Wakefulness-Promoting Agents: A specific category of drugs that prevent sleepiness by specifically targeting sleep-mechanisms in the brain. They are used to treat DISORDERS OF EXCESSIVE SOMNOLENCE such as NARCOLEPSY. Note that this drug category does not include broadly-acting central nervous system stimulants such as AMPHETAMINES.Receptors, Adrenergic, alpha-2: A subclass of alpha-adrenergic receptors found on both presynaptic and postsynaptic membranes where they signal through Gi-Go G-PROTEINS. While postsynaptic alpha-2 receptors play a traditional role in mediating the effects of ADRENERGIC AGONISTS, the subset of alpha-2 receptors found on presynaptic membranes signal the feedback inhibition of NEUROTRANSMITTER release.Fenofibrate: An antilipemic agent which reduces both CHOLESTEROL and TRIGLYCERIDES in the blood.PPAR alpha: A nuclear transcription factor. Heterodimerization with RETINOID X RECEPTOR GAMMA is important to metabolism of LIPIDS. It is the target of FIBRATES to control HYPERLIPIDEMIAS.Bezafibrate: An antilipemic agent that lowers CHOLESTEROL and TRIGLYCERIDES. It decreases LOW DENSITY LIPOPROTEINS and increases HIGH DENSITY LIPOPROTEINS.Receptors, Cytoplasmic and Nuclear: Intracellular receptors that can be found in the cytoplasm or in the nucleus. They bind to extracellular signaling molecules that migrate through or are transported across the CELL MEMBRANE. Many members of this class of receptors occur in the cytoplasm and are transported to the CELL NUCLEUS upon ligand-binding where they signal via DNA-binding and transcription regulation. Also included in this category are receptors found on INTRACELLULAR MEMBRANES that act via mechanisms similar to CELL SURFACE RECEPTORS.Hypolipidemic Agents: Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.Peroxisome Proliferators: A class of nongenotoxic CARCINOGENS that induce the production of hepatic PEROXISOMES and induce hepatic neoplasms after long-term administration.Propionates: Derivatives of propionic acid. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain the carboxyethane structure.Pyrimidines: A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (CYTOSINE; THYMINE; and URACIL) and form the basic structure of the barbiturates.Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.RNA, Messenger: RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.Dopamine Agonists: Drugs that bind to and activate dopamine receptors.alpha 1-Antitrypsin: Plasma glycoprotein member of the serpin superfamily which inhibits TRYPSIN; NEUTROPHIL ELASTASE; and other PROTEOLYTIC ENZYMES.Receptors, Adrenergic, alpha: One of the two major pharmacological subdivisions of adrenergic receptors that were originally defined by the relative potencies of various adrenergic compounds. The alpha receptors were initially described as excitatory receptors that post-junctionally stimulate SMOOTH MUSCLE contraction. However, further analysis has revealed a more complex picture involving several alpha receptor subtypes and their involvement in feedback regulation.GABA Agonists: Endogenous compounds and drugs that bind to and activate GAMMA-AMINOBUTYRIC ACID receptors (RECEPTORS, GABA).Hypoxia-Inducible Factor 1, alpha Subunit: Hypoxia-inducible factor 1, alpha subunit is a basic helix-loop-helix transcription factor that is regulated by OXYGEN availability and is targeted for degradation by VHL TUMOR SUPPRESSOR PROTEIN.Nicotinic Agonists: Drugs that bind to and activate nicotinic cholinergic receptors (RECEPTORS, NICOTINIC). Nicotinic agonists act at postganglionic nicotinic receptors, at neuroeffector junctions in the peripheral nervous system, and at nicotinic receptors in the central nervous system. Agents that function as neuromuscular depolarizing blocking agents are included here because they activate nicotinic receptors, although they are used clinically to block nicotinic transmission.Adrenergic alpha-2 Receptor Agonists: Compounds that bind to and activate ADRENERGIC ALPHA-2 RECEPTORS.Adrenergic alpha-Agonists: Drugs that selectively bind to and activate alpha adrenergic receptors.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Purinergic P1 Receptor Agonists: Compounds that bind to and stimulate PURINERGIC P1 RECEPTORS.Muscarinic Agonists: Drugs that bind to and activate muscarinic cholinergic receptors (RECEPTORS, MUSCARINIC). Muscarinic agonists are most commonly used when it is desirable to increase smooth muscle tone, especially in the GI tract, urinary bladder and the eye. They may also be used to reduce heart rate.Methyldopa: An alpha-2 adrenergic agonist that has both central and peripheral nervous system effects. Its primary clinical use is as an antihypertensive agent.Guanabenz: An alpha-2 selective adrenergic agonist used as an antihypertensive agent.Adrenergic Agonists: Drugs that bind to and activate adrenergic receptors.Clonidine: An imidazoline sympatholytic agent that stimulates ALPHA-2 ADRENERGIC RECEPTORS and central IMIDAZOLINE RECEPTORS. It is commonly used in the management of HYPERTENSION.Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.Platelet Membrane Glycoproteins: Surface glycoproteins on platelets which have a key role in hemostasis and thrombosis such as platelet adhesion and aggregation. Many of these are receptors.Platelet Aggregation: The attachment of PLATELETS to one another. This clumping together can be induced by a number of agents (e.g., THROMBIN; COLLAGEN) and is part of the mechanism leading to the formation of a THROMBUS.Drug Partial Agonism: Drug agonism involving selective binding but reduced effect. This can result in some degree of DRUG ANTAGONISM.Cell Membrane: The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.Receptors, Adrenergic, beta-2: A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-2 receptors are more sensitive to EPINEPHRINE than to NOREPINEPHRINE and have a high affinity for the agonist TERBUTALINE. They are widespread, with clinically important roles in SKELETAL MUSCLE; LIVER; and vascular, bronchial, gastrointestinal, and genitourinary SMOOTH MUSCLE.Spectrophotometry, Atomic: Spectrophotometric techniques by which the absorption or emmision spectra of radiation from atoms are produced and analyzed.Syringes: Instruments used for injecting or withdrawing fluids. (Stedman, 25th ed)Anesthesiology: A specialty concerned with the study of anesthetics and anesthesia.Masks: Devices that cover the nose and mouth to maintain aseptic conditions or to administer inhaled anesthetics or other gases. (UMDNS, 1999)Chromatography, Supercritical Fluid: A CHROMATOGRAPHY method using supercritical fluid, usually carbon dioxide under very high pressure (around 73 atmospheres or 1070 psi at room temperature) as the mobile phase. Other solvents are sometimes added as modifiers. This is used both for analytical (SFC) and extraction (SFE) purposes.Laryngeal Masks: A type of oropharyngeal airway that provides an alternative to endotracheal intubation and standard mask anesthesia in certain patients. It is introduced into the hypopharynx to form a seal around the larynx thus permitting spontaneous or positive pressure ventilation without penetration of the larynx or esophagus. It is used in place of a facemask in routine anesthesia. The advantages over standard mask anesthesia are better airway control, minimal anesthetic gas leakage, a secure airway during patient transport to the recovery area, and minimal postoperative problems.Nebulizers and Vaporizers: Devices that cause a liquid or solid to be converted into an aerosol (spray) or a vapor. It is used in drug administration by inhalation, humidification of ambient air, and in certain analytical instruments.Low Back Pain: Acute or chronic pain in the lumbar or sacral regions, which may be associated with musculo-ligamentous SPRAINS AND STRAINS; INTERVERTEBRAL DISK DISPLACEMENT; and other conditions.Back Pain: Acute or chronic pain located in the posterior regions of the THORAX; LUMBOSACRAL REGION; or the adjacent regions.Pain: An unpleasant sensation induced by noxious stimuli which are detected by NERVE ENDINGS of NOCICEPTIVE NEURONS.Heat Stress Disorders: A group of conditions that develop due to overexposure or overexertion in excessive environmental heat.Heat Exhaustion: A clinical syndrome caused by heat stress, such as over-exertion in a hot environment or excessive exposure to sun. It is characterized by SWEATING, water (volume) depletion, salt depletion, cool clammy skin, NAUSEA, and HEADACHE.Extreme Heat: High temperature weather exceeding the average and of several weeks duration. Extreme heat is a dangerous situation that can bring on health emergencies in susceptible people.Heat Stroke: A condition caused by the failure of body to dissipate heat in an excessively hot environment or during PHYSICAL EXERTION in a hot environment. Contrast to HEAT EXHAUSTION, the body temperature in heat stroke patient is dangerously high with red, hot skin accompanied by DELUSIONS; CONVULSIONS; or COMA. It can be a life-threatening emergency and is most common in infants and the elderly.Dehydration: The condition that results from excessive loss of water from a living organism.Athletes: Individuals who have developed skills, physical stamina and strength or participants in SPORTS or other physical activities.Agricultural Workers' Diseases: Diseases in persons engaged in cultivating and tilling soil, growing plants, harvesting crops, raising livestock, or otherwise engaged in husbandry and farming. The diseases are not restricted to farmers in the sense of those who perform conventional farm chores: the heading applies also to those engaged in the individual activities named above, as in those only gathering harvest or in those only dusting crops.

Modulation of long-term synaptic depression in visual cortex by acetylcholine and norepinephrine. (1/2158)

In a slice preparation of rat visual cortex, we discovered that paired-pulse stimulation (PPS) elicits a form of homosynaptic long-term depression (LTD) in the superficial layers when carbachol (CCh) or norepinephrine (NE) is applied concurrently. PPS by itself, or CCh and NE in the absence of synaptic stimulation, produced no lasting change. The LTD induced by PPS in the presence of NE or CCh is of comparable magnitude with that obtained with prolonged low-frequency stimulation (LFS) but requires far fewer stimulation pulses (40 vs 900). The cholinergic facilitation of LTD was blocked by atropine and pirenzepine, suggesting involvement of M1 receptors. The noradrenergic facilitation of LTD was blocked by urapidil and was mimicked by methoxamine, suggesting involvement of alpha1 receptors. beta receptor agonists and antagonists were without effect. Induction of LTD by PPS was inhibited by NMDA receptor blockers (completely in the case of NE; partially in the case of CCh), suggesting that one action of the modulators is to control the gain of NMDA receptor-dependent homosynaptic LTD in visual cortex. We propose that this is a mechanism by which cholinergic and noradrenergic inputs to the neocortex modulate naturally occurring receptive field plasticity.  (+info)

Modulation of basal intracellular calcium by inverse agonists and phorbol myristate acetate in rat-1 fibroblasts stably expressing alpha1d-adrenoceptors. (2/2158)

In rat-1 fibroblasts stably expressing alpha1d-adrenoceptors BMY 7378, phentolamine, chloroethylclonidine and 5-methyl urapidil decreased basal [Ca2+]i. WB 4101 induced a very small effect on this parameter but when added before the other antagonists it blocked their effect. All these agents inhibited the action of norepinephrine. Phorbol myristate acetate also blocked the effect of norepinephrine and decreased basal [Ca2+]i. Staurosporine inhibited these effects of the phorbol ester. Our results suggest that: (1) alpha1d-adrenoceptors exhibit spontaneous ligand-independent activity, (2) BMY 7378, phentolamine, chloroethylclonidine and 5-methyl urapidil act as inverse agonists and (3) protein kinase C activation blocks spontaneous and agonist-stimulated alpha1d-adrenoceptor activity.  (+info)

Uninjured C-fiber nociceptors develop spontaneous activity and alpha-adrenergic sensitivity following L6 spinal nerve ligation in monkey. (3/2158)

We investigated whether uninjured cutaneous C-fiber nociceptors in primates develop abnormal responses after partial denervation of the skin. Partial denervation was induced by tightly ligating spinal nerve L6 that innervates the dorsum of the foot. Using an in vitro skin-nerve preparation, we recorded from uninjured single afferent nerve fibers in the superficial peroneal nerve. Recordings were made from 32 C-fiber nociceptors 2-3 wk after ligation and from 29 C-fiber nociceptors in control animals. Phenylephrine, a selective alpha1-adrenergic agonist, and UK14304 (UK), a selective alpha2-adrenergic agonist, were applied to the receptive field for 5 min in increasing concentrations from 0.1 to 100 microM. Nociceptors from in vitro control experiments were not significantly different from nociceptors recorded by us previously in in vivo experiments. In comparison to in vitro control animals, the afferents found in lesioned animals had 1) a significantly higher incidence of spontaneous activity, 2) a significantly higher incidence of response to phenylephrine, and 3) a higher incidence of response to UK. In lesioned animals, the peak response to phenylephrine was significantly greater than to UK, and the mechanical threshold of phenylephrine-sensitive afferents was significantly lower than for phenylephrine-insensitive afferents. Staining with protein gene product 9.5 revealed an approximately 55% reduction in the number of unmyelinated terminals in the epidermis of the lesioned limb compared with the contralateral limb. Thus uninjured cutaneous C-fiber nociceptors that innervate skin partially denervated by ligation of a spinal nerve acquire two abnormal properties: spontaneous activity and alpha-adrenergic sensitivity. These abnormalities in nociceptor function may contribute to neuropathic pain.  (+info)

Homologous regulation of the alpha2C-adrenoceptor subtype in human hepatocarcinoma, HepG2. (4/2158)

1. Previous studies of the regulation of the alpha2C-adrenoceptor in OK and in transfected cells have led to discrepant conclusions. In the present work, we examined the homologous regulation of the human alpha2C-adrenoceptor in the hepatocarcinoma cell-line, HepG2; a model which expresses this subtype spontaneously. 2. Short-period treatment of the cells with UK14304 provoked neither a diminution of the potency of the alpha2-agonist to inhibit forskolin-induced cyclic AMP-accumulation nor a change in the degree of receptor coupling to G-proteins. 3. Long-period exposure to UK14304 resulted in a large reduction of [3H]MK912 binding sites (55% decrease). The action of UK14304 was dose-dependent (EC50 = 190 +/- 45 nM), rapid (t1/2 = 4.2 h) and reversible. Receptor down-regulation was also observed with clonidine or (-)adrenaline (38 and 36% decrease, respectively) and was blocked by the addition of alpha2-antagonists. 4. Conversely to that observed with alpha2-agonists, treatment of the cells with RX821002 or yohimbine alone, but not with phentolamine, promoted a significant increase of the receptor expression. 5. The observed alterations of receptor density are not the reflection of changes at the alpha2C4 mRNA level. Estimation of the receptor protein turnover and measurement of its half-life demonstrated that down-regulation by alpha2-agonists and up-regulation by alpha2-antagonists, with inverse-agonist efficacy, are respectively the consequence of increased and decreased rate of receptor degradation. 6. In conclusion, our data show that alpha2C-adrenoceptor does not undergo desensitization but is down-regulated in HepG2. The lack of desensitization agrees with previous results obtained in cells transfected with the alpha2C4 gene, but not with observations made in OK cells. Inversely, down-regulation fits with results obtained in OK but not in transfected cells. The reasons for these discrepancies are discussed. Our results also demonstrated that certain alpha2-antagonists behave as inverse agonist on the HepG2 model and thus provide for the first time evidence of inverse efficacy of antagonists on a cellular model expressing physiological level of a wild-type alpha2-adrenoceptor.  (+info)

Effects of heptanol on the neurogenic and myogenic contractions of the guinea-pig vas deferens. (5/2158)

1. The effects of the putative gap junction uncoupler, 1-heptanol, on the neurogenic and myogenic contractile responses of guinea-pig vas deferens were studied in vitro. 2. Superfusion of 2.0 mM heptanol for 20-30 min produced the following reversible changes in the biphasic neurogenic contractile response (8 trials): (i) suppression of both phases; (ii) delayed development of both the first as well as the second phase, accompanied by complete temporal separation of the two phases; (iii) prominent oscillations of force during the second (noradrenergic) phase only. 3. To eliminate prejunctional effects of heptanol, myogenic contractions were evoked by field stimulation of the vas in the presence of suramin (200 microM) and prazosin (1 microM). Heptanol (2.0 mM) abolished these contractions reversibly. 4. These results show that (i) heptanol inhibits both excitatory junction potential (EJP)-dependent and non EJP-dependent contractions of the vas; (ii) a postjunctional site of action of heptanol, probably intercellular uncoupling of smooth muscle cells, contributes to the inhibition of contraction.  (+info)

alpha1-Adrenergic stimulation of FGF-2 promoter in cardiac myocytes and in adult transgenic mouse hearts. (6/2158)

Fibroblast growth factor (FGF-2), a mitogenic, angiogenic, and cardioprotective agent, is reported to be released from the postnatal heart by a mechanism of transient remodeling of the sarcolemma during contraction. This release can be increased with adrenergic stimulation. RNA blotting was used to assess whether FGF-2 synthesis in neonatal rat cardiomyocytes might also be regulated by adrenergic stimulation. FGF-2 RNA levels were increased after treatment with norepinephrine for 6 h or with the alpha-adrenergic agonist phenylephrine for 48 h. To assess an effect on transcription, neonatal rat cardiomyocytes were transfected with a hybrid rat FGF-2 promoter/luciferase gene (-1058FGFp.luc) and treated with norepinephrine or phenylephrine for 6 or 48 h, respectively. FGF-2 promoter activity was increased two- to sevenfold in an alpha1-specific manner. Putative phenylephrine-responsive elements (PEREs) were identified at positions -780 and -761 relative to a major transcription initiation site. However, deletion analysis of -1058FGFp.luc showed that the phenylephrine response was independent of the putative PEREs, cell contraction, and Ca2+ influx. In transgenic mice expressing -1058FGFp.luc, a significant three- to sevenfold stimulation of FGF-2 promoter activity was detected in the hearts of two independent lines 6 h after intraperitoneal administration of phenylephrine (50 mg/kg). This increase was still apparent at 24 h but was not detected at 48 h posttreatment. Analysis of FGF-2 mRNA in normal mouse hearts revealed accumulation of the 6.1-kb transcript at 24 h. Control of local FGF-2 synthesis at the transcriptional level through adrenergic stimulation may be important in the response to injury as well as in the maintenance of a healthy myocardium.  (+info)

Endothelin antagonists block alpha1-adrenergic constriction of coronary arterioles. (7/2158)

We have previously observed that intracoronary administration of the alpha1-adrenergic agonist phenylephrine (PE) over a period of minutes induced both an immediate and long-lasting (2 h) vasoconstriction of epicardial coronary arterioles. Because it is unlikely that alpha1-adrenergic constriction would persist for hours after removal of the agonist, this observation supports the view that another constrictor(s) is released during alpha1-adrenergic activation and induces the prolonged vasoconstriction. Therefore, we hypothesized that the prolonged microvascular constriction after PE is due to the production of endothelin (ET). We focused on ET not only because this peptide produces potent vasoconstriction but also because its vasoconstrictor action is characterized by a long duration. To test this hypothesis, the diameters of coronary arterioles (<222 micrometers) in the beating heart of pentobarbital-anesthetized dogs with stroboscopic intravital microscopy were measured during a 15-min intracoronary infusion of PE (1 microgram. kg-1 . min-1) and at 15-min intervals for a total of 120 min. All experiments were performed in the presence of beta-adrenergic blockade with propranolol. At 120 min, arterioles in the PE group were constricted (-23 +/- 9% change in diameter vs. baseline). Pretreatment with the ET-converting enzyme inhibitor phosphoramidon or the ETA-receptor antagonist FR-139317 prevented the PE-induced constriction at 120 min (-1 +/- 3 and -6 +/- 3%, respectively, P < 0.01 vs. PE). Pretreatment with the selective alpha1-adrenergic antagonist prazosin (Prz) also prevented the sustained constriction (0 +/- 2%, P < 0.01 vs. PE) but Prz given 60 min after PE infusion did not (-13 +/- 3%). In the aggregate, these results show that vasoconstriction of epicardial coronary arterioles via alpha1-adrenergic activation is blocked by an ET antagonist and an inhibitor of its production. From these data, we conclude that alpha1-adrenergic activation promotes the production and/or release of ET, which produces or facilitates microvascular constriction of epicardial canine coronary arterioles.  (+info)

Effect of bolus epinephrine on systemic hemodynamics in canine anaphylactic shock. (8/2158)

OBJECTIVE: Epinephrine (Epi) is considered to be the drug of choice for anaphylactic shock (AS). However, the benefit of this drug on improving systemic hemodynamics in AS has never been shown. We used a canine ragweed model of AS to determine if an intravenous bolus of Epi hastened the recovery of hemodynamics and modified mediator release (Med) compared with no treatment (NT). METHODS: In one protocol (n = 8), the effects on hemodynamics of two intravenous doses of Epi (0.01 and 0.025 mg/kg) were examined for 3 h postshock in respective studies approximately three weeks apart under pentobarbital anesthesia in the same animal. In five other dogs, left ventricular (LV) mechanics were additionally determined by sonomicrometric techniques to determine changes in contractility as defined by the preload recruitable stroke-work (SW) relationship. RESULTS: Compared with NT values, Epi treatments produced only transient increases in mean arterial pressure (MAP) and cardiac output (CO) post-challenge. By 20 min postshock, CO in the Epi studies were generally lower (p < 0.05) and BP was not different from NT values. With Epi treatment, SW was reduced for a given LV end-diastolic volume compared with the control study. Epi treatments also caused relatively higher plasma thromboxane B2 concentrations postshock. CONCLUSION: Our findings indicate that, when given immediately postshock, bolus-Epi did not hasten recovery and caused impairment in LV mechanics in canine AS.  (+info)

Removal of endothelial cells on rings of rat aorta increased the sensitivity to the selective alpha-1 adrenoceptor agonist phenylephrine, to the nonselective alpha adrenoceptor agonist norepinephrine and to the selective alpha-2 adrenoceptor agonist clonidine. In the case of the first two, which are strong agonists for the alpha-1 adrenoceptor-mediating contraction, removal of endothelium increased sensitivity 4- and 6-fold at the EC30 level, but produced little or no increase in maximum. In the case of clonidine, a partial agonist for the alpha-1 adrenoceptor, which gave only about 15% of the maximum given by phenylephrine on endothelium-containing rings, removal of the endothelium not only shifted the curve to the left but also increased the maximum to about 50% of that given by phenylephrine. The depression of sensitivity to these agonists in rings with endothelium appeared to be due to the vasodepressor action of endothelium-derived relaxing factor (EDRF), as hemoglobin, a specific blocking ...
Ample experimental evidence supports the existence of two distinct types of vasoconstrictor α-adrenoceptors in vascular smooth muscle at postjunctional sites, showing similarities with α1 and α2-adrenoceptors. Especially in vivo, the characterization of an α2-adrenoceptor mediating an increase in diastolic pressure has been most successful. In this respect the model of the pithed rat has been employed most frequently (for reviews see [1, 2]).. At present, the agents cirazoline, (−) phenylephrine, (±)-erythro-methoxamine, (−)-amidephrine, SKF89748, St587 and Sgd 101/75 fulfil the criteria for selective α1-adrenoceptor agonists; their log dose-vasopressor effect curves are virtually unaffected by previous treatment with yohimbine or rauwolscine (selective dose in pithed rats: 1 mg/kg), whereas prazosin (selective dose in pithed rats: 0.1 mg/kg) causes an appreciable parallel rightward displacement. The reverse holds true for the stimulants B-HT 920, B-HT 933, B-HT 958, UK-14304, ...
Amibegron, a highly selective β3-adrenoceptor agonist originated by Sanofi (now sanofi-aventis), stimulates neuronal activity in a specific area of the
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TY - JOUR. T1 - Cooling and α1- and α2-adrenergic responses in cutaneous veins. T2 - Role of receptor reserve. AU - Flavahan, Nicholas. AU - Lindblad, L. E.. AU - Verbeuren, T. J.. PY - 1985. Y1 - 1985. N2 - Experiments were designed to determine the effects of cooling on α1- and α2-adrenergic responses in isolated canine cutaneous veins. Rings of saphenous veins were suspended for isometric tension recording in physiological salt solution. Cooling (from 37 to 24°C) augmented contractions to norepinephrine under control conditions and after α1-adrenergic blockade (prazosin) but not following α2-adrenergic blockade (rauwolscine). Cooling augmented contractions evoked by the α2-adrenergic agonists B-HT 920 and UK 14304 but did not affect responses to the full α1-adrenergic agonist phenylephrine. These experiments suggest that cooling augments α2-adrenergic responsiveness without affecting α1-adrenergic responsiveness. However, the contractions evoked by the partial α1-adrenergic ...
Tablet. Patients who engage in potentially hazardous activities, such as operating machinery or driving, should be advised of a potential sedative effect of clonidine. Patients should be cautioned against interruption of clonidine hydrochloride therapy without a physicians advice.. Epidural Injection. Patients should be instructed about the risks of rebound hypertension and warned not to discontinue clonidine except under the supervision of a physician. Patients should notify their physician immediately if clonidine administration is inadvertently interrupted for any reason. Patients who engage in potentially hazardous activities, such as operating machinery or driving, should be advised of the potential sedative and hypotensive effects of epidural clonidine. They should also be informed that sedative effects may be increased by CNS-depressing drugs such as alcohol and barbiturates, and that hypotensive effects may be increased by opiates.. ...
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1. Earlier studies have shown that exposure of fat-cells to insulin results in the rapid increased phosphorylation of an acid-soluble 22 kDa protein and that increases in phosphorylation were also evident in cells exposed to adrenaline [Belsham & Denton (1980) Biochem. Soc. Trans. 8, 382-383; Belsham, Brownsey, Hughes & Denton (1980) Diabetologia 18, 307-312]. 2. The effects of adrenaline are shown to be brought about through beta-adrenergic receptors and to be mimicked by other agents which increase cell cyclic AMP concentrations. The maximum extent of phosphorylation is about 60% of that observed with insulin. Increased phosphorylation is also observed in fat-cells exposed to vasopressin, oxytocin and phorbol esters, but not to alpha-adrenergic agonists. 3. No changes in the phosphorylation of the protein are evident in epididymal fat-pads from fat-fed, starved or starved/refed animals, despite the large changes in protein composition of fat-cells which accompany these nutritional alterations. ...
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Phenylephrine is a selective ?1-adrenergic receptor agonist used primarily as a decongestant, as an agent to dilate the pupil, and to increase blood...
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Alpha-2 adrenergic receptor agonistsEdit. Central alpha agonists lower blood pressure by stimulating alpha-receptors in the ... Heart failure may be worsened with nondihydropyridine calcium channel blockers, the alpha blocker doxazosin, and the alpha-2 ... an alpha-adrenergic receptor blocker, had a higher incidence of heart failure events, and the doxazosin arm of the study was ... Central alpha agonists, such as clonidine, are usually prescribed when all other anti-hypertensive medications have failed. For ...
Alpha-adrenergic agonists are the first treatment of choice. They relieve congestion by constricting the blood vessels in the ...
... is an alpha-adrenergic agonist. Fox K, Dargie HJ, de Bono DP, Oliver MF, Wülfert E, Kharkevitch T (September 1999). " ... "Effect of an alpha(2) agonist (mivazerol) on limiting myocardial ischaemia in stable angina". Heart. 82 (3): 383-5. doi:10.1136 ...
Important vasoactive substances are angiotensin-11, endothelin-1, and alpha-adrenergic agonists. Various vasoactive agents, ...
Alpha-adrenergic agonists work by decreasing production of fluid and increasing drainage. Brimonidine and Apraclonidine are two ... less selective alpha agonists such as [epinephrine] may decrease the production of aqueous humor through vasoconstriction of ... commonly prescribes alpha agonists for glaucoma treatment. Alphagan P uses a purite preservative, which is better tolerated ...
... is in the alpha-2 adrenergic receptor agonist family of medication. It works by stimulating the brain to decrease ... α-methylnorepinephrine is an agonist of presynaptic central nervous system α2 adrenergic receptors. Activation of these ... with increased use of other safer and more tolerable agents such as alpha blockers, beta blockers, and calcium channel blockers ... This inhibition results in reduced dopaminergic and adrenergic neurotransmission in the peripheral nervous system. This effect ...
Medications used include stimulants, atomoxetine, alpha-2 adrenergic receptor agonists, and sometimes antidepressants. In those ...
Alpha-adrenergic agonists may cause urinary retention by stimulating the contraction of the urethral sphincter. Calcium channel ...
"Quantitative relationships between alpha-adrenergic activity and binding affinity of alpha-adrenoceptor agonists and ... "Electrophysiologic and Hemodynamic Effects of Chronic Oral Therapy With the Alpha 2-agonists Clonidine and Tiamenidine in ... It acts as a centrally-acting α1 and α2 adrenergic receptor antagonist (with IC50 4.85 μM and 0.0091 μM, respectively). In ...
Adverse effects in mammals are caused by amitraz' alpha-adrenergic agonist activity. Symptoms can include low blood pressure ... Its effectiveness is traced back on alpha-adrenergic agonist activity, interaction with octopamine receptors of the central ...
... is in the decongestant and alpha-adrenergic agonist families of medication. Xylometazoline was patented in 1956 ... It binds to α1 and α2 adrenergic receptors in the nasal mucosa. Due to its sympathomimetic effects, it should not be used by ... The drug works by stimulating adrenergic receptors on the lamina propria of blood vessels in the nose. The decongestant effect ... Haenisch, B.; Walstab, J.; Herberhold, S.; Bootz, F.; Tschaikin, M.; Ramseger, R.; Bönisch, H. (2009). "Alpha-adrenoceptor ...
It is an α1-blocker which acts as an inverse agonist at alpha-1 adrenergic receptors. These receptors are found on vascular ... Day, H. E.; Campeau, S.; Watson Jr, S. J.; Akil, H. (1997). "Distribution of alpha 1a-, alpha 1b- and alpha 1d-adrenergic ... A larger controlled Phase II "Clinical Trial of the Adrenergic Alpha-1 Antagonist Prazosin for Alcohol Dependence" is currently ... "A pilot trial of the alpha-1 adrenergic antagonist, prazosin, for alcohol dependence". Alcoholism: Clinical and Experimental ...
... is a partial agonist/antagonist on serotonergic, dopaminergic and alpha-adrenergic receptors. Its specific ... dopaminergic and adrenergic receptors". In Vladimír Křen,Ladislav Cvak. Ergot: the genus Claviceps. CRC Press. pp. 411-440. ... which is also an agonist at the 5HT2A-mGlu2 receptor protomer and increases the chances of a patient experiencing ...
"Simultaneous treatment of hypertension and opiate withdrawal using an alpha 2 adrenergic agonist" (PDF). J Natl Med Assoc. 75: ... Hydromorphone is a semi-synthetic μ-opioid agonist. As a hydrogenated ketone of morphine, it shares the pharmacologic ...
Another countermeasure includes administration of Midodrine, which is a selective alpha-1 adrenergic agonist. Midodrine ... The use of beta-2 adrenergic agonists to increase muscle mass, and the use of essential amino acids in conjunction with ...
Alpha-adrenergic agonist medications, such as decongestants with pseudoephedrine can increase bladder outlet resistance. In ... Effects may take longer to appear than alpha blockers, but they persist for many years. When used together with alpha blockers ... As men age, the enzymes aromatase and 5-alpha reductase increase in activity. Aromatase and 5-alpha reductase are responsible ... Alpha blockers relax smooth muscle in the prostate and the bladder neck, thus decreasing the blockage of urine flow. Common ...
... s must not be used in the treatment of selective alpha-adrenergic agonist overdose. The blockade of only beta ... β1-adrenergic receptors are located mainly in the heart and in the kidneys. β2-adrenergic receptors are located mainly in the ... Newer, third-generation beta blockers can cause vasodilation through blockade of alpha-adrenergic receptors. Accordingly, ... These agents are capable of exerting low-level agonist activity at the β-adrenergic receptor while simultaneously acting as a ...
... is a transcriptional activator in alpha 1-adrenergic agonist-stimulated cardiac myocytes". The Journal of Biological Chemistry ...
... is a potent sedative drug which acts as a selective alpha-2 adrenergic agonist. It is closely related to dexmedetomidine ... ethyl-1H-imidazoles on alpha 1- and alpha 2-adrenergic receptors". Journal of Medicinal Chemistry. 37 (15): 2328-33. doi: ... Like other alpha-2 agonists, it produces sedative and muscle relaxant effects but without producing respiratory depression. It ... "Medetomidine analogs as alpha 2-adrenergic ligands. 3. Synthesis and biological evaluation of a new series of medetomidine ...
It was found to be an active Alpha-1 adrenergic receptor agonist in rabbit ear arteries. It has binding affinity towards 5-HT2C ... Very little data exists about the pharmacological properties, metabolism, and toxicity of 2C-H. It exhibits agonist activity at ...
... a selective alpha-2 adrenergic receptor agonist, and timolol, a non-selective beta-adrenergic receptor inhibitor. Elevated IOP ... It is a combination of brimonidine (an α2 adrenergic agonist) and timolol (a β adrenergic blocker), in concentrations of 0.2% ...
It is an alpha-2 adrenergic agonist that causes sedation and does have some analgesic properties. It has minimal effect on ...
doi:10.1111/j.1365-2125.1983.tb00311.x. PMC 1427667 . Arnsten AF (October 2010), "The use of α2A adrenergic agonists for the ... Belkin, MR; Schwartz, TL (2015). "Alpha-2 receptor agonists for the treatment of posttraumatic stress disorder". Drugs in ... Guanfacine is a highly selective agonist of the α2A adrenergic receptor, with negligible affinity for any other receptor. ... Adrenergic Receptor Agonist For Attention-Deficit/Hyperactivity Disorder". P & T : a peer-reviewed journal for formulary ...
Drugs that work to suppress NAN include anticholinergics, benzodiazepines, barbiturates and agonists at the alpha-2 adrenergic ... Conversely, coadministration of NMDA-antagonists with alpha-2 adrenergic antagonists, like yohimbine could theoretically ...
"Beta-3 Adrenergic Agonist, BRL-26830A, and Alpha/Beta Blocker, Arotinolol, Markedly Increase Regional Blood Flow in the Brown ... "Arotinolol is a weak partial agonist on beta 3-adrenergic receptors in brown adipocytes". Can J Physiol Pharmacol. 79 (7): 585- ... Arotinolol (INN, marketed under the tradename Almarl) is a medication in the class of mixed alpha/beta blockers. It also acts ... "β-adrenergic blocking, antiarrhythmic compound S-596". It is used in the treatment of high blood pressure and essential tremor ...
"Inhibition of the lipolytic action of beta-adrenergic agonists in human adipocytes by alpha-adrenergic agonists". J. Lipid Res. ... Khan ZP, Ferguson CN, Jones RM (1999). "alpha-2 and imidazoline receptor agonists. Their pharmacology and therapeutic role". ... Elliott J (1997). "Alpha-adrenoceptors in equine digital veins: evidence for the presence of both α1 and α2-receptors mediating ... 11,0 11,1 Haenisch B, Walstab J, Herberhold S, Bootz F, Tschaikin M, Ramseger R, Bönisch H. (2010). "Alpha-adrenoceptor ...
An adrenergic alpha-agonist (or alpha-adrenergic agonists) are a class of sympathomimetic agents that selectively stimulates ... Alpha blocker Adrenergic agonist Beta-adrenergic agonist Declerck I, Himpens B, Droogmans G, Casteels R (September 1990). "The ... α Adrenergic agonists have the opposite function of alpha blockers. Alpha adrenoreceptor ligands mimic the action of ... alpha adrenergic receptors. The alpha-adrenergic receptor has two subclasses α1 and α2. Alpha 2 receptors are associated with ...
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Alpha/Beta Adrenergic Agonists. Class Summary. These agents augment coronary and cerebral blood flow during the low-flow states ... It has alpha-agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, ... Jorge A Martinez, MD, JD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency ... Suzanne White, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Clinical Toxicology, ...
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... , Central Adrenergic Agonist, Methyl-Dopa, Methyldopa, Aldomet, Guanabenz, Wytensin. ... Alpha Adrenergic Central Agonist. Aka: Alpha Adrenergic Central Agonist, Central Adrenergic Agonist, Methyl-Dopa, Methyldopa, ... Central alpha-adrenocep agon., Central alpha-adrenoceptor agonist, Central alpha-adrenoceptor agonist (product), Central alpha- ... which is a potent alpha-2 adrenergic agonist that binds to and stimulates potent central inhibitory alpha-2 adrenergic ...
Alpha2 adrenergic agonists for the management. of opioid withdrawal (Cochrane Review) by. Gowing L, Farrell M, Ali R, White J. ... Ten studies compared a treatment regime based on an alpha2 adrenergic agonist with one based on reducing doses of methadone. ... From the comparison of alpha2 adrenergic agonist regimes with reducing doses of methadone, withdrawal intensity is similar to, ... REVIEWERS CONCLUSIONS: Treatment regimes based on the alpha2 adrenergic agonists clonidine and lofexidine, and those based on ...
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... and alpha 2-adrenoceptors. This class of agents has been shown to have potent and selective agonist activity at the alpha 2- ... imidazoles was synthesized and evaluated for activity at alpha 1- ... Synthesis and evaluation of 2-(arylamino)imidazoles as alpha 2-adrenergic agonists J Med Chem. 1997 Jan 3;40(1):18-23. doi: ... and alpha 2-adrenoceptors. This class of agents has been shown to have potent and selective agonist activity at the alpha 2- ...
Alpha-adrenergic agonists were more efficacious than placebo in the management of opioid withdrawal, but are best reserved as ... ALPHA-ADRENERGIC AGONISTS FOR THE MANAGEMENT OF OPIOID WITHDRAWAL. Benefits. Harms. NNT = 3 to prevent one episode of severe ... ALPHA-ADRENERGIC AGONISTS FOR THE MANAGEMENT OF OPIOID WITHDRAWAL. Benefits. Harms. NNT = 3 to prevent one episode of severe ... Alpha2-adrenergic agonists for the management of opioid withdrawal. Cochrane Database Syst Rev. 2016;(5):CD002024. ...
0/Adrenergic alpha-Agonists; 0/Iodine Radioisotopes; 0/Receptors, Adrenergic, alpha; 108294-53-7/4-iodoclonidine; 146-48-5/ ... 125I]PIC bound to the same number of high affinity sites as the alpha 2-adrenergic receptor (alpha 2-AR) full agonist [3H] ... Adrenergic alpha-Agonists / pharmacokinetics*. Blood Platelets / metabolism*. Cell Membrane / metabolism. Chromatography, Thin ... 8267204 - Methylprednisolone increases sensitivity to beta-adrenergic agonists within 48 hours in.... 6147954 - Adrenergic ...
Selective aortic arch perfusion using perfluorochemical and alpha adrenergic agonist to treat cardiac arrest ... 5. A method according to claim 1, wherein said alpha adrenergic receptor agonist is selected from the group consisting of ... administering said subject an alpha adrenergic receptor agonist in an amount effective to enhance coronary perfusion with said ... and other alpha adrenergic receptor agonists. Epinephrine is currently preferred. Vasoconstrictors may be administered by any ...
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Clonidine is classified as a centrally acting alpha adrenergic agonist.Clonidine acts centrally as an imidazoline receptor ... Clonidine hydrochloride Alpha adrenergic agonist Clonidine is classified as a centrally acting alpha adrenergic agonist. ... Clonidine is classified as a centrally acting alpha adrenergic agonist.Clonidine acts centrally as an imidazoline receptor ... Clonidine is classified as a centrally acting alpha adrenergic agonist.Clonidine acts centrally as an imidazoline receptor ...
... a new alpha 2-adrenergic agonist, blunts cardiovascular effects following surgical stress in pentobarbital-anesthetized rats ... Mivazerol, a new alpha 2-adrenergic agonist, blunts cardiovascular effects following surgical stress in pentobarbital- ... Mivazerol is a new and selective alpha 2-adrenoceptor agonist, devoid of hypotensive effects, which has been designed to ... Pretreatment with the alpha 2-adrenoceptor antagonist rauwolscine (0.5 mg/kg, i.v.) blocked the bradycardia induced by ...
Central Alpha-Agonist Agents, Alpha-Adrenergic Receptor Blockers, Direct Vasodilators, and Exogenous Nitric Oxide Donors. ... Central Alpha-Agonist Agents, Alpha-Adrenergic Receptor Blockers, Direct Vasodilators, and Exogenous Nitric Oxide Donors", ... Central Alpha-Agonist Agents, Alpha-Adrenergic Receptor Blockers, Direct Vasodilators, and Exogenous Nitric Oxide Donors ... alpha blockers, direct vasodilating agents, and exogenous nitric oxide donors. These antihypertensive drugs are considered as ...
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239000000464 Adrenergic Agents Substances 0 description 1 * 239000000695 Adrenergic alpha-Agonists Substances 0 claims ... Selective aortic arch perfusion using perfluorochemical and alpha adrenergic agonist to treat cardiac arrest Download PDF Info ... 5. A method according to claim 1, wherein said alpha adrenergic receptor agonist is selected from the group consisting of ... US07/769,132 1991-09-30 1991-09-30 Selective aortic arch perfusion using perfluorochemical and alpha adrenergic agonist to ...
6.2.7. Alpha2 adrenergic agonists. Alpha2 adrenergic agonists (such as clonidine and lofexidine) act to reduce the ... Alpha2 adrenergic agonists. The evidence for alpha2 adrenergic agonists is described in 6.2.7. ... alpha2 adrenergic agonists) to manage withdrawal symptoms.. Opioid agonists. All opioids, including heroin and methadone, are ... in addition to their opioid agonist reducing regimen or in addition to an adjunctive alpha-2 adrenergic agonist (for example, ...
Learn about Alpha-2-Adrenergic Agonists, see related evidence, and find other smart treatments for Back Pain at FoundHealth. ... Alpha-2-Adrenergic Agonists can be effective in treating Back Pain. ... Effect of Alpha-2-Adrenergic Agonists on Back Pain , Treatments Tried or prescribed Alpha-2-Adrenergic Agonists for Back Pain? ... Effect of Alpha-2-Adrenergic Agonists on Back Pain. There are alpha-2-Adrenergic Agonists that have shown to to relieve pain, ...
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Midodrine is a prodrug, i.e., the therapeutic effect of orally administered midodrine is due to the major metabolite desglymidodrine formed by deglycination of midodrine. Desglymidodrine diffuses poorly across the blood-brain barrier, and is therefore not associated with effects on the central nervous system. Administration of midodrine results in a rise in standing, sitting, and supine systolic and diastolic blood pressure in patients with orthostatic hypotension of various etiologies. Standing systolic blood pressure is elevated by approximately 15 to 30 mmHg at 1 hour after a 10-mg dose of midodrine, with some effect persisting for 2 to 3 hours. Midodrine has no clinically significant effect on standing or supine pulse rates in patients with autonomic failure ...
Dexmedetomidine activates 2-adrenoceptors, and causes the decrease of sympathetic tone, with attenuation of the neuroendocrine and hemodynamic responses to anesthesia and surgery; it reduces anesthetic and opioid requirements; and causes sedation and analgesia ...
Find your preferred Alpha-Adrenergic Agonists right here. ... Largest database of Alpha-Adrenergic Agonists listed for your ... Home - Human - Miscellaneous Central Nervous System Agents - Alpha-Adrenergic Agonists - Alpha- and Beta-Adrenergic Agonists ... Alpha- and Beta-Adrenergic Agonists (5167)*Alpha-Adrenergic Agonists (250). *Central Alpha-Agonists (203) ... Non-Selective Beta-Adrenergic Agonists (57). *Sympatholytic Adrenergic Blocking Agents (220). *Alpha-Adrenergic Blocking Agents ...
... alpha 1 receptors. Agonists induce the formation of a guanine nucleotide-sensitive high-affinity state of alpha 2 but not alpha ... Agonist versus antagonist binding to alpha-adrenergic receptors. Proceedings of the National Academy of Sciences of the United ... The binding properties of two alpha-adrenergic radioligands, [3H]epinephrine (an agonist) and [3H]dihydroergocryptine (an ... However, in the liver, alpha-adrenergic effects such as glycogen phosphorylase activation are shown to be mediated via alpha 1 ...
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  • We found that the α 2A -AR agonist guanfacine selectively inhibited this PBN input to the BNST, preferentially reducing the excitatory response in ex vivo mouse brain slices. (jneurosci.org)
  • Furthermore, we addressed whether guanfacine, an α 2 -adrenergic agonist that reduces stress-triggered maladaptive behavioral responses to drugs of abuse, could relief from SDPS-induced anhedonia. (frontiersin.org)
  • The binding properties of two alpha-adrenergic radioligands, [3H]epinephrine (an agonist) and [3H]dihydroergocryptine (an antagonist), were compared in two model systems--membranes derived from human platelets and membranes from rat liver. (meta.org)
  • Beta-adrenergic blockers have yellow or blue bottle caps. (visionaware.org)
  • Apart from the well-known angioedema/urticaria from ACE inhibitors, lichen planus / lichenoid reaction from beta adrenergic blockers and photosensitivity from thiazid diuretics, ACDR from CV drugs might be seen in a wide spectrum extending to rare but life-threatening conditions such as erythroderma, Stevens-Johnson syndrome, toxic epidermal necrolysis or drug hypersensitivity syndrome. (springer.com)
  • SELECTION CRITERIA: Randomised or quasi-randomised controlled trials that compared alpha2 adrenergic agonists with another form of treatment (or placebo) to modify the signs and symptoms of withdrawal in participants who were primarily opioid dependent. (opioids.com)
  • in the presence of high levels of an opioid agonist, it behaves like an antagonist. (nih.gov)
  • A better understanding of which excitatory inputs to the BNST are selectively modulated by α 2A -ARs may help elucidate neural circuitry underlying the ability of α 2 -AR agonists to block stress-induced reinstatement of drug-seeking in rodent models. (jneurosci.org)
  • 1 Several factors (drug prescribing regulations, dislike for the prolonged nature of methadone withdrawal, and desire to find alternatives for opiate treatment) led to the investigation of alpha-adrenergic agonists (AAAs) to decrease the severity of withdrawal symptoms. (aafp.org)
  • Low doses of α-adrenergic agonists constrict veins and may often shift blood from the Vu to the Vs, subsequently increasing the venous return and cardiac output, whereas higher drug doses constrict arteries and usually decrease cardiac output. (springer.com)
  • The sedative effects of the α 2 - adrenergic agonists is mainly attributed to its capacity to reduce the activity of noradrenergic neurons of Locus coeruleus ( LC) on the pons and lower brainstem and thus to diminish activity of the noradrenergic activator projections ascending towards superior cerebral structures. (vin.com)
  • Injection of either alpha 2 agonist resulted in respiratory arrhythmias with a greater than seven-fold increase in TE and a 30% reduction in TI. (mcw.edu)
  • The investigators intend to determine the effect of adrenergic blockade on 1) short-term physiology, behavior, and cognition and 2) long-term neuropsychological outcomes after severe Traumatic Brain Injury (TBI). (clinicaltrials.gov)
  • The primary hypothesis is that adrenergic blockade after severe TBI will be associated with increased ventilator-free days. (clinicaltrials.gov)
  • The purpose of this study was to test the hypothesis that respiratory and apneas induced by alpha 2 agonists in anesthetized goats are associated with an increase of upper airway expiratory-related activity, rather than a general depression of breathing. (mcw.edu)