A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.
Drugs that bind to but do not activate beta-adrenergic receptors thereby blocking the actions of beta-adrenergic agonists. Adrenergic beta-antagonists are used for treatment of hypertension, cardiac arrhythmias, angina pectoris, glaucoma, migraine headaches, and anxiety.
A beta-1 adrenergic antagonist that has been used in the emergency treatment of CARDIAC ARRYTHMIAS.
AMINO ALCOHOLS containing the propanolamine (NH2CH2CHOHCH2) group and its derivatives.
A nonselective alpha-adrenergic antagonist. It is used in the treatment of hypertension and hypertensive emergencies, pheochromocytoma, vasospasm of RAYNAUD DISEASE and frostbite, clonidine withdrawal syndrome, impotence, and peripheral vascular disease.
Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.
One of two major pharmacologically defined classes of adrenergic receptors. The beta adrenergic receptors play an important role in regulating CARDIAC MUSCLE contraction, SMOOTH MUSCLE relaxation, and GLYCOGENOLYSIS.
The number of times the HEART VENTRICLES contract per unit of time, usually per minute.
A non-selective beta-adrenergic antagonist with a long half-life, used in cardiovascular disease to treat arrhythmias, angina pectoris, and hypertension. Nadolol is also used for MIGRAINE DISORDERS and for tremor.
A cardioselective beta-1 adrenergic blocker possessing properties and potency similar to PROPRANOLOL, but without a negative inotropic effect.
A moderately lipophilic beta blocker (ADRENERGIC BETA-ANTAGONISTS). It is non-cardioselective and has intrinsic sympathomimetic actions, but little membrane-stabilizing activity. (From Martindale, The Extra Pharmocopoeia, 30th ed, p638)
A cardioselective beta-1 adrenergic antagonist with little effect on the bronchial receptors. The drug has stabilizing and quinidine-like effects on cardiac rhythm, as well as weak inherent sympathomimetic action.
Cell-surface proteins that bind epinephrine and/or norepinephrine with high affinity and trigger intracellular changes. The two major classes of adrenergic receptors, alpha and beta, were originally discriminated based on their cellular actions but now are distinguished by their relative affinity for characteristic synthetic ligands. Adrenergic receptors may also be classified according to the subtypes of G-proteins with which they bind; this scheme does not respect the alpha-beta distinction.
Drugs that inhibit the actions of the sympathetic nervous system by any mechanism. The most common of these are the ADRENERGIC ANTAGONISTS and drugs that deplete norepinephrine or reduce the release of transmitters from adrenergic postganglionic terminals (see ADRENERGIC AGENTS). Drugs that act in the central nervous system to reduce sympathetic activity (e.g., centrally acting alpha-2 adrenergic agonists, see ADRENERGIC ALPHA-AGONISTS) are included here.
The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.
Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.
A selective adrenergic beta-1 blocking agent that is commonly used to treat ANGINA PECTORIS; HYPERTENSION; and CARDIAC ARRHYTHMIAS.
A beta-adrenergic antagonist used in the treatment of hypertension, angina pectoris, arrhythmias, and anxiety.
Drugs that selectively bind to and activate beta-adrenergic receptors.
An alkaloid, originally from Atropa belladonna, but found in other plants, mainly SOLANACEAE. Hyoscyamine is the 3(S)-endo isomer of atropine.
Drugs that bind to but do not activate alpha-adrenergic receptors thereby blocking the actions of endogenous or exogenous adrenergic agonists. Adrenergic alpha-antagonists are used in the treatment of hypertension, vasospasm, peripheral vascular disease, shock, and pheochromocytoma.
An alpha-adrenergic antagonist with long duration of action. It has been used to treat hypertension and as a peripheral vasodilator.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
A general class of ortho-dihydroxyphenylalkylamines derived from tyrosine.
A salicylamide derivative that is a non-cardioselective blocker of BETA-ADRENERGIC RECEPTORS and ALPHA-1 ADRENERGIC RECEPTORS.
Drugs that bind to but do not activate ADRENERGIC RECEPTORS. Adrenergic antagonists block the actions of the endogenous adrenergic transmitters EPINEPHRINE and NOREPINEPHRINE.
Compounds possessing both a hydroxyl (-OH) and an amino group (-NH2).
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.
Expenditure of energy during PHYSICAL ACTIVITY. Intensity of exertion may be measured by rate of OXYGEN CONSUMPTION; HEAT produced, or HEART RATE. Perceived exertion, a psychological measure of exertion, is included.
Cyclical movement of a body part that can represent either a physiologic process or a manifestation of disease. Intention or action tremor, a common manifestation of CEREBELLAR DISEASES, is aggravated by movement. In contrast, resting tremor is maximal when there is no attempt at voluntary movement, and occurs as a relatively frequent manifestation of PARKINSON DISEASE.
Drugs that mimic the effects of stimulating postganglionic adrenergic sympathetic nerves. Included here are drugs that directly stimulate adrenergic receptors and drugs that act indirectly by provoking the release of adrenergic transmitters.
The relationship between the dose of an administered drug and the response of the organism to the drug.
The phenomenon whereby compounds whose molecules have the same number and kind of atoms and the same atomic arrangement, but differ in their spatial relationships. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed)
The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
The action of a drug that may affect the activity, metabolism, or toxicity of another drug.
One of the ADRENERGIC BETA-ANTAGONISTS used as an antihypertensive, anti-anginal, and anti-arrhythmic agent.
A cardioselective beta-1-adrenergic antagonist with no partial agonist activity.
The thoracolumbar division of the autonomic nervous system. Sympathetic preganglionic fibers originate in neurons of the intermediolateral column of the spinal cord and project to the paravertebral and prevertebral ganglia, which in turn project to target organs. The sympathetic nervous system mediates the body's response to stressful situations, i.e., the fight or flight reactions. It often acts reciprocally to the parasympathetic system.
The rhythmical expansion and contraction of an ARTERY produced by waves of pressure caused by the ejection of BLOOD from the left ventricle of the HEART as it contracts.
A vascular anomaly due to proliferation of BLOOD VESSELS that forms a tumor-like mass. The common types involve CAPILLARIES and VEINS. It can occur anywhere in the body but is most frequently noticed in the SKIN and SUBCUTANEOUS TISSUE. (from Stedman, 27th ed, 2000)
A dull red, firm, dome-shaped hemangioma, sharply demarcated from surrounding skin, usually located on the head and neck, which grows rapidly and generally undergoes regression and involution without scarring. It is caused by proliferation of immature capillary vessels in active stroma, and is usually present at birth or occurs within the first two or three months of life. (Dorland, 27th ed)
Drugs that bind to and activate adrenergic receptors.
Drugs that bind to and block the activation of ADRENERGIC BETA-2 RECEPTORS.
A nonselective beta-blocker used as an antihypertensive and an antianginal agent.
An alkaloid found in the roots of Rauwolfia serpentina and R. vomitoria. Reserpine inhibits the uptake of norepinephrine into storage vesicles resulting in depletion of catecholamines and serotonin from central and peripheral axon terminals. It has been used as an antihypertensive and an antipsychotic as well as a research tool, but its adverse effects limit its clinical use.
The hollow, muscular organ that maintains the circulation of the blood.
A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.
Dosage forms of a drug that act over a period of time by controlled-release processes or technology.
An imidazole antithyroid agent. Carbimazole is metabolized to METHIMAZOLE, which is responsible for the antithyroid activity.
Drugs that selectively bind to and activate alpha adrenergic receptors.
A beta-2 selective adrenergic antagonist. It is used primarily in animal and tissue experiments to characterize BETA-2 ANDRENERGIC RECEPTORS.
AMINO ALCOHOLS containing the ETHANOLAMINE; (-NH2CH2CHOH) group and its derivatives.
Any dummy medication or treatment. Although placebos originally were medicinal preparations having no specific pharmacological activity against a targeted condition, the concept has been extended to include treatments or procedures, especially those administered to control groups in clinical trials in order to provide baseline measurements for the experimental protocol.
An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.
The decrease in a measurable parameter of a PHYSIOLOGICAL PROCESS, including cellular, microbial, and plant; immunological, cardiovascular, respiratory, reproductive, urinary, digestive, neural, musculoskeletal, ocular, and skin physiological processes; or METABOLIC PROCESS, including enzymatic and other pharmacological processes, by a drug or other chemical.
Works about pre-planned studies of the safety, efficacy, or optimum dosage schedule (if appropriate) of one or more diagnostic, therapeutic, or prophylactic drugs, devices, or techniques selected according to predetermined criteria of eligibility and observed for predefined evidence of favorable and unfavorable effects. This concept includes clinical trials conducted both in the U.S. and in other countries.
Abnormal increase of resistance to blood flow within the hepatic PORTAL SYSTEM, frequently seen in LIVER CIRRHOSIS and conditions with obstruction of the PORTAL VEIN.
A method of studying a drug or procedure in which both the subjects and investigators are kept unaware of who is actually getting which specific treatment.
The L-Isomer of bunolol.
Use of electric potential or currents to elicit biological responses.
Contractile activity of the MYOCARDIUM.
A cardioselective beta-1 adrenergic antagonist that has intrinsic symopathomimetic activity. It is used in the management of ANGINA PECTORIS and HYPERTENSION.
Elements of limited time intervals, contributing to particular results or situations.
The volume of BLOOD passing through the HEART per unit of time. It is usually expressed as liters (volume) per minute so as not to be confused with STROKE VOLUME (volume per beat).
An antihypertensive agent that acts by inhibiting selectively transmission in post-ganglionic adrenergic nerves. It is believed to act mainly by preventing the release of norepinephrine at nerve endings and causes depletion of norepinephrine in peripheral sympathetic nerve terminals as well as in tissues.
The increase in a measurable parameter of a PHYSIOLOGICAL PROCESS, including cellular, microbial, and plant; immunological, cardiovascular, respiratory, reproductive, urinary, digestive, neural, musculoskeletal, ocular, and skin physiological processes; or METABOLIC PROCESS, including enzymatic and other pharmacological processes, by a drug or other chemical.

Drug-protein binding and blood-brain barrier permeability. (1/3372)

The permeability surface area (PS) product, an index of permeability of the blood-brain barrier (BBB), was measured by using the in situ perfusion method. In the cerebral circulation, the fraction of drug that permeates into the brain through the BBB is not only the unbound fraction but also the fraction dissociated from the protein in the perfusate. The sum of these two fractions, the apparent exchangeable fraction, was estimated by fitting the parameters of the BBB permeability under the condition of varying BSA concentrations in the perfusate. The unbound fraction of drugs in a buffer containing 0.5 mM BSA was measured by using the ultrafiltration method in vitro, and the apparent exchangeable fraction was measured in vivo by using the intracarotid artery injection method. The apparent exchange fraction was 100% for S-8510, 96.5% for diazepam, 90.9% for caffeine, 38.3% for S-312-d, 33.1% for propranolol, and 6.68% for (+)-S-145 Na, and each of these was higher than the corresponding unbound fraction in vitro in all drugs. The apparent exchangeable fractions, for example, were 8 times higher for diazepam and 38 times for S-312-d than the unbound fractions in vitro. The apparent exchangeable fraction of drugs was also estimated from the parameters obtained with the perfusion method. Because drugs can be infused for an arbitrary length of time in the perfusion method, substances with low permeability can be measured. The apparent exchangeable fractions obtained with this method were almost the same as those obtained with the intracarotid artery injection method.  (+info)

The role of the sympathetic nervous system in the regulation of leptin synthesis in C57BL/6 mice. (2/3372)

The objectives of this study were to determine whether leptin synthesis is regulated by the sympathetic nervous system and if so whether beta-adrenergic receptors mediate this effect. We show that sympathetic blockade by reserpine increases leptin mRNA levels in brown but not white adipose tissue, while acute cold-exposure decreases leptin expression 10-fold in brown adipose tissue and 2-fold in white adipose tissue. The cold-induced reduction in leptin mRNA can be prevented by a combination of propranolol and SR 59230A but not by either antagonist alone, indicating that beta3-adrenergic receptors and classical beta1/beta2-adrenergic receptors both mediate responses to sympathetic stimulation. Circulating leptin levels reflect synthesis in white adipose tissue but not in brown adipose tissue.  (+info)

Neuroregulation by vasoactive intestinal peptide (VIP) of mucus secretion in ferret trachea: activation of BK(Ca) channels and inhibition of neurotransmitter release. (3/3372)

1. The aims of this study were to determine: (1) whether vasoactive intestinal peptide (VIP) regulates cholinergic and 'sensory-efferent' (tachykininergic) 35SO4 labelled mucus output in ferret trachea in vitro, using a VIP antibody, (2) the class of potassium (K+) channel involved in VIP-regulation of cholinergic neural secretion using glibenclamide (an ATP-sensitive K+ (K(ATP)) channel inhibitor), iberiotoxin (a large conductance calcium activated K+ (BK(ca)) channel blocker), and apamin (a small conductance K(ca) (SK(ca)) channel blocker), and (3) the effect of VIP on cholinergic neurotransmission using [3H]-choline overflow as a marker for acetylcholine (ACh) release. 2. Exogenous VIP (1 and 10 microM) alone increased 35SO4 output by up to 53% above baseline, but suppressed (by up to 80% at 1 microM) cholinergic and tachykininergic neural secretion without altering secretion induced by ACh or substance P (1 microM each). Endogenous VIP accounted for the minor increase in non-adrenergic, non-cholinergic (NANC), non-tachykininergic neural secretion, which was compatible with the secretory response of exogenous VIP. 3. Iberiotoxin (3 microM), but not apamin (1 microM) or glibenclamide (0.1 microM), reversed the inhibition by VIP (10 nM) of cholinergic neural secretion. 4. Both endogenous VIP (by use of the VIP antibody; 1:500 dilution) and exogenous VIP (0.1 microM), the latter by 34%, inhibited ACh release from cholinergic nerve terminals and this suppression was completely reversed by iberiotoxin (0.1 microM). 5. We conclude that, in ferret trachea in vitro, endogenous VIP has dual activity whereby its small direct stimulatory action on mucus secretion is secondary to its marked regulation of cholinergic and tachykininergic neurogenic mucus secretion. Regulation is via inhibition of neurotransmitter release, consequent upon opening of BK(Ca) channels. In the context of neurogenic mucus secretion, we propose that VIP joins NO as a neurotransmitter of i-NANC nerves in ferret trachea.  (+info)

Wavelet transform to quantify heart rate variability and to assess its instantaneous changes. (4/3372)

Heart rate variability is a recognized parameter for assessing autonomous nervous system activity. Fourier transform, the most commonly used method to analyze variability, does not offer an easy assessment of its dynamics because of limitations inherent in its stationary hypothesis. Conversely, wavelet transform allows analysis of nonstationary signals. We compared the respective yields of Fourier and wavelet transforms in analyzing heart rate variability during dynamic changes in autonomous nervous system balance induced by atropine and propranolol. Fourier and wavelet transforms were applied to sequences of heart rate intervals in six subjects receiving increasing doses of atropine and propranolol. At the lowest doses of atropine administered, heart rate variability increased, followed by a progressive decrease with higher doses. With the first dose of propranolol, there was a significant increase in heart rate variability, which progressively disappeared after the last dose. Wavelet transform gave significantly better quantitative analysis of heart rate variability than did Fourier transform during autonomous nervous system adaptations induced by both agents and provided novel temporally localized information.  (+info)

Assessment of cardiac sympathetic regulation by respiratory-related arterial pressure variability in the rat. (5/3372)

1. Mechanical ventilation evokes a corresponding arterial pressure variability (APV) which is decreased by beta-adrenoceptor antagonism. Therefore, in this study we set out to determine whether the respiratory-related APV can be used to assess cardiac sympathetic tone. 2. Computer-generated broad-band mechanical ventilation (0-3 Hz) was applied to Sprague-Dawley rats that had been anaesthetized with ketamine and paralysed with pancuronium. APV and its relationship to lung volume variability (LVV-APV) was systematically quantified with auto- or cross-spectral frequency domain analysis. 3. APV and LVV-APV transfer magnitudes between 0.5 and 1.5 Hz showed dose-dependent suppression by propranolol from 0.01 to 1 mg kg-1, while the static value of arterial pressure remained unchanged. Stroke volume variability, assessed by the use of a pulse contour method, exhibited a similar pattern of suppression by propranolol. In contrast, heart rate variability was not lowered with propranolol. 4. The effect of propranolol on respiratory-related APV persisted even in the presence of combined alpha-adrenoceptor and muscarinic receptor blockade by phentolamine and atropine. 5. The frequency range of 0.5-1.0 Hz was optimal for LVV-APV transfer magnitude to correlate with cardiac sympathetic tone. 6. We conclude that respiratory-related APV may provide a valid assessment of cardiac sympathetic regulation which is independent of parasympathetic and vascular sympathetic influences in ketamine-anaesthetized and positive pressure-ventilated rats.  (+info)

beta2-adrenergic receptor-selective agonist clenbuterol prevents Fas-induced liver apoptosis and death in mice. (6/3372)

Stimulation of the cAMP-signaling pathway modulates apoptosis in several cell types and inhibits Jo2-mediated apoptosis in cultured rat hepatocytes. No information is yet available as to whether the hepatic beta2-adrenergic receptor (AR) expression level, including beta2-AR-dependent adenylyl cyclase activation, modulates hepatocyte sensitivity to apoptosis in vivo or whether this sensitivity can be modified by beta2-AR ligands. We have examined this using C57BL/6 mice, in which hepatic beta2-AR densities are low, and transgenic F28 mice, which overexpress beta2-ARs and have elevated basal liver adenylyl cyclase activity. The F28 mice were resistant to Jo2-induced liver apoptosis and death. The beta-AR antagonist propranolol sensitized the F28 livers to Jo2. In normal mice clenbuterol, a beta2-AR-specific agonist, considerably reduced Jo2-induced liver apoptosis and death; salbutamol, another beta2-AR-selective agonist, also reduced Jo2-induced apoptosis and retarded death but with less efficacy than clenbuterol; and propranolol blocked the protective effect of clenbuterol. This indicates that the expression level of functional beta2-ARs modulates Fas-regulated liver apoptosis and that this apoptosis can be inhibited in vivo by giving beta2-AR agonists. This may well form the basis for a new therapeutic approach to diseases involving abnormal apoptosis.  (+info)

Endothelin antagonists block alpha1-adrenergic constriction of coronary arterioles. (7/3372)

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)

beta2-adrenoceptor agonists reduce the decline of rat diaphragm twitch force during severe hypoxia. (8/3372)

The aim of the present study was to investigate the in vitro effects of the short-acting beta2-adrenoceptor agonist salbutamol and the long-acting beta2-adrenoceptor agonist salmeterol on hypoxia-induced rat diaphragm force reduction. In vitro diaphragm twitch force (Pt) and maximal tetanic force (Po) of isolated diaphragm muscle strips were measured for 90 min during hyperoxia (tissue bath PO2 83.8 +/- 0.9 kPa and PCO2 3.9 +/- 0.1 kPa) or severe hypoxia (PO2 7.1 +/- 0.3 kPa and PCO2 3.9 +/- 0.1 kPa) in the presence and absence of 1 microM salbutamol or 1 microM salmeterol. During hyperoxia, salbutamol and salmeterol did not significantly alter the time-related decreases in Pt and Po (to approximately 50% of initial values). Salbutamol had no effects on Po or the Pt-to-Po ratio. Salmeterol treatment significantly reduced Po and increased the Pt-to-Po ratio during hyperoxia (P < 0.05 compared with control value). Hypoxia resulted in a severe decrease in Pt (to approximately 30% of initial value) and Po after 90 min. Both salbutamol and salmeterol significantly reduced the decline in Pt during hypoxia (P < 0.05). The reduction in Po was not prevented. Salbutamol increased Pt rapidly but transiently. Salmeterol had a delayed onset of effect and a longer duration of action. Addition of 1 microM propranolol (a nonselective beta-adrenoceptor antagonist) did not alter Pt, Po, or the Pt-to-Po ratio during hypoxia but completely blocked the inotropic effects of salbutamol and salmeterol, indicating that these effects are dependent on beta2-adrenoceptor agonist-related processes.  (+info)

1. Essential tremor: This is the most common type of tremor, and it is characterized by a rhythmic shaking of the hands, arms, legs, or head. It can be inherited and can worsen over time.
2. Parkinson's disease: A neurodegenerative disorder that affects movement, including tremors, rigidity, and difficulty with walking.
3. Dystonia: A movement disorder that causes involuntary muscle contractions and spasms, which can result in tremors.
4. Huntington's disease: A rare genetic disorder that causes progressive damage to the brain, leading to involuntary movements, including tremors.
5. Medication-induced tremors: Certain medications, such as those used to treat psychosis, can cause tremors as a side effect.
6. Alcohol or drug withdrawal: Stopping the use of certain substances can cause tremors as part of the withdrawal process.
7. Metabolic disorders: Conditions such as hypoglycemia (low blood sugar) or hyperthyroidism (too much thyroid hormone) can cause tremors.
8. Trauma: A head injury or other trauma can sometimes cause tremors.

Tremors can be diagnosed through a physical examination and medical history, as well as through imaging tests such as CT or MRI scans. Treatment for tremors depends on the underlying cause, but may include medications, lifestyle changes, or surgery. In some cases, tremors can be managed with techniques such as physical therapy, relaxation exercises, or deep brain stimulation.

Note: This definition is intended for informational purposes only and should not be used to diagnose or treat a medical condition. If you suspect that you or your child may have a hemangioma, it is important to consult with a qualified healthcare professional for proper evaluation and treatment.

Note: Portal hypertension is a common complication of liver disease, especially cirrhosis. It is characterized by elevated pressure within the portal vein system, which can lead to splanchnic vasodilation, increased blood flow, and edema in the splanchnic organ.

Symptoms: Symptoms of portal hypertension may include ascites (fluid accumulation in the abdomen), encephalopathy (mental confusion or disorientation), gastrointestinal bleeding, and jaundice (yellowing of the skin and eyes).

Diagnosis: The diagnosis of portal hypertension is based on a combination of clinical findings, laboratory tests, and imaging studies. Laboratory tests may include liver function tests, blood counts, and coagulation studies. Imaging studies may include ultrasonography, computed tomography (CT), or magnetic resonance imaging (MRI).

Treatment: Treatment of portal hypertension depends on the underlying cause and may include medications to control symptoms, such as beta blockers to reduce portal pressure, antibiotics to treat infection, and nonsteroidal anti-inflammatory drugs (NSAIDs) to relieve pain. In severe cases, surgery or shunt procedures may be necessary.

Prognosis: The prognosis for patients with portal hypertension is generally poor, as it is often associated with advanced liver disease. The 5-year survival rate for patients with cirrhosis and portal hypertension is approximately 50%.

... , sold under the brand name Inderal among others, is a medication of the beta blocker class. It is used to treat ... Propranolol appears in the blood after 30 minutes and has a maximum effect between 60 and 90 minutes when taken by mouth. ... Propranolol was patented in 1962 and approved for medical use in 1964. It is on the World Health Organization's List of ... Propranolol is available as a generic medication. In 2020, it was the 88th most commonly prescribed medication in the United ...
Morphine is the prototype of opioid analgesics Propranolol is the prototype of the beta blockers Chlorpromazine is the ... ". "Propranolol". DrugBank. 16 October 2018. Retrieved 16 October 2018. Watanabe, T.; Wada, H. (1991). Histaminergic Neurons ( ...
Effect of propranolol". The American Journal of Medicine. 57 (4): 584-90. doi:10.1016/0002-9343(74)90010-2. PMID 4432863. (CS1 ... In 1974 it was discovered that propranolol could prevent attacks. The concept of channelopathies and the link with specific ion ... such as propranolol (as most of the symptoms are driven by increased levels of adrenaline and its effect on the β-adrenergic ...
The first beta blocker, propranolol, was introduced in the early 1960s by the winner of The Nobel Prize in Physiology or ... Linde, K.; Rossnagel, K. (2004). Hobson, Anna (ed.). "Propranolol for migraine prophylaxis". The Cochrane Database of ... Phenoxybenzamine Phentolamine Prazosin Tamsulosin Yohimbine Propranolol Timolol Atenolol Metoprolol Butaxamine Still under ...
D. K. Ganguly (1976). "Antioxotremorine action of propranolol". British Journal of Pharmacology. 56 (1): 21-24. doi:10.1111/j. ...
Additionally, increased blood-levels of Maprotiline are possible, if certain beta-blocking agents (e.g. Propranolol) are given ...
Propranolol. The addition of isosorbide mononitrate to propranolol treatment in patients with cirrhosis and portal hypertension ... effect of isosorbide mononitrate was especially evident in patients whose portal pressure was not reduced by propranolol.[ ...
A meta-analysis found that propranolol had an "overall relative risk of response to treatment (here called the 'responder ratio ... 2012). "Randomized, placebo-controlled trial of propranolol added to topiramate in chronic migraine". Neurology. 78 (13): 976- ... "Propranolol for migraine prophylaxis". Cochrane Database Syst Rev (2): CD003225. doi:10.1002/14651858.CD003225.pub2. PMID ... massage and relaxation might be as effective as propranolol or topiramate in the prevention of migraine headaches; however, the ...
One example is propranolol. Propranolol is a beta blocker that has been approved to treat hypertension, angina, anxiety, and ... Ramoska, Edward; Sacchetti, Alfred D (1985-11-01). "Propranolol-induced hypertension in treatment of cocaine intoxication". ... due to propranolol (n=3), esmolol (n=3), and metoprolol (n=1). Some detractors of beta-blockers for cocaine-induced chest pain ...
Stapleton MP (1997). "Sir James Black and propranolol. The role of the basic sciences in the history of cardiovascular ...
... response with propranolol and steroids". Clinical Sarcoma Research. 10 (1): 12. doi:10.1186/s13569-020-00134-8. PMC 7394668. ...
The discovery of propranolol was hailed as the greatest breakthrough in the treatment of heart disease since the discovery of ... Propranolol has been described as the greatest breakthrough in heart disease treatments since the 18th century discovery of ... His invention of propranolol, the beta adrenergic receptor antagonist that revolutionised the medical management of angina ... He went to work for ICI Pharmaceuticals in 1958 and, while there, developed propranolol, a beta blocker used for the treatment ...
Stapleton MP (1997). "Sir James Black and propranolol. The role of the basic sciences in the history of cardiovascular ... and was superseded by propranolol from 1965 onward. Beta blocker Discovery and development of beta-blockers Quirke V (January ...
James W. Black synthesises propranolol, the first beta blocker (used for regulation of angina pectoris), which becomes the ... 122-4. ISBN 978-3-540-19587-0. Stapleton, Melanie P. (1997). "Sir James Black and Propranolol". Texas Heart Institute Journal. ...
Benzodiazepines, such as lorazepam; beta blockers such as propranolol; anticholinergics such as benztropine; and serotonin ... particularly propranolol. The term was first used by Czech neuropsychiatrist Ladislav Haškovec, who described the phenomenon in ... "Cyproheptadine versus propranolol for the treatment of acute neuroleptic-induced akathisia: a comparative double-blind study". ...
... propranolol Propranolol is the only agent indicated for the control of tremor, portal hypertension, and esophageal variceal ... Elman MJ, Sugar J, Fiscella R, Deutsch TA, Noth J, Nyberg M, Packo K, Anderson RJ (1998). "The effect of propranolol versus ... Discusses the use of propranolol by a North Korean pistol shooter in the 2008 Olympics) beta-Adrenergic+Blockers at the US ... "Propranolol hydrochloride" (PDF). Retrieved September 3, 2020. National Heart, Lung, and Blood Institute (2007). "Expert Panel ...
Inderal (propranolol) - a beta blocker; it is used for acute anxiety, panic attacks, hypertension. Invega (paliperidone) - ...
... alprazolam and propranolol; alprazolam weakly agonizes dopamine receptors and causes catecholamine release while propranolol ...
Its potency is similar to propranolol. Like other beta blockers, oral bupranolol can be used to treat hypertension and ...
Diazepam and propranolol are common examples; ethanol and cannabis are also used occasionally.[citation needed] Blood doping ...
Treatment involves propranolol and trigger avoidance. Aquagenic urticaria Urticaria Skin lesion List of cutaneous conditions ...
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  • The extended-release propranolol capsule (brand name: Inderal LA) usually is taken once a day. (medlineplus.gov)
  • In this paper, the authors propose an update on the latest recommendations for the management of patients with infantile hemangiomas and indication for treatment with oral propranolol. (rcaap.pt)
  • Melo IS, Gonçalves V, Anjos R. Propranolol nos hemangiomas infantis: casuística nacional com 30 doentes. (rcaap.pt)
  • Pereira J, Banquart-Leitão J. Propranolol como tratamento de primeira linha dos hemangiomas da infância. (rcaap.pt)
  • hemangiomas and propranolol 2: 32. (gatech.edu)
  • Evidence from June 2008 suggests that propranolol can be used to treat severe infantile hemangiomas (IHs). (curecrowd.com)
  • Early propranolol treatment of infantile hemangiomas improves outcome. (bvsalud.org)
  • To evaluate aesthetic and functional outcome in propranolol -treated infantile hemangiomas according to the age of treatment onset. (bvsalud.org)
  • The present results strongly suggest that early (before 3 months of age) initiation of treatment of infantile hemangiomas with propranolol results in significantly higher aesthetic and functional improvement rates and a higher percentage of total resolution. (bvsalud.org)
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  • Studies have shown that individuals given propranolol immediately after a traumatic experience show less severe symptoms of PTSD compared to their respective control groups that did not receive the drug (Vaiva et al. (curecrowd.com)
  • However, results remain inconclusive as to the success of propranolol in treatment of PTSD, including nightmares experienced by those with PTSD. (curecrowd.com)
  • Since 2008, the use of oral propranolol has been growing with superior efficacy compared to systemic corticosteroids and good safety profile, assuming a frontline position in the treatment of infantile hemangioma. (rcaap.pt)
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  • tell your doctor and pharmacist if you are allergic to propranolol, any other medications, or any ingredients in propranolol products. (medlineplus.gov)
  • In fact, many are surprised to learn that the typical Propranolol dosage for anxiety is actually quite low, with most doctors recommending taking a small dose of 10-20 mg one hour before a pivotal moment like a presentation, job interview, or crucial exam. (gokick.com)
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  • Animals receiving the propranolol treatment were given a single dose (20 mg/kg, i.p.) either four or 11 days prior to the LPS challenge. (cdc.gov)
  • Propranolol reduces the effects of nightmare -related cardiac activity by keeping sinus rhythm low during nightmares, as a higher pulse and increased adrenaline are associated with severe nightmares. (curecrowd.com)
  • Propranolol was investigated for possible effects on resting energy expenditure and muscle catabolism in patients with severe burns. (curecrowd.com)
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  • If you also take certain drugs to lower your cholesterol (bile acid-binding resins such as cholestyramine or colestipol ), take propranolol at least 1 hour before or at least 4 hours after these medications. (webmd.com)
  • There are also many ethical and legal questions surrounding the use of Propranolol-based medications for use as a "memory dampener," including: altering (memory-recalled) evidence during an investigation, modifying behavioral response to past (albeit traumatic) experiences, the regulation of these drugs, and others. (curecrowd.com)
  • Propranolol along with a number of other membrane-acting drugs have been investigated for possible effects on Plasmodium falciparum and so the treatment of malaria . (curecrowd.com)
  • [ 20 ] However, a single study from 2006 has suggested that propranolol may reduce the dosages required for existing drugs to be effective against P. falciparum by 5- to 10-fold, suggesting a role for combination therapies. (curecrowd.com)
  • Initiation and use of propranolol for infantile hemangioma: report of a consensus conference. (rcaap.pt)
  • Though Propranolol is largely considered to be a safe medication, it simply isn't the right solution for everyone. (gokick.com)
  • Propranolol is in a class of medications called beta blockers. (medlineplus.gov)
  • Since 2008, oral propranolol has been widely considered to be the first-line treatment for IH. (bvsalud.org)
  • Propranolol in the Treatment of infantile hemangioma: clinical effectiveness, risks and recommendations. (rcaap.pt)
  • Sucessful Treatment of infantile haemangiomas of the orbit with propranolol. (rcaap.pt)
  • Propranolol is currently being investigated as a potential treatment for post-traumatic stress disorder . (curecrowd.com)
  • Propranolol in combination with etodolac is currently being investigated in a Phase 3 trial of 400 colorectal cancer patients as a potential treatment for prevention of colorectal cancer recurrence. (curecrowd.com)
  • [ 18 ] In children with burns, treatment with propranolol during hospitalization attenuated hypermetabolism and reversed muscle wasting. (curecrowd.com)
  • Propranolol treatment abrogated the elaboration of inflammatory cytokine mRNA expression in the brain instigated in our model, having no treatment effects in non-DFP exposed groups. (cdc.gov)
  • IMSEAR at SEARO: Propranolol on plasma fibrinogen, fibrinolytic activity and cardiac injury following isoprenaline challenge in rats. (who.int)
  • Propranolol is used to treat high blood pressure, irregular heart rhythms, pheochromocytoma (tumor on a small gland near the kidneys), certain types of tremor, and hypertrophic subaortic stenosis (a heart muscle disease). (medlineplus.gov)
  • Propranolol is used for treating certain types of irregular heartbeat. (canadianolpharmacy.com)
  • Propranolol comes as a tablet, solution (liquid),and as an extended-release (long-acting) capsule to take by mouth. (medlineplus.gov)
  • Retrospective, observational study of infantile hemangioma patients under 4 years of age at the time of diagnosis , treated with oral propranolol . (bvsalud.org)
  • The goal of the current study was to evaluate the potential for the β-adrenergic receptor inhibitor and anti-inflammatory drug, propranolol, to treat neuroinflammation in a novel long-term mouse model of GWI. (cdc.gov)
  • Significance: Our results indicate that propranolol may be a promising therapy for GWI with the potential to treat the underlying neuroinflammation associated with the illness. (cdc.gov)
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  • Propranolol works by decreasing the action of pacemaker cells and slowing certain impulses in the heart. (canadianolpharmacy.com)
  • it may increase the risk of Propranolol 's side effects. (canadianolpharmacy.com)
  • The potential anti-neuroinflammatory effects of propranolol were interrogated by analysis of cytokine mRNA expression. (cdc.gov)
  • [ 16 ] The aim of this study is to assess the use of perioperative medical intervention using a combination of a propranolol and etodolac in order to attenuate the surgically induced immunosuppression and other physiological perturbations, aiming to reduce the rate of tumor recurrence and distant metastatic disease. (curecrowd.com)
  • Ask your health care provider any questions you may have about how to use Propranolol. (canadianolpharmacy.com)