Thiamylal
Thiopental
Anesthetics, Intravenous
Ultrashort-acting anesthetics that are used for induction. Loss of consciousness is rapid and induction is pleasant, but there is no muscle relaxation and reflexes frequently are not reduced adequately. Repeated administration results in accumulation and prolongs the recovery time. Since these agents have little if any analgesic activity, they are seldom used alone except in brief minor procedures. (From AMA Drug Evaluations Annual, 1994, p174)
Differential inhibitory effects of thiopental, thiamylal and phenobarbital on both voltage-gated calcium channels and NMDA receptors in rat hippocampal slices. (1/21)
Although it is known that there are some pharmacological differences between the structurally similar barbiturates, the underlying mechanism of action remains unclear. We have compared the effects of thiopental, thiamylal and phenobarbital on both voltage-gated calcium channels (VGCC) and N-methyl-D-aspartate (NMDA) receptors in rat hippocampal slices by determining changes in intracellular calcium ([Ca2+]i). Experiments were performed in adult rat hippocampal slices perfused with Krebs solution (37 degrees C). Concentrations of [Ca2+]i in the pyramidal cell layer of the CA1 region were measured using a calcium indicator dye, fura-2. To activate VGCC and NMDA receptors, slices were exposed to K+ 60 mmol litre-1 (< or = 60 s) and NMDA 100 mumol litre-1 (30 s), respectively. Thiopental, thiamylal and phenobarbital were present 5 min before, during and 1 min after high K+ or NMDA application. Both thiamylal and thiopental (50-600 mumol litre-1) attenuated the increases in [Ca2+]i produced by high K+ or NMDA in a concentration-dependent manner, while phenobarbital 50-1000 mumol litre-1 only slightly attenuated the [Ca2+]i increase produced by high K+ at concentrations of more than 200 mumol litre-1 and was ineffective on the [Ca2+]i response produced by NMDA. Although the increases in [Ca2+]i caused by membrane depolarization with high K+ were reduced equally with thiamylal and thiopental, thiamylal was more effective in attenuating the increase in [Ca2+]i produced by NMDA receptor activation than thiopental. We conclude that the depressant effects of barbiturates on both VGCC and NMDA receptors varied between agents. Differential inhibition of both VGCC and NMDA receptors may determine the pharmacological properties of barbiturates and their ability to protect neurones against ischaemia. (+info)Blockade of adenosine triphosphate-sensitive potassium channels by thiamylal in rat ventricular myocytes. (2/21)
BACKGROUND: The adenosine triphosphate (ATP)-sensitive potassium (KATP) channels protect myocytes during ischemia and reperfusion. This study investigated the effects of thiamylal on the activities of KATP channels in isolated rat ventricular myocytes during simulated ischemia. METHODS: Male Wistar rats were anesthetized with ether. Single, quiescent ventricular myocytes were dispersed enzymatically. Membrane currents were recorded using patch-clamp techniques. In the cell-attached configuration, KATP channel currents were assessed before and during activation of these channels by 2,4-dinitrophenol and after administration of 25, 50, and 100 mg/l thiamylal. The open probability was determined from current-amplitude histograms. In the inside-out configuration, the current-voltage relation was obtained before and after the application of thiamylal (50 mg/1). RESULTS: In the cell-attached configuration, 2,4-dinitrophenol caused frequent channel opening. 2,4-Dinitrophenol-induced channel activities were reduced significantly by glibenclamide, suggesting that the channels studied were KATP channels. Open probability of KATP channels was reduced by thiamylal in a concentration-dependent manner. KATP channels could be activated in the inside-out configuration because of the absence of ATP. Thiamylal inhibited KATP channel activity without changing the single-channel conductance. CONCLUSIONS: The results obtained in this study indicate that thiamylal inhibits KATP channel activities in cell-attached and inside-out patches, suggesting a direct action of this drug on these channels. (+info)Dual effects of intravenous anesthetics on the function of norepinephrine transporters. (3/21)
BACKGROUND: Norepinephrine transporters (NETs) terminate the neuronal transmission of norepinephrine, which is released from noradrenergic neurons. To investigate the interaction with NET, the authors examined the effects of short- and long-term treatment with anesthetics on the activity and mRNA level of NET. METHODS: To assay [3H]norepinephrine uptake, bovine adrenal medullary cells in culture were incubated with [3H]norepinephrine in the presence of intravenous anesthetics, including propofol, thiamylal, and diazepam. To study the direct interaction between the anesthetics and NET, the effect of propofol on the binding of [3H]desipramine to the plasma membrane was examined. To study the long-term effect of anesthetics, [3H]norepinephrine uptake by cells pretreated with propofol for 6-24 h and [3H]desipramine binding after pretreatment for 12 h were measured. Simultaneously, we examined the effect of anesthetics on the expression of NET mRNA using the reverse transcriptase-polymerase chain reaction. RESULTS: All of the intravenous anesthetics inhibited [3H]norepinephrine uptake in a concentration-dependent manner. The active concentrations of propofol (1-3 microm) and thiamylal (< or = 30 microm) were similar to those encountered clinically. The kinetic analysis revealed that all the anesthetics noncompetitively inhibited [3H]norepinephrine uptake. Propofol inhibited [3H]desipramine binding with a potency similar to that observed in [3H]norepinephrine uptake. Scatchard analysis showed that propofol competitively inhibited [3H]desipramine binding. On the other hand, long-term treatment of cells with propofol (10 microm) enhanced the NET functional activity and [3H]desipramine binding, and also increased the level of NET mRNA. CONCLUSIONS: These results suggest that intravenous anesthetics have a dual effect on NET; short-term treatment causes inhibition, whereas long-term treatment leads to up-regulation. The interaction of intravenous anesthetics with NET may modulate the neuronal transmission of norepinephrine during anesthesia. (+info)Complete recovery of consciousness in a patient with decorticate rigidity following cardiac arrest after thoracic epidural injection. (4/21)
A 46-yr-old man with dysaesthesia (burning sensation) following herpes zoster in the left upper chest region was treated with a single thoracic (T2/T3) epidural injection (1.0% lidocaine 3 ml + 0.125% bupivacaine 3 ml) as an outpatient. Twenty minutes after the injection, a nurse noticed the patient to be unconscious with dilated pupils, apnoea and cardiac arrest. Following immediate cardiopulmonary resuscitation, the patient was treated with an i.v. infusion of thiamylal sodium 2-4 mg kg-1 h-1 and his lungs were mechanically ventilated. When the patient developed a characteristic decorticate posture, mild hypothermia (oesophageal temperature, 33-34 degrees C) was induced. On the 17th day of this treatment, after rewarming (35.5 degrees C) and discontinuation of the barbiturate, the patient responded to command. Weaning from the ventilator was successful on the 18th day. About 4 months after the incident, the patient was discharged with no apparent mental or motor disturbances. We suggest that mild hypothermia with barbiturate therapy may have contributed to the successful outcome in this case. (+info)Effects of propofol on ischemia and reperfusion in the isolated rat heart compared with thiamylal. (5/21)
The aim of the present study was to investigate whether clinical doses of propofol and thiamylal affect oxygen free radical production and intracellular calcium concentration ([Ca2+]i) in the post-ischemic reperfused heart. Forty-eight rat hearts were perfused with a Langendorff system and loaded with Fura-2 / AM as a [Ca2+]i marker. The hearts were divided into 6 groups as follows (each group: n = 8); Group S (saline), Group TL (thiamylal 100 microM), Group TH (thiamylal 300 microM), Group I (Intralipid), Group PL (propofol 3 microM), and Group PH (propofol 10 microM). All hearts were initially perfused for 5 min as control aerobic perfusion. Afterwards, no-flow ischemia was induced for 15 min, followed by reperfusion for 20 min. The formation of hydroxyl radicals in the coronary effluent was measured with high performance liquid chromatography using salicylic acid. At the beginning of the ischemia and reperfusion periods, increases in systolic and diastolic [Ca2+]i were observed in all groups except Group TH. The high dose of thiamylal significantly suppressed this initial increase in cytosolic [Ca2+]i (Group S 1.30+/-0.15; Group TL 0.99+/-0.17; Group TH 0.70+/-0.09, at 1 min after reperfusion; systolic [Ca2+]i : p < 0.05). Total DHBAs in the coronary effluent of all groups increased significantly 1 min after reperfusion, however, there were no significant differences among the groups. Clinical doses of propofol had no significant effect on myocardial function and [Ca2+]i before and after ischemia, whereas thiamylal suppressed the increase in [Ca2+]i during ischemia and reperfusion. However, free radical formation during reperfusion was unaffected by thiamylal and propofol. (+info)Anesthesia rapidly suppresses insulin pulse mass but enhances the orderliness of insulin secretory process. (6/21)
Induction of anesthesia is accompanied by modest hyperglycemia and a decreased plasma insulin concentration. Most insulin is secreted in discrete pulses occurring at approximately 6- to 8-min intervals. We sought to test the hypothesis that anesthesia inhibits insulin release by disrupting pulsatile insulin secretion in a canine model by use of direct portal vein sampling. We report that induction of anesthesia causes an abrupt decrease in the insulin secretion rate (1.1 +/- 0.2 vs. 0.7 +/- 0.1 pmol. kg(-1). min(-1), P < 0.05) by suppressing insulin pulse mass (630 +/- 121 vs. 270 +/- 31 pmol, P < 0.01). Anesthesia also elicited an approximately 30% higher increase in insulin pulse frequency (P < 0.01) and more orderly insulin concentration profiles (P < 0.01). These effects were evoked by either sodium thiamylal or nitrous oxide and isoflurane. In conclusion, anesthesia represses insulin secretion through the mechanism of a twofold blunting of pulse mass despite an increase in orderly pulse frequency. These data thus unveil independent amplitude and frequency controls of beta-cells' secretory activity in vivo. (+info)Presynaptic inhibition in man during anesthesia and sleep. (7/21)
The slow positive (P2) wave of the evoked electrospinogram was recorded from the dorsal epidural space in man. The waveform characteristics of the P2 wave were similar to those of the dorsal cord positive wave (P wave), which is believed to be caused by the primary afferent depolarization (PAD) and to be related to presynaptic inhibitory action in animals. The "second" component of the P2 wave appeared during excitement or following strong stimulation and disappeared after thiamylal administration and during natural slow-wave sleep. The second component, also demonstrated in the P wave of rabbits during ketamine anesthesia, was abolished by spinal transection. Therefore, these second components in man and rabbits may originate from a feedback loop via supraspinal structures. Thus, supraspinal influences might play an important role in the regulation of presynaptic inhibition in the spinal cord of man during wakefulness and anesthesia. (+info)Effects of change in frequency of stimulation on myocardial depression produced by thiamylal and halothane. (8/21)
The effects of change in the frequency of stimulation on the myocardial contractility depressed by thiamylal and halothane were studied in isolated dog heart muscle. An increase in the frequency of stimulation from 0.1 to 0.6 cps resulted in a progressive in increase in net-shortening (delta1) and maximum velocity of shortening at 0.4 g preload (V'max), namely a positive staircase. The myocardium previously depressed to a similar degree by thiamylal or halothane still showed a positive staircase. This result indicates that the mechanism to produce the myocardial depression by thiamylal or halothane is not a complete inhibition of Ca++ influx across the cell membrane. The time to reach a steady state of contraction following an increase in the frequency of stimulation was longer in the presence than in the absence of these anesthetics. The degree of recovery from the myocardial depression by increasing the frequency of stimulation was much higher in the presence of thiamylal than in the presence of halothane. This fact suggests that the mechanism to produce the myocardial depression may be different in there two anesthetics. (+info)Thiamylal is a rapidly acting, ultrashort-acting barbiturate drug primarily used for the induction of anesthesia due to its rapid onset and short duration of action, characterized by its water-soluble property and minimal cardiovascular effects.
Thiamylal is a fast-acting, ultra-short-acting barbiturate drug that is primarily used for the induction of anesthesia before surgical procedures. It works by depressing the central nervous system, producing sedation, relaxation, and hypnosis. Thiamylal has a rapid onset of action and its effects last only a short time, making it useful for quickly achieving a desired level of anesthesia while minimizing the risk of prolonged sedation or respiratory depression.
It is important to note that thiamylal should be administered under the close supervision of trained medical personnel, as its use carries certain risks and potential complications, such as cardiovascular and respiratory depression. Additionally, patients with a history of drug allergies, liver or kidney disease, or other medical conditions may require special precautions before receiving thiamylal.
Thiopental is a rapid-onset, ultrashort-acting barbiturate sedative-hypnotic drug, primarily used for the induction of anesthesia due to its quick reduction of consciousness levels, although its use in medical practice has significantly declined because of associated risks such as cardiovascular depression and respiratory arrest.
Thiopental, also known as Thiopentone, is a rapid-onset, ultrashort-acting barbiturate derivative. It is primarily used for the induction of anesthesia due to its ability to cause unconsciousness quickly and its short duration of action. Thiopental can also be used for sedation in critically ill patients, though this use has become less common due to the development of safer alternatives.
The drug works by enhancing the inhibitory effects of gamma-aminobutyric acid (GABA), a neurotransmitter in the brain that produces a calming effect. This results in the depression of the central nervous system, leading to sedation, hypnosis, and ultimately, anesthesia.
It is worth noting that Thiopental has been largely replaced by newer drugs in many clinical settings due to its potential for serious adverse effects, such as cardiovascular and respiratory depression, as well as the risk of anaphylaxis. Additionally, it has been used in controversial procedures like capital punishment in some jurisdictions.
Intravenous anesthetics are medications that, when administered into a vein, induce or maintain general anesthesia, providing sedation, amnesia, and muscle relaxation, with the onset of action being more rapid than other types of anesthetics.
Intravenous anesthetics are a type of medication that is administered directly into a vein to cause a loss of consciousness and provide analgesia (pain relief) during medical procedures. They work by depressing the central nervous system, inhibiting nerve impulse transmission and ultimately preventing the patient from feeling pain or discomfort during surgery or other invasive procedures.
There are several different types of intravenous anesthetics, each with its own specific properties and uses. Some common examples include propofol, etomidate, ketamine, and barbiturates. These drugs may be used alone or in combination with other medications to provide a safe and effective level of anesthesia for the patient.
The choice of intravenous anesthetic depends on several factors, including the patient's medical history, the type and duration of the procedure, and the desired depth and duration of anesthesia. Anesthesiologists must carefully consider these factors when selecting an appropriate medication regimen for each individual patient.
While intravenous anesthetics are generally safe and effective, they can have side effects and risks, such as respiratory depression, hypotension, and allergic reactions. Anesthesia providers must closely monitor patients during and after the administration of these medications to ensure their safety and well-being.
2,4-Dinitrophenol (DNP) is a chemical compound that functions as an uncoupler of oxidative phosphorylation, disrupting the production of ATP and increasing cellular respiration rate, thereby leading to elevated body temperature and potentially toxic effects.
2,4-Dinitrophenol (DNP) is a chemical compound with the formula C6H4N2O5. It is an organic compound that contains two nitro groups (-NO2) attached to a phenol molecule. DNP is a yellow, crystalline solid that is slightly soluble in water and more soluble in organic solvents.
In the medical field, DNP has been used in the past as a weight loss agent due to its ability to disrupt mitochondrial function and increase metabolic rate. However, its use as a weight loss drug was banned in the United States in the 1930s due to serious side effects, including cataracts, skin lesions, and hyperthermia, which can lead to death.
Exposure to DNP can occur through ingestion, inhalation, or skin contact. Acute exposure to high levels of DNP can cause symptoms such as nausea, vomiting, sweating, dizziness, headache, and rapid heartbeat. Chronic exposure to lower levels of DNP can lead to cataracts, skin lesions, and damage to the nervous system, liver, and kidneys.
It is important to note that DNP is not approved for use as a weight loss agent or any other medical purpose in the United States. Its use as a dietary supplement or weight loss aid is illegal and can be dangerous.
Thiamylal - Wikipedia
Thiamylal is still in current use, primarily for induction in surgical anaesthesia or as an anticonvulsant to counteract side ... Thiamylal (Surital) is a barbiturate derivative invented in the 1950s. It has sedative, anticonvulsant, and hypnotic effects, ... Hsieh MY, Hung GY, Hsieh YL, Chang CY, Hwang B (2005). "Deep sedation with methohexital or thiamylal with midazolam for ...
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Effects of diazepam, acepromazine, detomidine, and xylazine on thiamylal anesthesia in horses. Muir, W.W., Mason, D.E. J. Am. ... The cardiorespiratory effects of thiamylal (10 mg/kg of body weight, IV) and the effects of preanesthetic medication with ... diazepam, acepromazine, detomidine, or xylazine administered prior to a thiamylal dosage of 6 mg/kg, IV, were evaluated in 6 ...
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R-134a began being phased out from use in the European Union, starting in the mid 2010s, by a directive of 2006, recommending the replacement of gases in air conditioning systems with a GWP above 100. [13] 1,1,1,2-tetrafluoroethane is subject to use restrictions in the US and other countries as well. The Society of Automotive Engineers (SAE) has proposed that it be best replaced by a new fluorochemical refrigerant HFO-1234yf (CF3CF=CH2) in automobile air-conditioning systems.[14] By model year 2021, newly manufactured light-duty vehicles in the United States will no longer use R-134a.[3] California may also prohibit the sale of canned R-134a to individuals to avoid non-professional recharge of air conditioners.[15] A ban had been in place in Wisconsin since October 1994 under ATCP 136 prohibiting sales of container sizes holding less than 15 lbs of 1,1,1,2-tetrafluoroethane, but this restriction applied only when the chemical was intended to be a refrigerant. However, the ban was lifted in ...
Paraldehyde - Wikipedia
Paraldehyde is the cyclic trimer of acetaldehyde molecules.[2] Formally, it is a derivative of 1,3,5-trioxane, with a methyl group substituted for a hydrogen atom at each carbon. The corresponding tetramer is metaldehyde. A colourless liquid, it is sparingly soluble in water and highly soluble in ethanol. Paraldehyde slowly oxidizes in air, turning brown and producing an odour of acetic acid. It attacks most plastics and rubbers and should be kept in glass bottles. Paraldehyde was first observed in 1835 by the German chemist Justus Liebig; its empirical formula was determined in 1838 by Liebigs student Hermann Fehling.[3][4] The German chemist Valentin Hermann Weidenbusch (1821-1893), another of Liebigs students, synthesized paraldehyde in 1848 by treating acetaldehyde with acid (either sulfuric or nitric acid) and cooling to 0°C. He found it quite remarkable that when paraldehyde was heated with a trace of the same acid, the reaction went the other way, recreating acetaldehyde.[5][6] ...
MedicoNotebook: Anaesthetic drugs - Active / Inactive metabolites
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Wheezing during induction of general anesthesia in patients with and without asthma: A randomized, blinded trial<...
All patients received 1.5 μg/kg fentanyl, oxygen, followed by either 5 mg/kg thiopental or thiamylal, 1.75 mg/kg methohexital ... All patients received 1.5 μg/kg fentanyl, oxygen, followed by either 5 mg/kg thiopental or thiamylal, 1.75 mg/kg methohexital ... All patients received 1.5 μg/kg fentanyl, oxygen, followed by either 5 mg/kg thiopental or thiamylal, 1.75 mg/kg methohexital ... All patients received 1.5 μg/kg fentanyl, oxygen, followed by either 5 mg/kg thiopental or thiamylal, 1.75 mg/kg methohexital ...
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The Effects of Thiamylal Sodium on Electrical Activities of the Central and Peripheral Nervous Systems in Man ... Room D, 10/16/2000 9: 00 AM - 11: 00 AM (PS) Effects of Thiamylal on Adenosine Triphosphate-Sensitive Potassium Channels during ... Blockade of Adenosine Triphosphate-sensitive Potassium Channels by Thiamylal in Rat Ventricular Myocytes ... Molecular Mechanisms of the Inhibitory Effects of Propofol and Thiamylal on Sarcolemmal Adenosine Triphosphate-sensitive ...
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