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At least 19 recordsLinked to original sources
PubMed1996

Effectiveness of a manually controlled infusion scheme of propofol and alfentanil mixture for endotracheal intubation in hypertensive patients: in comparison with thiamylal and nifedipine plus thiamylal.

BACKGROUND: Bolus administration of propofol for induction causes hypotension, especially in elderly hypertensive patient. Carefully titrated infusion of propofol minimizes adverse effects, such as hypotension, and permits a rapid recovery of its central effects. The objective of this study was to investigate the effect of a manually controlled infusion scheme of propofol and alfentanil mixture on hemodynamic stability during induction and endotracheal intubation for hypertensive patient. At the same time, the effectiveness of this scheme was compared with two other induction regimens (thiamylal or nifedipine plus thiamylal). METHODS: Sixty hypertensive patients undergoing orthopedic surgery were randomized into 3 groups (n = 20 per each group), None of the patients received premedication. Anesthesia was induced in group 1 (G1) with alfentanil 10 micrograms/kg. 30 s later, manual infusion of a mixture of propofol (10-12 mg/kg/h) and alfentanil (25 micrograms/kg/h) was performed for 2 min, followed by atracurium (5 mg) and propofol (1-1.5 mg/kg) as a bolus induction dose over 20 s, and then Suxamethonium (1.5 mg/kg) at 30-40 s later. Intubation was done while giving a continuous infusion of propofol and alfentanil. After intubation, the infusion rate was adjusted according to the blood pressure (BP) variation. Group 2 patients (G2) were induced with fentanyl (2 micrograms/kg), thiamylal (4-5 mg/kg), atracurium (5 mg) and succinylcholine (1.5 mg/kg). Induction of anesthesia in group 3 patients (G3) was the same as for G2, with additional sublingual nifedipine (1/2 capsule) 10 min prior to induction. Extra bolus dose of propofol (20 mg) or thiamylal (20 mg) was given at every 15 s if the systolic BP was still higher than 160 mmHg after induction by the above 3 regimens. The radial arterial pressure and electrocardiogram were continuously recorded for evaluation of hemodynamic changes. RESULTS: Post-intubation peak mean arterial pressure (MAP) in G1 and G3 were below to awake baseline values, while MAP of G2 was significantly higher than over awake baseline level (p < 0.001). The lowest MAP of G3 at post-intubation period before surgical stimulation were significantly lower than those of G1 and G2 (p < 0.001). Peak tachycardiac response to intubation in G2 was significantly higher than G1 (p < 0.05). After intubation, the peak rate pressure product were significantly higher in G2 compared with that in G1 (p < 0.05) and G3 (p < 0.001). CONCLUSIONS: The proposed manual infusion scheme of propofol and alfentanil mixture performed during induction and intubation attenuated the subsequent peak pressor response to incubation and reduced the hypotensive effect, in comparison to thiamylal or thiamylal plus nifedipine treatment, during post-intubation period. The same infusion scheme also attenuated the tachycardiac response to intubation.

Aged↗
PubMed1994

Effects of phenylbutazone on thiamylal disposition and anaesthesia in ponies.

Phenylbutazone given during the perisurgical period has been reported to increase the intensity and duration of thiamylal anaesthesia in horses. A possible mechanism of competitive plasma protein binding has been suggested. The purpose of the present study was to experimentally reproduce the phenomenon of increased intensity and/or duration of thiamylal anaesthesia and to determine if there is competitive displacement of plasma protein bound thiamylal by phenylbutazone. Six ponies each received one of three treatments, 11 mg/kg intravenous (i.v.) thiamylal; 8.8 mg/kg i.v. phenylbutazone; and 11 mg/kg i.v. thiamylal with 8.8 mg/kg i.v. phenylbutazone given 9 min later. Thirteen blood samples were collected from 0 time through 600 min following drug administration and plasma drug concentrations quantified by high performance liquid chromatography. The pharmacokinetics of thiamylal and phenylbutazone were best described by three- and two-compartment models, respectively. There were no significant differences in pharmacokinetic parameters for thiamylal in the presence of phenylbutazone. However, there were differences in phenylbutazone pharmacokinetics when preceded by thiamylal administration. Unbound phenylbutazone concentrations were increased at 171, 231 and 351 min when given with thiamylal, accompanied by decreases in per cent bound phenylbutazone (P < 0.05). There were also significant (P < 0.05) changes in per cent plasma protein binding of thiamylal and phenylbutazone between 120 and 360 min, when in combination. No changes in intensity or duration of anaesthesia were observed.

Anesthesia↗
PubMed1994

[Induction of anesthesia with midazolam and thiamylal].

Midazolam has a slow onset of action, while thiamylal causes pain on injection and circulatory changes. To compensate for these drawbacks, the usefulness of a combination of midazolam and thiamylal in anesthesia induction was studied. The combination method was compared to the induction with single use of thiamylal in 40 patients (20 patients in each group). The combination of 0.2 mg.kg-1 of midazolam and 1.9 mg.kg-1 of thiamylal showed a shorter onset of action than the 4-5 mg.kg-1 of thiamylal. Pain on injection was observed in 5 cases of thiamylal group but in no cases of combination group. The changes in blood pressure, heart rate and rate pressure product were obviously smaller in combination group than in thiamylal group. Although the recovery time from anesthesia of combination group (13.2 minutes) was longer than that of thiamylal group (10.5 minutes), this was not clinically important. It is concluded that anesthesia induction with the combination of midazolam 0.2 mg.kg-1 and thiamylal 1.9 mg.kg-1 is more useful than that of thiamylal alone.

Abdomen↗
PubMed1993

Effects of diazepam, acepromazine, detomidine, and xylazine on thiamylal anesthesia in horses.

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 adult horses. The quality of recovery from thiamylal anesthesia also was evaluated. Intravenous administration of thiamylal at a dosage of 10 mg/kg increased heart rate, systemic arterial, pulmonary artery, and central venous blood pressures, as well as cardiac output and arterial partial pressure of CO2 (PaCO2). The maximal rate of right ventricular pressure increase (RVdP/dtmax), respiratory rate, and arterial partial pressure of O2 (PaO2) decreased, whereas arterial pH and systemic vascular resistance remained unchanged. Preanesthetic medication with diazepam prior to IV administration of thiamylal (6 mg/kg) did not change the pattern of this response, but diazepam did increase heart rate, cardiac output, and respiratory rate during the recovery period. Administration of acepromazine (0.1 mg/kg, IV) prior to administration of thiamylal increased heart rate and decreased systemic arterial and central venous blood pressures and systemic vascular resistance. Detomidine (10 micrograms/kg, IV), administered prior to thiamylal, decreased heart rate, cardiac output, and respiratory rate, and increased right atrial blood pressure. Administration of xylazine (0.5 and 1.0 mg/kg, IV) prior to thiamylal induced effects qualitatively similar to detomidine. Thiamylal decreased RVdP/dtmax and PaO2 in horses that received diazepam, acepromazine, detomidine, or xylazine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acepromazine↗
PubMed2000

Protein binding and the metabolism of thiamylal enantiomers in vitro.

UNLABELLED: Thiamylal, a chiral thiobarbiturate, is marketed as a racemic product. We studied the serum protein binding and microsomal metabolism of thiamylal enantiomers in vitro. The unbound fraction of R(+)-thiamylal was greater than that of S(-)-thiamylal. The analysis of binding data revealed that both enantiomers bound to human serum albumin through only one site. In displacement studies with site-specific probes, dansylsarcosine, but not warfarin, significantly decreased the binding of both enantiomers. The bindings of enantiomers were also decreased by octanoate and a large concentration of oleate. These findings suggest that both enantiomers bind to Site II of albumin with higher affinity for S(-)-enantiomer. R(+)-thiamylal was metabolized more rapidly than S(-)-enantiomer by human liver microsomes. An experiment with isoform-selective inhibitors and cytochrome P-450 (CYP) isoforms showed that CYP2C9 had the highest activity for the metabolism of both enantiomers, the activity being 7 to 10 times that of CYP2E1 and CYP3A4. CYP2C9 showed a significantly rapid metabolism of R(+)-enantiomer, suggesting that CYP2C9 is mainly involved in the enantioselective metabolism of thiamylal. IMPLICATIONS: Because clinically marketed thiamylal is a racemic compound, a pharmacokinetic study of each enantiomer may be beneficial. We found that the enantioselectivity of thiamylal existed in protein binding and metabolism. This may be caused by the differences in the affinities of enantiomers for albumin and cytochrome P-450 isoform.

Adult↗
PubMed1989

[A possible circadian rhythm of susceptibility to thiamylal].

A circadian rhythm of the susceptibility to thiamylal was evaluated in 30 patients. They were divided into two groups; 15 patients were induced around 9 AM (Morning-group) and the rest were in the early afternoon (Afternoon-group). The induction was performed by intravenous administration of thiamylal sodium. Parameters measured were the time and doses of thiamylal sodium to obtain the loss of consciousness and the loss of eyelash reflex. The results were as follows; the doses of thiamylal sodium to obtain the loss of consciousness were 3.5 +/- 0.6 mg.kg-1 (mean +/- SD) in Morning-group, and 4.1 +/- 0.4 mg.kg-1 in Afternoon-group, respectively. Thus, larger doses of thiamylal were necessary to obtain the loss of consciousness in Afternoon-group than in Morning-group (P less than 0.01). The doses of thiamylal sodium to obtain the loss of eyelash reflex were 4.4 +/- 0.8 mg.kg-1 in Morning-group and 5.0 +/- 0.6 mg.kg-1 in Afternoon-group, respectively. Also, larger doses of thiamylal were necessary to obtain the loss of eyelash reflex in Afternoon-group than in Morning-group (P less than 0.05). This study suggests that a circadian rhythm of the susceptibility to thiamylal exists in humans.

Adult↗
PubMed1997

Pharmacokinetics of thiamylal enantiomers in humans.

Thiamylal, a chiral thiobarbiturate, is marketed as the racemate. The pharmacokinetic behavior of thiamylal enantiomers was studied in patients undergoing thiamylal treatment. The percentage of R(+)-thiamylal unbound to serum protein was 1.5 times greater than that of S(-)-enantiomer (17.5 +/- 2.6% and 11.7 +/- 2.0% mean +/- SD, p < 0.001, n = 7). The pharmacokinetic parameters of enantiomers were estimated in 6 patients. S(-)-thiamylal serum concentration was higher than R(+)-enantiomer in all patients at all time points examined. Total clearance of R(+)-thiamylal (0.27 +/- 0.23 1/hr/kg) was 1.8 times greater (p < 0.05) than that of S(-)-thiamylal (0.15 +/- 0.13). The volume of distribution at steady state of R(+)-thiamylal (3.66 +/- 1.99 l/kg) was 1.4 times higher (p < 0.05) than that of S(-)-enantiomer (2.60 +/- 1.35). The differences in these parameters may be due mainly to enantioselective binding to serum protein.

Adult↗
PubMed2004

Molecular mechanisms of the inhibitory effects of propofol and thiamylal on sarcolemmal adenosine triphosphate-sensitive potassium channels.

BACKGROUND: Both propofol and thiamylal inhibit adenosine triphosphate-sensitive potassium (KATP) channels. In the current study, the authors investigated the effects of these anesthetics on the activity of recombinant sarcolemmal KATP channels encoded by inwardly rectifying potassium channel (Kir6.1 or Kir6.2) genes and sulfonylurea receptor (SUR1, SUR2A, or SUR2B) genes. METHODS: The authors used inside-out patch clamp configurations to investigate the effects of propofol and thiamylal on the activity of recombinant KATP channels using COS-7 cells transfected with various types of KATP channel subunits. RESULTS: Propofol inhibited the activities of the SUR1/Kir6.2 (EC50 = 77 microm), SUR2A/Kir6.2 (EC50 = 72 microm), and SUR2B/Kir6.2 (EC50 = 71 microm) channels but had no significant effects on the SUR2B/Kir6.1 channels. Propofol inhibited the truncated isoform of Kir6.2 (Kir6.2DeltaC36) channels (EC50 = 78 microm) that can form functional KATP channels in the absence of SUR molecules. Furthermore, the authors identified two distinct mutations R31E (arginine residue at position 31 to glutamic acid) and K185Q (lysine residue at position 185 to glutamine) of the Kir6.2DeltaC36 channel that significantly reduce the inhibition of propofol. In contrast, thiamylal inhibited the SUR1/Kir6.2 (EC50 = 541 microm), SUR2A/Kir6.2 (EC50 = 248 microm), SUR2B/Kir6.2 (EC50 = 183 microm), SUR2B/Kir6.1 (EC50 = 170 microm), and Kir6.2DeltaC36 channels (EC50 = 719 microm). None of the mutants significantly affects the sensitivity of thiamylal. CONCLUSIONS: These results suggest that the major effects of both propofol and thiamylal on KATP channel activity are mediated via the Kir6.2 subunit. Site-directed mutagenesis study suggests that propofol and thiamylal may influence Kir6.2 activity by different molecular mechanisms; in thiamylal, the SUR subunit seems to modulate anesthetic sensitivity.

ATP-Binding Cassette Transporters↗
PubMed1985

Pharmacokinetics of pentobarbital and thiamylal as combined anesthetics in sheep.

This study was performed to investigate the possible mechanisms underlying prolongation of anesthesia times in sheep caused by the sequential administration of thiamylal and pentobarbital. Sodium thiamylal was injected as an intravenous bolus dose (13.2 mg/kg) followed in 7 min by sodium pentobarbital (14.3 mg/kg) by the same route to seven sheep. Separate studies were conducted for each of the two drugs administered separately to the same animals at the same doses. Mean anesthesia times (to the return of the palpebral reflex) were 7.89 min (thiamylal), 5.39 min (pentobarbital) and 34.1 min (the sequential combination). The kinetic parameters Vd(area), Vd(ss), t 1/2 beta, and ClB for either drug were not affected by the other when given in combination. The t 1/2 alpha was shorter, and the Vc was smaller, for pentobarbital when administered with thiamylal, while there were no changes in thiamylal disposition for the combination regimen. Computer-generated curves, associated with the two-compartment open model showing the fraction of dose in each compartment as a function of time, illustrated that pentobarbital rapidly achieved higher concentrations in the peripheral compartment after prior thiamylal administration. Protein-binding studies showed that this could not be attributed to displacement of pentobarbital from plasma albumin by thiamylal. Calculation of total and free drug concentrations at the time of awakening showed that, when the drugs were combined, the concentration of each drug was less than half of that observed at awakening when they were studied separately. It can be concluded that the prolonged sleeping times associated with the sequential combination of the two agents were not due to an alteration in kinetic parameters of either drug caused by the other, but rather to an additive effect of the subanesthetic concentrations of the two drugs when combined. The fact that sleeping times were supra-additive is attributed to a shift of awakening time from the distribution (alpha) phase, when given independently, to the elimination (beta) phase when administered in combination.

Anesthesia, Intravenous↗
PubMed2003

Effects of the intravenously administered anaesthetics ketamine, propofol, and thiamylal on the cortical renal blood flow in rats.

Intravenous anaesthetics such as ketamine, propofol, and thiamylal are widely used, although the direct effects of these anaesthetics on the renal blood flow (RBF) have not been well elucidated. In this study, we examined the effects of bolus and continuous administrations of ketamine, propofol, and thiamylal on cortical RBF and the effects of noradrenaline (NA) on RBF under continuous administration of these anaesthetics. We used laser Doppler flowmetry to measure the effects of bolus injection and continuous infusion of ketamine, propofol, and thiamylal on cortical RBF in male Wistar rats. We also examined the effects of the anaesthetics on mean arterial blood pressure (MAP) and heart rate (HR). Bolus injections of ketamine, propofol, or thiamylal (1-8 mg/kg each, n = 10) at clinically relevant concentrations did not affect MAP, HR, or RBF. Continuous administration of ketamine, propofol, or thiamylal (1-8 mg/kg/h each, n = 10) did not affect MAP, HR or RBF. Exogenous NA (2 microg/kg) caused an increase in MAP and a decrease in RBF and HR. In experiments with continuous infusions of propofol or thiamylal (1-8 mg/kg/h each, n = 10), similar results were observed without infusion of any anaesthetics. However, bolus injection of NA did not result in a decrease in RBF during continuous ketamine infusion (98.8 +/- 6.7% of control, n = 6, p < 0.05), while ketamine did not affect the NA-induced increase in MAP. In conclusion, bolus and continuous administrations of ketamine, propofol, and thiamylal did not affect the RBF. From our present findings, ketamine would be useful for maintaining the RBF.

Anesthetics, Intravenous↗
PubMed1993

Inotropic and electrophysiologic effects of propofol and thiamylal in isolated papillary muscles of the guinea pig and the rat.

We compared the inotropic and electrophysiologic effects of propofol and thiamylal in isolated papillary muscles of the guinea pig and rat. Propofol applied in clinical 10% intralipid emulsion showed concentration-dependent negative inotropic effects, accompanied by decreased action potential duration, in the guinea pig. Intralipid alone had no effect. Although thiamylal showed a concentration-dependent depression similar to propofol in the guinea pig, depolarization of resting membrane potential was seen at 0.1 and 0.3 mM, and a slight prolongation of action potential duration at 90% repolarization at 0.1 mM, and then a decrease of action potential duration at 0.3 mM. In rat papillary muscles, propofol did not produce any depression of contractile force, whereas thiamylal produced a concentration-dependent negative inotropic effect. The important findings observed in the action potential in rat papillary muscles were the modest shortening of action potential duration after propofol application, and the significant decrease of resting membrane potential and the significant prolongation of action potential duration caused by thiamylal. Both propofol and thiamylal depressed slow action potentials and contractile force in guinea pig papillary muscles depolarized by 25 mM K+ solution. In conclusion, the negative inotropic effects of propofol and thiamylal might be caused by inhibition of trans-sarcolemmal Ca2+ influx accompanied by shortening of action potential duration in guinea pig papillary muscles. The action potential of thiamylal might be affected by the suppression of K+ current in guinea pig and rat papillary muscles that was never observed in the propofol-treated tissue.

Action Potentials↗
PubMed1994

Clonidine decreases the dose of thiamylal required to induce anesthesia in children.

Clonidine is a useful drug to give preoperatively because it produces anxiolysis, sedation, and hemodynamic stability, and reduces intravenous and volatile anesthetic requirements. Several premedicants, including midazolam and diazepam, have been shown to reduce the induction dose of intravenous anesthetics, such as thiopental, ketamine, or propofol. A randomized, double-blind controlled study was conducted to evaluate the effect of premedication with oral clonidine on thiamylal requirement for the induction of anesthesia and on associated hemodynamic changes in children. Sixty children (ASA grades I-II, 7-12 yr old) were assigned randomly to receive one of three treatments (n = 20, for each group): placebo (control), clonidine 2 micrograms/kg, or clonidine 4 micrograms/kg 105 min before the induction of anesthesia. Thiamylal was injected at a dose of 1 mg/kg every 15 s until loss of the eyelash reflex and the dose was recorded. Blood pressure (BP), heart rate (HR), and arterial oxygen saturation were recorded every minute from the beginning of injection of thiamylal for 5 min. Significant decreases in thiamylal dose were observed in patients receiving clonidine. The induction dose of thiamylal (mean +/- SD) was 5.4 +/- 0.9, 4.5 +/- 1.1, and 3.4 +/- 0.9 mg/kg for patients receiving placebo, clonidine 2 micrograms/kg, and clonidine 4 micrograms/kg, respectively (P < 0.05). Systolic BP decreased by 6.8%, 5.6%, and 6.6% and HR increased by 5.7%, 4.8%, and 4.1% after administration of thiamylal in the control (placebo) group and the clonidine 2 micrograms/kg and clonidine 4 micrograms/kg groups, respectively (P > 0.05). Premedication with oral clonidine reduced the dose of intravenous thiamylal required for the induction of anesthesia in children.

Anesthesia, Intravenous↗
PubMed1991

Effect of midazolam preanesthetic administration on thiamylal induction requirement in dogs.

The thiamylal sparing effect of midazolam was studied in 30 healthy Beagle and mixed-breed dogs. Using a replicated Latin square design, all dogs were given placebo (saline solution) and 0.025, 0.05, 0.1, and 0.2 mg of midazolam/kg of body weight prior to IV administration of thiamylal sodium. The 0.1 and 0.2 mg/kg dosages significantly decreased the amount of thiamylal required to obtund swallowing reflex and easily achieve endotracheal intubation. Midazolam at 0.1 and 0.2 mg/kg reduced thiamylal requirement by 16.4% and 18.9%, respectively, whereas the 0.05 mg/kg dosage decreased thiamylal requirement by only 6.8%. The 0.2 mg/kg dosage did not further decrease thiamylal requirement beyond that achieved with the 0.1 mg/kg dosage of midazolam. This study demonstrates that the preanesthetic IV administration of midazolam reduces the thiamylal dose necessary to accomplish intubation. The optimal preanesthetic dosage (lowest dosage with significant effect) was 0.1 mg/kg.

Animals↗
PubMedDate not supplied

Electroconvulsive therapy-induced cardiac arrhythmias during anesthesia with methohexital, thiamylal, or thiopental sodium.

STUDY OBJECTIVE: To determine the frequency of electroconvulsive therapy (ECT)-induced arrhythmias under methohexital, thiamylal, or thiopental sodium anesthesia with and without atropine premedication. DESIGN: A randomized, double-blind study, placebo-controlled for atropine. SETTING: The inpatient psychiatric unit at a university medical center. PATIENTS: Forty-nine patients scheduled for ECT. INTERVENTIONS: Atropine 0.6 mg intravenously (IV) or an equal volume of normal saline IV was given before IV induction of anesthesia with methohexital 0.5 to 1.0 mg/kg, thiamylal 1.5 to 2.5 mg/kg, or thiopental sodium 1.5 to 2.5 mg/kg. MEASUREMENTS AND MAIN RESULTS: Single-lead electrocardiogram (ECG) recordings were made for 1 minute before induction, during induction of anesthesia, and for 5 minutes after the ECT stimulus. Each ECG was evaluated for arrhythmias and evidence of ischemia in a blinded fashion. Blood pressure and ECG evidence of ischemia did not differ among the groups. Seizure duration was significantly (p less than 0.05) prolonged by a mean of 5 seconds during methohexital anesthesia compared with thiopental sodium and thiamylal (47.6 +/- 18.6 seconds, 42.7 +/- 13.2 seconds, and 42.7 +/- 15.2 seconds, respectively). The frequency of sinus bradycardia was decreased (p less than 0.05) with methohexital (8%) compared with thiopental sodium (20%) and thiamylal (20%). The frequency of premature atrial contractions was decreased (p less than 0.05) with methohexital (43%) compared with thiamylal (61%) but not with thiopental sodium (57%). The frequency of premature ventricular contractions was decreased (p less than 0.05) with methohexital (27%) compared with thiopental sodium (44%) but not with thiamylal (40%). Atropine decreased the frequency of bradycardia (9% vs. 24%) and premature atrial contractions (47% vs. 61%) and increased the frequency of sinus tachycardia (88% vs. 75%). CONCLUSIONS: These data suggest that anesthesia for ECT therapy should be induced with methohexital to minimize the possibility of potentially life-threatening cardiac arrhythmias. Atropine premedication may further decrease the frequency of premature atrial contractions and bradycardia, while increasing the frequency of tachycardia.

Adult↗
PubMed1999

The effect of propofol and thiamylal on hypertensive responses to a rapid increase in isoflurane concentration.

STUDY OBJECTIVE: To compare the effects of propofol and thiamylal on the hyperdynamic circulatory response caused by a rapid increase in isoflurane concentration. DESIGN: Prospective, randomized, double-blind study. SETTING: Operating rooms of a university hospital. PATIENTS: 30 ASA physical status I adult patients scheduled for elective surgery with general anesthesia. INTERVENTIONS: Patients were anesthetized with either propofol 2 mg/kg (propofol group, n = 15) or thiamylal 4 mg/kg (thiamylal group, n = 15). Two minutes after anesthesia induction, the inspired isoflurane concentration was rapidly increased from 0.5% to 5% and maintained for 5 minutes. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure significantly increased after the increase in isoflurane concentration in the thiamylal group, but it did not change in the propofol group. The isoflurane-induced increase in rate-pressure product was significantly greater in the thiamylal group than in the propofol group. CONCLUSION: Propofol induction of anesthesia more effectively attenuates the circulatory responses to a sudden increase in isoflurane concentration than does thiamylal.

Adult↗
PubMed2000

Blockade of adenosine triphosphate-sensitive potassium channels by thiamylal in rat ventricular myocytes.

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.

2,4-Dinitrophenol↗
PubMed2003

Thiamylal and pentobarbital have opposite effects on human platelet aggregation in vitro.

UNLABELLED: The effects of barbiturates on human platelet function are not fully understood. We designed the present study to clarify the effects of thiamylal and pentobarbital on human platelet aggregation and to elucidate the underlying mechanisms in vitro. Human platelet aggregation induced by adenosine diphosphate (ADP), epinephrine, arachidonic acid (AA), and (+)-9,11-epithia-11,12-methano-thromboxane A(2) (STA(2)), measured with an 8-channel light transmission aggregometer, was compared in the absence and presence of thiamylal or pentobarbital. To estimate thromboxane A(2) (TXA(2)) receptor binding affinity, Scatchard analysis was done using [(3)H]-S145, a specific TXA(2) receptor antagonist. STA(2)-TXA(2) receptor binding assay was also examined. The release of AA was determined in platelets preincubated with [(3)H]-AA and stimulated by ADP, using a liquid scintillation analyzer. Cytosolic free calcium concentration ([Ca(2+)](i)) was measured in fluo-3/AM-loaded platelets using a fluorometer. Thiamylal enhanced, but pentobarbital suppressed, ADP- and epinephrine-induced platelet aggregation, but they did not affect AA- or STA(2)-induced platelet aggregation. They had no effect on TXA(2) receptor binding affinity. Although thiamylal increased and pentobarbital decreased release of [(3)H]-AA from ADP-stimulated platelets, both barbiturates had no effect on ADP-induced [Ca(2+)](i) increase. We conclude that thiamylal enhances but pentobarbital suppresses human platelet aggregation in vitro. These effects of barbiturates are mediated by altered AA release without affecting [Ca(2+)](i) increase. IMPLICATIONS: Thiamylal enhances but pentobarbital suppresses human platelet aggregation in vitro. These effects are attributed to altered arachidonic acid release from platelets, possibly by the effects of phospholipase A(2), but not secondary to altered cytosolic free calcium concentration.

Anesthetics, Intravenous↗