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PubMed2001

Effects of propofol on ischemia and reperfusion in the isolated rat heart compared with thiamylal.

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.

Analysis of Variance↗

PubMed1984

Inhibition of platelet shape-change by sodium thiamylal.

Canine platelets were treated in vitro with sodium thiamylal and allowed to surface activate on glass coverslips. Platelet surface activation was markedly inhibited by sodium thiamylal at concentrations as low as 2 X 10(-4) M and this inhibitory effect was most pronounced after pretreating the platelets for 30 minutes with sodium thiamylal. Treatment with sodium thiamylal prevented spreading platelets from reaching the fully spread stage. Additional experiments demonstrated that sodium thiamylal need not be present in the medium during the activation process in order to exert its effect. Preliminary platelet aggregation studies show sodium thiamylal in the 10(-4) - 10(-3) M range to be capable of inhibiting aggregation induced by adenosine diphosphate.

Animals↗

PubMed1998

[Circulatory changes at the time of anesthetic induction and endotracheal intubation--comparison of thiamylal induction group and propofol induction group].

We examined the circulatory changes after intravenous thiamylal with additional injection of thiamylal 1 minute before intubation and after propofol at the time of anesthetic induction and endotracheal intubation. Sixty ASA I or II patients were studied after the institutional and informed consents. We compared the following three groups. Group I (n = 20): Anesthesia was induced with thiamylal 5 mg.kg-1 and intubation with the aid of vecuronium 0.1 mg.kg-1. Group II (n = 20): Anesthesia was induced with thiamylal 3 mg.kg-1 and vecuronium 0.1 mg.kg-1. One minute before the intubation, the patients received additional thiamylal 4 mg.kg-1. Group III (n = 20): Anesthesia was induced with propofol 2.5 mg.kg-1 and intubation was performed with the aid of vecuronium 0.1 mg.kg-1. We examined the systolic, diastolic and mean blood pressures, heart rate, and rate pressure product (RPP) in the three groups. The examinations were performed before and after induction, soon after intubation, and every one minute after intubation for 5 minutes. After the endotracheal intubation, the systolic blood pressure and heart rate increased in Group I. But the systolic and diastolic pressures were significantly more stable in Group II and Group III. The change of the RPP was slight and most stable in Group II compared with the other two groups. We conclude that additional injection of thiamylal 4 mg.kg-1 following induction of anesthesia with thyamylal 3 mg.kg-1 1 minute before endotracheal intubation is an effective method for minimizing the increase in blood pressure and circulatory changes at the time of rapid induction of anesthesia and endotracheal intubation.

Adjuvants, Anesthesia↗

PubMed2000

Changes in left ventricular end-diastolic area, end-systolic wall stress, and fractional area change during anesthetic induction with propofol or thiamylal.

PURPOSE: To elucidate the mechanisms of the more profound hypotensive effects of propofol relative to thiamylal, we monitored changes in left ventricular (LV) preload, afterload, and contractility during the course of anesthetic induction with propofol and thiamylal. METHODS: Thirty-two patients (ASA I) were randomly assigned into two groups and injected with propofol (2 mg.kg(-1)) or thiamylal (4 mg.kg(-1)) as anesthetic induction agents. Transthoracic echocardiography (TTE) was used to assess LV performance before and during induction by the two anesthetics. The LV end-diastolic area (EDA) and LV end-systolic wall stress (ESWS) were used as indices of LV preload and LV afterload, respectively, while LV contractility was assessed by the fractional area change (FAC). RESULTS: Both propofol and thiamylal significantly reduced EDA and ESWS without significant change in FAC. Propofol-induced reductions in EDA and ESWS were significantly greater than those of thiamylal. CONCLUSION: The more profound hypotension observed during induction of anesthesia with propofol is due to the greater decrease in preload and afterload than with thiamylal, but not to a decrease in LV contractility.

Clinical Trial↗

PubMed1995

Phosphatidylinositol responses are involved in the vascular effects of thiamylal and fentanyl.

Although thiobarbiturates potentiate, and fentanyl attenuates peripheral vasoconstriction, the intracellular mechanism involved in this phenomenon is not clear. Because smooth muscle contraction induced by alpha 1-adrenoceptor agonists is mediated by the phosphatidylinositol (PI) response, this study was carried out to clarify if thiamylal and fentanyl affect the norepinephrine-induced PI response in rat aortic slices. Rat aortic slices were incubated in Krebs-Henseleit solution containing 5 mM LiCl, [3H]myo-inositol, and varying concentrations of thiamylal or fentanyl. The Pl response was stimulated by 0.9 microM (ED50) norepinephrine (NE). The [3H]inositol monophosphate (IP1) was separated from [3H]myo-inositol by column chromatography and counted with a liquid scintillation counter. The basal IP1 accumulation was not affected by thiamylal and fentanyl. Norepinephrine-induced IP1 accumulation was potentiated by thiamylal at concentrations of 10 microM and 100 microM. Norepinephrine-induced IP1 accumulation was attenuated by 1 microM and 10 microM fentanyl. The results suggest that thiamylal stimulates the NE-induced PI response, which potentiates the vasoconstriction, and fentanyl attenuates NE-induced PI response, which would attenuate the vasoconstriction.

Anesthetics, Intravenous↗

PubMed1995

Enantioselective determination of thiamylal in human serum by high-performance liquid chromatography.

Thiamylal, a widely used anesthetic drug, has two enantiomers. We developed a novel and simple method for measuring thiamylal enantiomers in human serum using reversed-phase high-performance liquid chromatography. R(+)- and S(-)-Thiamylal were separated using a chiral mobile phase containing beta-cyclodextrin, and detected at the range of 50 ng/ml-25 micrograms/ml in serum. The relative standard deviations of R(+)- and S(-)-thiamylal were 3.4-8.7% and 2.8-8.7% for the intra-day assay, and 2.8-12.0% and 2.8-13.0% for the inter-day assay. This method may be applied to enantioselective pharmacokinetic studies of thiamylal.

Chromatography, High Pressure Liquid↗

PubMed2002

Effects of GABAergic agents on anesthesia induced by halothane, isoflurane, and thiamylal in mice.

The effects of gamma-aminobutyric acid (GABA) receptor modulators and GABA uptake inhibitors on volatile and intravenous anesthetic-induced anesthesia were examined in male ICR mice, as assessed by the loss of righting reflex (LORR). The GABA uptake inhibitors, NO-711 and SKF89976A, which are permeable to the blood-brain barrier (BBB), but not nipecotic acid or guvacine, which poorly permeate BBB, shortened the onset of LORR but did not affect the duration of LORR induced by 1.5% halothane and 2% isoflurane. NO-711 and SKF89976A shortened the onset of and prolonged the duration of LORR induced by thiamylal (45 mg/kg i.p.). The GABA mimetics, muscimol and diazepam, shortened the onset of and prolonged the duration of LORR induced by halothane, isoflurane, and thiamylal. On the other hand, picrotoxin, a GABAA receptor antagonist, prolonged the onset of LORR induced by all anesthetics tested. Another GABAA receptor antagonist, bicuculline, prolonged the onset of LORR induced by halothane, but not by isoflurane or thiamylal. Both antagonists failed to affect the duration of LORR induced by halothane, isoflurane, or thiamylal. Baclofen, a GABAB receptor agonist, enhanced both volatile anesthetics- and thiamylal-induced anesthesia. These results suggest that anesthesia induced by volatile and intravenous anesthetics might be correlated with the modification of the pre- and/or postsynaptic GABAergic activities.

Anesthesia↗

PubMed1999

Improved method of determining thiamylal enantiomers in human serum by high-performance liquid chromatography.

Thiamylal, a widely used anesthetic drug, has two enantiomers. We developed a simple and rapid method for measuring the thiamylal enantiomers in human serum. The method involves a liquid-liquid extraction procedure followed by chiral resolution using a 5 microm silica-bonded alpha1-acid glycoprotein column (Chiral-AGP). The thiamylal enantiomers and internal standard were eluted within 15 min and were well-resolved. At concentrations of 1, 5 and 20 microg ml(-1), the relative standard deviations of R(+)- and S(-)-thiamylal were 1.35-2.88% and 1.37-3.01%, respectively, for the intra-day assay, and 2.93-4.46% and 2.46-4.84%, respectively, for the inter-day assay. This method facilitates the routine monitoring and pharmacokinetic studies of thiamylal enantiomers.

Anesthetics, Intravenous↗

PubMed1998

Differential inhibitory effects of thiopental, thiamylal and phenobarbital on both voltage-gated calcium channels and NMDA receptors in rat hippocampal slices.

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.

Anesthetics, Intravenous↗

PubMed1981

Antianalgesic action of thiamylal sodium in cats.

The effects of thiamylal on the nociceptor-driven neural activity in the spinal cord were studied in decerebrate, non-anesthetized cats. Noxious stimulation was induced by the injection of bradykinin into the femoral artery and the neutral response in the lateral funiculus was measured by the multi-unit activity technique. The effects of thiamylal on the bradykinin-induced response were compared before and after the spinal cord transection, above the recording site. Thiamylal, 5 mg/kg i.v., potentiated the response significantly before the cord transection and depressed it after the transection. These findings indicate that the antianalgesic action of thiamylal is induced at the spinal cord level: although this anesthetic agent does have a direct intraspinal depressant action, the multisynaptic neural network of the supraspinal pain inhibition system is more susceptible to the actions of anesthetics, and the depression of this descending system by thiamylal results in a release of spinal cord nociceptive neural mechanisms from the supraspinal control.

Animals↗

PubMedDate not supplied

Thiamylal-sparing effect of midazolam for canine endotracheal intubation. A clinical study of 118 dogs.

One hundred eighteen dogs were studied at three veterinary teaching hospitals after the administration of midazolam (0.1 mg/kg, intravenously [IV]) or a placebo. Midazolam and placebo treatments were randomized and blinded to the investigators. The dose of thiamylal required for tracheal intubation 3 to 5 minutes after midazolam or placebo was calculated. The dose of thiamylal at the three hospitals was 10.6, 9.8, and 10.1 mg/kg i.v. after midazolam, and 12.1, 11.2, and 11.6 mg/kg i.v. after placebo. Pooled data from the three hospitals yielded a significant (p < .001) decrease in mean IV thiamylal dose after midazolam (10.2 mg/kg) compared with placebo (11.6 mg/kg). Overall, there was a 12% decrease in the dose of thiamylal required for tracheal intubation after midazolam compared to that after the placebo. The thiamylal dose was significantly (p < .001) decreased after midazolam compared with placebo for dogs weighing more than 15 kg but not for dogs weighing less than 15 kg.

Anesthesia, Endotracheal↗

PubMed1991

The vasodilator effect of thiamylal in dog mesenteric artery: contribution of intracellular action.

The effects of thiamylal on contractions induced by various mechanisms were investigated in mesenteric arteries isolated from dogs. Thiamylal (10(-4) to 10(-3) M) significantly inhibited contractions induced by KCl (20 mM) in normal media, and those induced by norepinephrine (10(-5) M) in normal and Ca(2+)-free media. Caffeine-induced contraction was significantly inhibited by thiamylal in the concentrations greater than 3 x 10(-5) M in intact fibers and 10(-5) M in chemically skinned fibers. Chemically skinned fibers that were precontracted with Ca2+ were relaxed by thiamylal in concentrations lower than those required to relax intact fibers that were precontracted with KCl (20 mM); the ED50 was 1.52 x 10(-5) M in skinned fibers and 5.50 x 10(-4) M in intact fibers. These results suggest that intracellular mechanisms are involved in thiamylal-induced vasodilatation of dog mesenteric artery.

Animals↗

PubMed2003

Intravenous alprostadil, an analog of prostaglandin E1, prevents thiamylal-fentanyl-induced bronchoconstriction in humans.

UNLABELLED: Prostaglandin (PG) E(1) relaxes airway smooth muscle in animals. However, no clinical data have been published on the bronchorelaxant effects of IV alprostadil, an analog of PGE(1). We have described experimental thiamylal-fentanyl-induced bronchoconstriction in humans; we now report the effect of IV alprostadil on thiamylal-fentanyl-induced bronchoconstriction. Thirty-two patients were allocated randomly to a control group (n = 16) and alprostadil group (n = 16). Anesthesia was induced with thiamylal 5 mg/kg and vecuronium 0.3 mg/kg and maintained with a continuous infusion of thiamylal 15 mg. kg(-1). h(-1). The lungs of the patients were ventilated with 50% nitrous oxide in oxygen. Twenty minutes after the induction of anesthesia, patients in the control group were given a continuous infusion of normal saline 20 mL/h, and those in the alprostadil group received a continuous infusion of alprostadil 0.2 micro g. kg(-1). min(-1) (20 mL/h), both for 60 min. Both groups were then given fentanyl 5 micro g/kg. Systolic and diastolic arterial blood pressure, heart rate, mean airway resistance (Rawm), expiratory airway resistance (Rawe), and dynamic lung compliance (Cdyn) were measured at the baseline, just before the fentanyl injection (T30), at three consecutive 6-min intervals after fentanyl injection (T36, T42, and T48), and 30 min after fentanyl injection (T60). Baseline Rawm, Rawe, and Cdyn values were comparable between groups. In the control group, both Rawm and Rawe were significantly increased at T36-60, and Cdyn was significantly decreased at T36-60 compared with the baseline. Patients given alprostadil showed no change in Rawm, Rawe, or Cdyn at T36-60. Thus, IV alprostadil seems to have a bronchodilator effect in humans. IMPLICATIONS: IV alprostadil, an analog of prostaglandin E(1), prevents thiamylal-fentanyl-induced bronchoconstriction in humans. This finding suggests that IV alprostadil has a bronchodilator effect.

Adult↗

PubMed1986

Reduction in the myocardial sodium current by halothane and thiamylal.

Effects of two general anesthetics, halothane and thiamylal, on the fast sodium inward current (INa) of enzymatically isolated single rat ventricular cells were studied under current clamp and voltage clamp conditions. A suction pipette technique was used for potential measurement, current injection and internal perfusion of isolated cells. In current clamp experiments, sodium action potential was elicited in a Ca-free Co Krebs solution and the action potential was reduced by 0.5% halothane and 5 X 10(-5) M thiamylal. In voltage clamp experiments, the calcium current was suppressed by replacing Ca with Co and the potassium current was eliminated by replacing K with Cs and adding 4-aminopyridine and tetraethylammonium. Both anesthetics decreased INa, in a dose dependent manner, without changing the shape of the current-voltage curve. Halothane (1%) shifted the steady state inactivation curve in a negative direction along the potential axis by 8.5 +/- 2 mV (mean +/- S.D., n = 4). Thiamylal, 5 X 10(-5) and 10(-4) M, shifted the curve in a negative direction by 4.4 +/- 0.8 mV (n = 5) and 8.6 +/- 3.2 mV (n = 5), respectively. Both agents slightly reduced the maximum sodium conductance (gNa). Halothane (1%) increased half recovery time from inactivation measured at -80 mV from 30 +/- 15 to 80 +/- 25 ms (n = 4). Thiamylal (10(-4) M) prolonged it at - 75 mV from 50 +/- 20 to 110 +/- 15 ms (n = 5). With a test pulse duration of 50 ms, neither drug produced a use-dependent inhibition of INa. Halothane and thiamylal depress the INa of cardiac muscles mainly by shifting the steady state inactivation curve in a negative direction along the potential axis. Relatively small prolongation of half recovery time from inactivation and no sign of use-dependent inhibition suggest a molecular mechanism which differs in some respects from the local anesthetics.

Animals↗

PubMed1990

Thiamylal: review of the literature and report of a suicide.

A 28-year-old white male medical student was found hanging by the neck from the bathroom closet of a hotel room. An intravenous infusion line leading from a bottle of thiamylal sodium (an ultrashort-acting barbiturate) was inserted into the antecubital vein of the left arm. Blood was analyzed for alcohol and other volatiles and for acidic, basic, and neutral drugs. Only thiamylal was detected. Thiamylal was quantified by high-performance liquid chromatography with ultraviolet detection, and its presence was confirmed by gas chromatography/mass spectrometry. The tissue distribution of thiamylal was 29 mg/L in blood, 1.4 mg/L in urine, 16 mg/L in bile, 135 mg/kg in liver, 25 mg/kg in kidney, and 0.4 mg in the stomach contents. The uptake and distribution of thiamylal is similar to thiopental. The distribution of the drug in this case was compared to that of other fatalities involving ultrashort-acting barbiturates.

Adult↗

PubMed1980

Influence of time interval between administration of chloramphenicol and thiamylal on the sleeping time of mice.

The influence of the time interval between chloramphenicol and thiamylal administrations on the sleeping time of mice was studied. Two hundred 20- to 25-g mice were given (intraperitoneally) chloramphenicol or isotonic saline solution and then thiamylal at different time intervals between drugs. The duration of anesthesia was measured as the time between the loss and the return of the righting reflex. The results indicated that in mice given chloramphenicol simultaneously with thiamylal (0 time interval), the sleeping time was increased by a factor of about 10 as compared with the sleeping time in mice given thiamylal alone. As the time interval between administrations of thiamylal and chloramphenicol was increased (from 0.25 to 4 hours), the prolongation of sleeping time decreased correspondingly.

Animals↗

PubMed1998

[Comparison of propofol and pentazocine combined with thiamylal for laryngeal mask insertion].

We evaluated the combination of pentazocine and thiamylal as induction agents for laryngeal mask airway (LMA) insertion and compared this with propofol. Ninety-four patients, ASA grade 1 or 2, were randomly assigned to one of four induction groups as follows; group P: propofol 2.5 mg.kg-1, group p 0.3: pentazocine 0.3 mg.kg-1 followed by thiamylal 5 mg.kg-1, group p 0.6: pentazocine 0.6 mg.kg-1 followed by thiamylal 5 mg.kg-1, and group T: thiamylal 5 mg.kg-1. In group T (n = 5), insertion of LMA was impossible due to inadequate anesthesia. In contrast, good and acceptable conditions for LMA insertion were obtained in 85.2%, 86.7%, and 96.9% of group P, p 0.3, and p 0.6, respectively. Apneic interval, endtidal CO2 and arterial CO2 were significantly greater in pentazocine groups than in propofol group (group P < p 0.3 < p 0.6). Systolic pressure decreased after induction in all groups. Decreases in systolic and diastolic pressure were significantly greater in group P. Heart rate did not show any significant change. We conclude that the induction with the combination of pentazocine and thiamylal provides suitable conditions for LMA insertion with more stable hemodynamics compared with propofol. Doses of 0.3 mg.kg-1 seem to be desirable for LMA insertion.

Adjuvants, Anesthesia↗

PubMed1996

Optimal dose of thiamylal in combination with midazolam for induction of anaesthesia.

PURPOSE: The optimal dose range of thiamylal, combined with midazolam, in the induction of anaesthesia was evaluated using haemodynamic variables. METHODS: The 200 patients, aged 30 to 70 yr, were randomly divided into five groups by midazolam dosage. Anaesthesia was induced with midazolam 0.05, 0.075, 0.10, 0.15, or 0.20 mg.kg-1. Two minutes later, 50 mg thiamylal was administered followed by 25 mg increments until verbal response and eyelash reflex disappeared and blood pressure decreased to a level less than that of preinduction. Tracheal intubation was performed with 0.15 mg.kg-1 vecuronium. Blood pressure and heart rate were monitored during induction. Optimal induction was defined as a systolic blood pressure one minute after intubation within +/- 20% of that before induction. RESULTS: There were 164 patients whose systolic blood pressure were within these criteria. Blood pressure decreased two minutes after induction and 3 to 15 min after intubation in all groups. Heart rate increased one minute after intubation in 0.05 mg.kg-1, 0.075 mg.kg-1 and 0.10 mg.kg-1 midazolam groups. The optimal range of thiamylal was 4.0 +/- 1.1 (mean + SD), 3.1 +/- 1.2, 2.8 +/- 1.1, 2.3 +/- 1.2, and 1.7 +/- 1.0 mg.kg-1 in combination with midazolam 0.05, 0.075, 0.10, 0.15, and 0.20 mg.kg-1, respectively. CONCLUSION: The optimal dose range, to maintain haemodynamic stability, for thiamylal induction of anaesthesia in combination with midazolam, 0.05-0.2 mg.kg-1 was found to range from 4.0 to 1.7 mg.kg-1.

Adult↗