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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↗
PubMed2003

Pharmacological effects of intravenous melatonin: comparative studies with thiopental and propofol.

BACKGROUND: Possible utility of high-dose i.v. melatonin as an anaesthetic adjuvant has not been studied. This study compared its effects with thiopental and propofol. METHODS: Sprague Dawley rats were assigned to receive bolus or cumulative i.v. doses of melatonin, thiopental or propofol. Righting reflex, hindpaw withdrawal to a noxious stimulus, response to tail clamping and haemodynamic effects were assessed. RESULTS: Melatonin caused a dose-dependent increase in paw withdrawal threshold and the percent of rats displaying loss of the righting reflex. Melatonin was comparable to thiopental and propofol in terms of its rapid onset of hypnosis. The mean ED(50) values for loss of righting reflex were 5.4 (SEM 1.2), 12.5 (1.1) and 178 (1.1) mg kg(-1) for propofol, thiopental and melatonin, respectively. The percent of rats displaying loss of response to tail clamping was greater with propofol than with melatonin (P<0.05). Haemodynamic changes produced by melatonin or propofol were similar in onset and magnitude. CONCLUSIONS: I.V. melatonin can exert hypnotic effects similar to those observed with thiopental and propofol. Melatonin exhibited significant antinociceptive effects but was less effective in abolishing the response to tail clamping.

Adjuvants, Anesthesia↗
PubMed1998

Pharmacologic electroencephalographic suppression during cardiopulmonary bypass: a comparison of thiopental and isoflurane.

UNLABELLED: In this study, we examined the cerebral oxygenation effects of two methods of pharmacologic burst suppression during cardiopulmonary bypass (CPB) in valvular heart surgery patients. Patients were randomly entered into one of three groups: control (n = 13, fentanyl and midazolam), control plus burst suppression doses of thiopental (n = 15), or control plus burst suppression doses of isoflurane (n = 16). Burst suppression (80% suppression) was accomplished in the thiopental and isoflurane groups 15 min before aortic cannulation and was maintained through aortic decannulation. Cerebral physiologic measurements were made during hypothermia (27-28 degrees C) and on rewarming to 36 degrees C. During hypothermia, burst suppression produced significant (P < 0.005) differences with regard to cerebral vascular resistance (P = 0.003), cerebral arterial venous oxygen difference [C(a-v)O2] (P = 0.032), cerebral blood flow (CBF) (P = 0.009), and cerebral oxygen delivery (P = 0.027). There was a similar pattern on rewarming, with groups differing significantly (P < 0.05) with respect to CBF (P = 0.016), cerebral vascular resistance (P = 0.008), oxygen delivery (P = 0.004), C(a-v)O2 (P = 0.043), and cerebral oxygen extraction (P = 0.046). Rewarming rates were similar among groups. There was no difference in neurologic outcome or requirement for inotropic support among groups. The time to awakening was increased (P = 0.0005) in the thiopental group. The thiopental group had lower cerebral oxygen delivery, but not lower cerebral metabolic rate of oxygen consumption, compared with the control group, resulting in widening C(a-v)O2 during CPB. This lack of coupling of oxygen delivery and consumption suggests that pharmacologic neuroprotective mechanisms are complex and involve more than an improvement in the ratio of global cerebral oxygen supply to demand. IMPLICATIONS: This study demonstrates that the balance of cerebral oxygen delivery to consumption during cardiopulmonary bypass is altered differently by thiopental and isoflurane. As others have noted, it seems that cerebral protection is more complex than a simple improvement in the balance of oxygen delivery and consumption.

Adult↗
PubMed1998

Propofol and thiopental in a 1:1 volume mixture is chemically stable.

UNLABELLED: Propofol and thiopental have been used clinically in combination for induction of anesthesia. Studies suggest that this mixture has synergistic activity, recovery characteristics similar to propofol alone, and bactericidal effects on multiple organisms. It may therefore be both clinically useful and cost-effective. In this study, we examined the chemical stability of this mixture. We used high-performance liquid chromatography to quantify the concentration of both propofol and thiopental in a given sample. This technique allows the detection of loss in total drug mass and of the appearance of breakdown products resulting from drug interaction. Ten samples of a 1:1 mixture by volume were prepared and assayed at Time 0 and Days 1, 3, and 7. Half the samples were incubated at 23 degrees C and the rest were stored at 4 degrees C. Other mixtures were assayed before and after filtration at Time 0 and Days 1 and 7 after storage at 23 degrees C. The assay was able to measure accurately the quantity of drug present in the samples. There was no significant decrease in the quantities of either propofol or thiopental in the mixture over the 7-day period. We conclude that the 1:1 volume mixture of propofol and thiopental is chemically stable for 1 wk at room temperature. IMPLICATIONS: A mixture of propofol and thiopental has been used to induce anesthesia. We investigated the chemical stability of this mixture using high-performance liquid chromatography and found it to be stable for at least 24 h.

Anesthetics, Intravenous↗
PubMed2000

The comparative effects of propofol versus thiopental on middle cerebral artery blood flow velocity during electroconvulsive therapy.

UNLABELLED: Electroconvulsive therapy provokes abrupt changes in both systemic and cerebral hemodynamics. An anesthetic that has a minor effect on cerebral hemodynamics might be more suitable for patients with intracranial complications, such as cerebral aneurysm. The purpose of our present study was to compare the effects of thiopental and propofol on cerebral blood flow velocity. We continuously compared cerebral blood flow velocity at the middle cerebral artery (MCA) during electroconvulsive therapy, using propofol (1 mg/kg, n = 20) versus thiopental (2 mg/kg, n = 20) anesthesia. Systemic hemodynamic variables and flow velocity at the MCA were measured until 10 min after the electrical shock. Heart rate and arterial blood pressure increased in the thiopental group until 5 min after the electrical shock. In the propofol group, an increase in mean blood pressure was observed to 1 min after the electrical shock. Mean flow velocity at the MCA decreased after anesthesia in both groups, and increased at 0.5-3 min after the electrical shock in the thiopental group and at 0.5 and 1 min after the shock in the propofol group. The flow velocities at 0.5-5 min after the electrical shock were significantly more rapid in the thiopental group compared with the propofol group. ¿abs¿ IMPLICATIONS: Cerebral blood flow velocity change, measured by transcranial Doppler sonography during electroconvulsive therapy, was minor using propofol anesthesia compared with barbiturate anesthesia. Propofol anesthesia may be suitable for patients who cannot tolerate abrupt cerebral hemodynamic change.

Adolescent↗
PubMed1975

Recovery and simulated driving after intravenous anesthesia with thiopental, methohexital, propanidid, or alphadione.

Recovery from anesthesia was assessed in a double-bind manner in 40 healthy volunteer students after intravenous anesthesia with thiopental (6.0 mg/kg), methohexital (2.0 mg/kg), propanidid (6.6 mg/kg), or alphadione (Althesin), 85 mul/kg using a driving simulator 2,4, 6, and 8 hours after injection of the drugs. Clinical recovery was faster after propanidid and methohexital than after thiopental or alphadione. Driving performances remained significantly (P less than 0.05) worse than in a control group for 6 hours after thiopental and for 8 hours after methohexital, and reaction times 8 hours after thiopental remained worse than in the control subjects. After alphadione driving skills were impaired at 6 hours only. Propanidid produced no impairment in driving skills at any time during the experiment. It is concluded that after the doses used in this study patients should not drive or operate machinery for at least 2 hours after propanidid and for at least 8 hours after alphadione. After methohexital and thiopental patients should probably not drive for 24 hours because of the severity of the disturbances at 8 hours.

Adult↗
PubMed1976

Binding of thiopental to plasma proteins: effects on distribution in the brain and heart.

Thiopental-14C (30 mg and 10 muCi/kg) was injected intravenously into rats 36-48 hours following bilateral nephrectomy and one minute after pretreatment with sulfadimethoxine (30 mg/kg, iv). Control groups of normal and sham-operated animals were used. The distributions of radioactivity in plasma, brain, and heart 1, 5, and 30 minutes after injection were examined. Uremic and sulfonamide-pretreated rats showed significantly higher levels of 14C in brain and heart and more free thiopental in plasma at each time than did control animals. There was a significant correlation between the free thiopental in plasma and total drug concentrations in the brain and heart. Uremic rats bound less thiopental in plasma compared with controls in spite of normal total plasma protein and albumin concentrations. It is concluded that reduced protein binding of thiopental leads to accelerated distribution and increased drug concentrations in the brain and and heart.

Animals↗
PubMed1977

Thiopental inhibition of tumor immunity.

The ability of leukocytes to kill tumor cells appears central to the defense against neoplastic growth. The authors determined the effect of thiopental on this phenomenon in vitro by incubating 51Cr-labelled YAAC-1 tumor cells obtained from the peritoneal cavities of syngeneic A/JAX white mice with immune leukocytes from the peritoneal cavities of allogeneic C57/black mice. Tumor-cell death was quantitated by the amount of 51Cr released into the medium following tumor-cell lysis. Thiopental, in concentrations used during routine anesthesia, inhibited tumor-cell killing in a dose-related manner. Inhibition of cytotoxicity ranged from 8.6 per cent at 2.8 x 10(-5) M thiopental to 38.1 per cent at 8.5 x 10(-5) M thiopental. Moreover, this inhibitory effect was additive to that previously demonstrated with halothane, and was related to the duration of exposure to the anesthetic. It is postulated that thiopental and other anesthetics contribute to the inhibition of leukocyte responsiveness observed in patients with malignancies who have undergone surgical procedures.

Animals↗
PubMed1978

Cardiovascular effects of plasma levels of thiopental necessary for anesthesia.

The cardiovascular effects of plasma levels of thiopental necessary for anesthesia were studied using systolic time intervals (STI). In ten healthy patients anesthesia was induced with thiopental, 2-2.5 mg/kg, intravenously, and maintained with an infusion of 1-1.5 mg/kg/min. STI and thiopental plasma levels were measured before induction and when corneal reflex and trapezius muscle response, indicators of anesthetic depth equivalent to response to surgical stimulation, were lost. Significant changes included: an increase in heart rate with induction of anesthesia; a decrease in 1/pre-ejection period2--indexed for heart rate (1/PEP2-I) at loss of corneal reflex; a decrease in systolic blood pressure and 1/PEP2-I at loss of trapezius muscle response. No other variable was significantly different from control. Control values for STI were in the high-normal range, indicating some sympathetic stimulation. With induction of anesthesia these values decreased to a normal range. Free and total plasma levels were 5.4 and 37.6 microgram/ml at loss of corneal reflex; 6.1 and 41.6 microgram/ml at loss of trapezius muscle response. In comparison with other studies, thiopental causes less cardiac depression than inhalational agents at approximately the same anesthetic depth. It is concluded from this study in healthy patients that plasma levels of thiopental producing surgical anesthesia result in minimal cardiac depression as determined by systolic time intervals.

Adult↗
PubMed1981

Pharmacokinetics and plasma binding of thiopental. I: Studies in surgical patients.

The pharmacokinetics and plasma protein binding of thiopental were investigated in 5 female patients who received a bolus intravenous dose of the drug for induction of anesthesia for gynecologic surgery. Blood samples were collected for 3 to 4 days after the dose. Plasma protein binding determinations were also carried out by ultrafiltration and equilibrium dialysis on samples from a panel of healthy volunteers. Plasma concentrations of thiopental were determined by reverse-phase, high-performance liquid chromatography. The coefficient of variation of the method was 2.8 per cent (n equals 10). In healthy volunteers, the plasma protein binding of thiopental was concentration dependent. Percentage bound ranged from 96.7 (n equals 4, SD equals 0.8) at 150 micrograms/ml. Therefore, saturation of binding sites on rapid administration of the drug may occur, exposing vital organs to unexpectedly high concentrations of free drug. Values of the fraction of thiopental bound in plasma obtained from the surgical patients during the hour following drug administration were similar to values obtained in healthy volunteers at comparable concentrations. Mean pharmacokinetic parameters obtained for thiopental in the surgical patients were as follows: initial distribution volume 13.81 (SD equals 9.4), apparent volume of distribution 233 1 (SD equals 98), volume of distribution at steady state 97.51 (SD equals 40), elimination half-life 11.5 h (SD equals 1.0) and systemic plasma clearance 0.150 l/min (SD equals 0.063). None of these parameters correlated with body weight. Values reported by other workers vary from ours and this variation may be explained by the much shorter duration of blood collection used in those studies.

Adult↗
PubMed1982

The neurologic effects of thiopental therapy following experimental cardiac arrest in cats.

To define the utility of high-dose barbiturate therapy following an episode of complete global cerebral ischemia, we investigate the effects of 60 mg/kg of thiopental given to cats five minutes after resuscitation from 12, 14, or 16 min of electrically induced ventricular fibrillation (VF). All aspects of the arrest, resuscitation, with post-arrest care were carefully controlled, with the EEG becoming isoelectric 20-25 s after the onset mean resuscitation time of 2.5 +/- 0.2 (SEM) min. For any given duration of VF, there were no differences (control vs thiopental) in any pre- or post-arrest parameters (blood pressure, blood gases, electrolytes, etc.) A total of 68 resuscitated cats were entered into various treatment and control groups, and all but one group received 20-24 h of post-resuscitation paralysis, mechanical ventilation, and ICU support before being extubated. Cats received an additional six days of aggressive nursing care, and daily examinations were performed with the assignment of a neurologic deficit score (NDS) between 0 (normal) and (brain dead). Autopsies were performed to determine the cause of death in animals which died before the end of the seven-day observation period. The early post-arrest period was marked by the occurrence of repetitive, rhythmic bursts of high-frequency electroencephalographic (EEG) activity (? seizures) in 38 per cent of control animals (16/42, all arrest times combined). Ten of these animals died as a result of severe neurologic injuries. By contrast, only 12 per cent of treated cats (3/26) developed similar EEG patterns (P less than 0.05) and there were no neurologic deaths in the thiopental groups. The differences in the incidence of neurologic deaths (control vs. thiopental) was significant (P less than 0.02). The change in overall mortality did not quite reach significance (36 per cent vs. 21 per cent), and treatment had no effect on the incidence of deaths due to cardiovascular causes (e.g., myocardial infarctions). In spite of the effects on mortality, treatment had no effect on the neurologic function of survivors (assessed by NDS). These findings suggest that thiopental improved survival rates by suppressing an unusual post-arrest EEG pattern (? anticonvulsant effect), but had no additional cerebral protective effects.

Animals↗
PubMed1982

Comparative evaluation of intravenous agents for rapid sequence induction--thiopental, ketamine, and midazolam.

The pharmacologic effects of ketamine, midazolam, and a midazolam-ketamine combination were compared with thiopental for rapid induction of general anesthesia. Thiopental, 4 mg/kg, 1.5 mg/kg ketamine, 0.3 mg/kg midazolam, or 0.15 mg/kg midazolam, and 0.75 mg/kg ketamine, were administered intravenously in a randomized fashion to 80 patients undergoing emergency surgery. Adequacy of induction, hemodynamic changes, and postoperative effects were assessed during and after a standardized induction-maintenance anesthetic technique. Midazolam had the slowest onset (15-60 s) and longest duration of action. During induction, thiopental decreased mean arterial pressure (MAP) by 11%, ketamine increased MAP by 10%, while neither midazolam nor the midazolam-ketamine combination significantly changed MAP. Heart rate (HR) increased during induction in all groups; however, the increase was significantly less in the combination group. After intubation, MAP and HR increased to the same extent in all four groups. Significantly more patients who received ketamine for induction were disoriented during emergence. Midazolam most effectively produced anxiolysis and antegrade amnesia. Significantly more patients who received thiopental felt depressed postoperatively, and 95% required parenteral opiate analgesics in the recovery room. Dreaming was highest after ketamine (55%) and lowest after midazolam (0%) and the combination (5%). Thus, midazolam effectively attenuated both the cardiostimulatory responses and unpleasant emergence reactions associated with ketamine. The author concludes that both midazolam and the midazolam-ketamine combination are safe and effective induction agents for emergency surgery, which may offer an advantage over thiopental in situations where hemodynamic stability is crucial. Furthermore, midazolam effectively attenuates the side effects of ketamine.

Adult↗
PubMed1982

Potentiation by thiopental of halothane--epinephrine-induced arrhythmias in dogs.

Epinephrine-induced arrhythmias were studied in 14 dogs (Group 1) anesthetized with halothane alone (1.09% end-tidal), and on another occasion, at the same halothane concentration following intravenous thiopental (20 mg/kg). Surface (Lead II), catheter His bundle and high right atrial electrocardiograms, and airway and femoral arterial pressures were recorded. Graded doses of epinephrine (EPI-least dose 0.25 microgram . kg-1 . min-1) were infused over five minutes, but terminated sooner if ventricular tachycardia occurred (maximal sensitization). Sensitizing EPI doses (microgram . kg-1) were calculated (dose X time to arrhythmia) for: Shift in or wandering atrial pacemaker (SAP-WAP), atrial ectopy (At Ect), A-V dissociation (AVD), and ventricular ectopy, bigeminy, or tachycardia (V Ect, V Bigem, V Tach). With halothane alone, SAP-WAP occurred at the least dose of EPI followed by At Ect, AVD, V Ect, V Bigem, and V Tach in order of increasing EPI dose. Following thiopental, EPI doses for AVD, V Ect, V Bigem, and V Tach were reduced, as well as EPI dose differences for At Ect, AVD, V Ect, and V Bigem. In an additional seven dogs (Group 2), anesthesia was induced with thiopental (20 mg/kg) followed by halothane (1.09% end-tidal). These animals were observed for arrhythmias during graded EPI infusions at 1-2 h and 3-4 h following thiopental. Sensitizing EPI doses for SAP-WAP and V Tach were similar at each time period. The authors concluded that with halothane and increasing EPI dose, sensitization constitutes a spectrum of arrhythmias, beginning with atrial and progressing to severe ventricular arrhythmias. Thiopental reduces the EPI dose needed for AVD and ventricular, but not atrial, arrhythmias. It also reduces the EPI dose discrepancies for atrial and ventricular arrhythmias.

Animals↗
PubMed1984

Cardiovascular and metabolic sequelae of inducing anesthesia with ketamine or thiopental in hypovolemic swine.

If further sympathetic stimulation is neither possible nor desirable during moderate hypovolemia, anesthetic agents capable of sympathetic stimulation would not be advantageous for induction of anesthesia during hypovolemia. To test this hypothesis, 21 swine were studied during normovolemia and after 30% of their estimated blood volume was removed. Swine were divided randomly into three equal groups to receive no anesthetic or the minimal anesthetic dose of ketamine (6.65 +/- 0.38 mg/kg, iv) or thiopental (5.77 +/- 0.21 mg/kg, iv). After the initial response to hypovolemia, animals given no drug did not exhibit further changes during the hypovolemic period. Five minutes after induction of anesthesia in the hypovolemic state, ketamine, but not thiopental, caused large increases in plasma epinephrine, norepinephrine, and renin activity. Despite these differences, both anesthetics equally depressed systemic vascular resistance, mean systemic arterial blood pressure, heart rate, and cardiac output. Ketamine, but not thiopental, decreased stroke volume. Neither anesthetic affected oxygen consumption. Both anesthetics caused similar increases in blood lactate concentration. Thirty minutes after induction of anesthesia, plasma epinephrine, norepinephrine, and renin activity remained higher in animals given ketamine than in those given thiopental. Stroke volume, systemic vascular resistance, cardiac output, and oxygen consumption did not differ among groups; however, only the animals given ketamine showed further increase in blood lactate concentration and base-deficit. Thirty minutes after infusion of shed blood, cardiac output and blood lactate concentration were greater in the animals given ketamine than in those given thiopental or no anesthetic. Ninety minutes after infusion of shed blood, no differences existed among groups. The authors conclude that after moderate hemorrhage, further increase in circulating catecholamines is possible but that the levels achieved either exceed the maximal effective concentration at site(s) of action or their effects are overwhelmed by the depressant effects of ketamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1985

Thiopental pharmacokinetics under conditions of long-term infusion.

Thiopental was used in long-term infusion (3-4.5 mg . kg-1 . h-1 during 4-8 days) to protect the brain from injury following trauma. Thiopental plasma concentrations were measured during infusion (48 patients) and after infusion (14 patients) to determine the kinetics of the drug in continuous infusion. All mean values were mean +/- SD. Steady state concentrations (Css) were 31.8 +/- 10.7 mg/l for an infusion rate of 3.05 +/- 0.37 mg . kg-1 . h-1 and 48.9 +/- 14.6 mg/l for a rate of 4.2 +/- 0.3 mg . kg-1 . h-1. Corresponding steady state clearance decreased when Css increased, indicating possible saturation of the metabolic enzymatic system. Michaelis-Menten kinetics were confirmed by postinfusion data that give, for higher Css, a nonlinear decay of log C versus time. First-order kinetics were only obtained with Css below 30 mg/l. The maximum rate of elimination (Vm) was 1.76 +/- 1.15 mg . l-1 . h-1 (n = 11), and the Michaelis constant (Km) was 26.7 +/- 22.9 mg/l (n = 11). Hepatic enzyme saturation was between 35 and 85%. The volume of distribution at steady state was 4.35 +/- 1.83 l/kg (n = 11). Apparent half-lives of elimination were between 18 and 36 h at the end of infusion, and predicted terminal half-lives were 10.15 +/- 5.43 h (n = 11). Phases of burst-suppression were observed on electroencephalographic traces for concentrations greater than 40 mg/l. The authors' results suggest that a continuous infusion at a dose of 4 mg . kg-1 . h-1 induces EEG changes consistent with a near-maximum reduction in cerebral metabolism. Because of the thiopental Michaelis-Menten kinetics at doses above 4 mg . kg-1 . h-1, the authors suggest that thiopental plasma concentrations be measured and/or the drug effect be measured with the EEG to prevent excessive thiopental overdosage, causing a prolonged recovery time.

Adolescent↗
PubMed1987

Hepatic oxygen supply and consumption in rats exposed to thiopental, halothane, enflurane, and isoflurane in the presence of hypoxia.

Hepatic oxygen supply and uptake were assessed in phenobarbital-pretreated male Sprague-Dawley rats receiving subanesthetic doses of thiopental, halothane, enflurane, or isoflurane combined with hypoxia (approximately 0.5 MAC and 12% oxygen) for the purpose of evaluating the role of these combinations in hepatic blood flow alterations and the concomitant hepatic oxygen supply and uptake. Hepatic blood flow was measured using microspheres; hepatic oxygen supply and consumption was calculated from measured hepatic blood flow and oxygen content in hepatic arterial, portal venous, and hepatic venous blood. In all anesthetic groups, total hepatic blood flow did not change from the control value. Oxygen supply to the liver was decreased from air control values in all anesthetic groups, but there were no significant differences among anesthetic groups. Hepatic oxygen consumption was significantly lower in animals exposed to halothane and isoflurane versus air controls, whereas it was not significantly decreased in animals receiving thiopental or enflurane. The hepatic oxygen supply/consumption ratio was higher in the air control and the isoflurane groups than in other groups; however, no significant differences in this ratio were observed among the thiopental, halothane, and enflurane groups. Oxygen content in hepatic venous blood correlated well with hepatic oxygen supply/consumption ratio in all five groups. These results show that, during exposure to mild hypoxia, a sub-MAC dose of isoflurane maintains the relationship of hepatic oxygen supply to uptake better than thiopental, halothane, or enflurane. However, a subanesthetic dose of halothane did not aggravate liver hypoxia specifically, compared with thiopental or enflurane.

Animals↗
PubMed1987

Morphine and fentanyl hypnotic interactions with thiopental.

The effects of morphine-thiopental and fentanyl-thiopental combinations on the righting reflex were studied in rats. Doses that block the righting reflex for the agents given alone and for their combinations were determined with a probit procedure and compared with an isobolographic analysis. Interaction between morphine or fentanyl and thiopental on blockade of the righting reflex were both found to be synergistic. The degree of synergism was relatively small for the fentanyl-thiopental combination; the maximal deviation from additive interaction (expected/observed ratio) for ED50 dose level was 1.15 (P less than 0.01). The degree of synergism was greater for the morphine-thiopental combination; the maximal deviation from additive interaction was 2.27 (P less than 0.001). Comparison of the results with the outcomes of opioid-barbiturate interactions in relation to blockade of purposeful movement response to tail clamping, which was antagonistic, shows that the combination of a barbiturate with an opioid gives different outcomes for different end-points of anesthesia. This suggests that the anesthetic effect of an agent is composed of several components, each with a different mechanism of action.

Animals↗
PubMed1990

Mechanism of thiopental-induced constriction of guinea pig trachea.

The authors studied the effects of thiopental on baseline airway tone in intact guinea pig tracheas using a preparation where the epithelial (inside) and serosal (outside) surfaces were isolated. Whole tracheas were excised, cannulated, and mounted in 50-ml tissue baths. The serosal and epithelial surfaces were perfused via separate circuits with Krebs-Henseleit solution. All data were expressed as a percent of constriction produced by 2 X 10(-6) M carbachol (a concentration that elicited a 90 + % of maximal constriction). Thiopental elicited a dose-dependent constriction in all 25 tracheas. Increases in tone were first seen at 10(-5) M (14.3 +/- 1.84%; mean +/- SEM) and reached a peak at 10(-3) M (29 +/- 3.16%; P less than .0001). Responses to thiopental were similar when the epithelium was removed, when thiopental was added to the inner perfusate, and when tracheas were pretreated with 10(-5) M pyrilamine. Constriction was entirely inhibited by pretreatment with indomethacin 10(-5) M. The authors conclude that thiopental, at concentrations in the clinical range, causes a reproducible dose-dependent constriction of guinea pig trachea. This effect is mediated by constrictor prostaglandins.

Animals↗