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Effects of medetomidine-midazolam, acepromazine-butorphanol, and midazolam-butorphanol on induction dose of thiopental and propofol and on cardiopulmonary changes in dogs.

OBJECTIVE: To evaluate dose-sparing effects of medetomidine-midazolam (MM), acepromazine-butorphanol (AB), and midazolam-butorphanol (MB) on the induction dose of thiopental and propofol and to examine cardiopulmonary changes in dogs. ANIMALS: 23 healthy Beagles. PROCEDURE: Dogs were administered MM, AB, MB, or physiologic saline (0.9% NaCI) solution (PS) IM, and anesthesia was induced with thiopental or propofol. Cardiopulmonary measurements were obtained before and after administration of medication and 0, 5, 10, and 15 minutes after endotracheal intubation. RESULTS: Induction doses were reduced significantly by preanesthetic administration of MM, AB, and MB (thiopental, 20, 45, and 46% after administration of PS; propofol, 42, 58, and 74% after administration of PS, respectively). Recovery time in dogs administered MM-thiopental or MM-propofol and AB-propofol were significantly prolonged, compared with recovery time in dogs administered PS-thiopental or PS-propofol. Relatively large cardiovascular changes were induced by administration of MM, which were sustained even after the induction of anesthesia. Administration of AB and MB induced cardiovascular changes during and immediately after endotracheal intubation that were significantly decreased by induction with thiopental or propofol. However, mild hypotension developed with AB-propofol. Apnea was observed in dogs administered MM during induction of anesthesia, but most respiratory variables did not change significantly. CONCLUSIONS AND CLINICAL RELEVANCE: Preanesthetic medication with MM greatly reduced the anesthesia induction dose of thiopental and propofol but caused noticeable cardiopulmonary changes. Preanesthetic medication with AB and MB moderately reduced the induction dose of thiopental and propofol and amelio rated cardiovascular changes induced by these anesthetics, although AB caused mild hypotension.

Acepromazine↗

Anesthetic and cardiorespiratory effects of a 1:1 mixture of propofol and thiopental sodium in dogs.

OBJECTIVE: To compare anesthetic and cardiorespiratory effects of a 1:1 (vol:vol) mixture of propofol and thiopental sodium with either drug used alone in dogs. DESIGN: Randomized crossover study. ANIMALS: 10 healthy Walker Hounds. PROCEDURE: Dogs received propofol (6 mg/kg [2.7 mg/lb] of body weight), thiopental (15 mg/kg [6.8 mg/lb]), or a mixture of propofol (6 mg/kg) and thiopental (15 mg/kg) at 1-week intervals. Drugs were slowly administered i.v. over 90 seconds or until dogs lost consciousness. Increments of 10% of the initial dose were administered until intubation was possible. Amount of drug required for intubation, quality of induction and recovery, times from induction to intubation and to walking with minimal ataxia, and duration of intubation and lateral recumbency were recorded. Heart and respiratory rates, mean, systolic, and diastolic blood pressure, hemoglobin saturation of oxygen (SpO2), and end-tidal CO2 concentration (ETCO2) were determined before and after intubation. RESULTS: Amounts of propofol and thiopental required to permit intubation were less, but not significantly so, when administered in combination than when administered alone. Duration of lateral recumbency and time from induction to walking were greater and recovery quality was worse in the thiopental group, compared with the other groups. Dogs in all groups remained normotensive. Respiratory rate, heart rate, ETCO2, and SpO2 did not differ among groups. CONCLUSIONS AND CLINICAL RELEVANCE: A 1:1 mixture of propofol and thiopental induced anesthesia of similar quality to propofol or thiopental alone. Recovery quality and recovery times were similar to those of propofol and superior to those of thiopental.

Anesthetics, Combined↗

Relationship between extra and intracellular sources of calcium and the contractile effect of thiopental in rat aorta.

To evaluate the relationship between the vasocontractile effect of thiopental and the extra and intracellular sources of Ca2+, we analyzed both the contractile effect of the barbiturate on rat aortic rings and its ability to modify the intracellular calcium concentration in cultured rat aorta smooth muscle cells. Thiopental (10-310 microg/mL) contracted aortic rings only in the presence of extracellular Ca2+, and this effect was not blocked by verapamil or diltiazem. On the contrary, Ca2+ (0.1-3.1 mM) evoked contractions only when thiopental (100 microg/mL) was present. Although in calcium-free solution thiopental (100 microg/mL) did not contract aortic rings, it abolished the contractile effect of either phenylephrine (10(-6) M) or caffeine (10 mM). Finally, thiopental augmented the intracellular calcium concentration in cultured smooth muscle cells incubated either in the presence or absence of calcium. In conclusion, thiopental's vasocontractile effect depends on extracellular calcium influx, which is independent of L-calcium channels. The increase in intracellular Ca2+ concentration elicited by thiopental in Ca2+-free solution and its ability to block the effect of phenylephrine and caffeine suggest that this barbiturate can deplete intracellular pools of calcium. Therefore, the calcium entry pathway associated with the contractile effect of thiopental may correspond to the capacitative calcium entry model.

Animals↗

Hemodynamic responses of thiopental and propofol in different-aged patients during endotracheal intubation.

BACKGROUND: Thiopental and propofol are 2 popularly used anesthetic induction agents that have different pharmacological and pharmacokinetic actions. It is not clear how the hemodynamic responses differ in different-aged patients using these 2 drugs for anesthetic induction. The aim of this study was to investigate the hemodynamic responses to propofol and thiopental of different-aged patients during endotracheal intubation. METHODS: Sixty patients, 20 to 83 years old, were included in this study. Patients were randomly divided into 6 groups according to age and different inductive anesthetics. Non-invasive blood pressure (NIBP) monitoring was performed every minute before anesthesia, during anesthetic induction with 5 mg.kg-1 thiopental or 2 mg.kg-1 propofol intravenously, and after intubation. RESULTS: Propofol induction produced a smaller mean arterial pressure increase immediately after intubation than did thiopental induction in adult and elderly groups (101.0 +/- 18.5 and 104.0 +/- 21.1 mmHg in the propofol groups vs. 138.3 +/- 17.1 and 138.9 +/- 16.1 mmHg in the thiopental groups at 1 minute after intubation, p < 0.001 and p = 0.001, respectively). Differences in heart rate between propofol and thiopental groups were found in young and adult groups (85.1 +/- 9.2 and 81.7 +/- 10.9 in the propofol groups vs. 94.5 +/- 9.9 and 95.0 +/- 14.0 beats per minute in the thiopental groups at 1 minute after intubation, p = 0.041 and p = 0.029, respectively). CONCLUSION: Propofol induction produced more stable hemodynamics after intubation in adult and elderly patients than did thiopental induction. Therefore, it is safer to use propofol for induction and intubation in adult and elderly patients.

Adult↗

[Influence of thiopental administration on peripheral circulation during cardiac surgery with extracorporeal circulation].

The influence of thiopental administration on peripheral circulation during cardiac surgery with extracorporeal circulation was examined. The subjects were 28 patients who were divided into one group of 14 patients receiving thiopental and the other group of 14 patients receiving no thiopental. The time lag of changes in peripheral temperature (sole) from that in central temperature (forehead) according to the deep body temperature determination, and base excess were used as indices of the quality of the peripheral circulation. A single shot of thiopental at a dose of 4 mg.kg-1 was initially given i.v. at the start of extracorporeal circulation and subsequently thiopental at a dose of 2 mg.kg-1.hr-1 was continuously infused i.v. up to the time of the aortic declamping. The results indicate a significantly smaller lag in the group receiving thiopental than in the group receiving no thiopental. Base excess was maintained within normal limits in the former group compared with negative base excess in the latter group as well as a significantly smaller requirement of postoperative catecholamine in the former group. The above findings suggest that thiopental administration during cardiac surgery with extracorporeal circulation is not only useful for maintaining peripheral circulation, but also beneficial for post-operative cardiac function.

Aged↗

Rectal thiopental versus an intramuscular cocktail for sedating children before computerized tomography.

The sedative effects of rectal thiopental sodium and an intramuscular cocktail of meperidine hydrochloride, chlorpromazine hydrochloride and promethazine hydrochloride were compared in 72 pediatric patients undergoing computerized tomography (CT). Pediatric patients scheduled were randomly assigned to receive either the i.m. cocktail (2.0 mg/kg of meperidine, 1.0 mg/kg of both chlorpromazine and promethazine) or 25--45 mg/kg of thiopental rectally before scanning. Side effects, and onset, duration and depth of sedation were recorded by 14 unblinded investigators. Clarity of CT scans was rated by two blinded radiologists. Additional doses of sedatives were administered as necessary. Sedation was not achieved in 3% of the thiopental group or in 14+ of the i.m. cocktail group. Additional sedatives were required by eight patients in the thiopental group and by five patients in the cocktail group. The mean time for onset of sedation was 8 minutes with thiopental and 18 minutes with the cocktail. The mean duration of sedation was 7 hours for the cocktail group and 2.75 hours for the 25-mg/kg rectal thiopental group. All scans were diagnostic (acceptable) in the rectal thiopental group, but 14% of those in the i.m. cocktail group were nondiagnostic. Rectal thiopental is an effective alternative to an i.m. cocktail for sedating children before CT scans and may reduce the number of nondiagnostic scans.

Child↗

Adrenoceptor mechanism involved in thiopental-induced potentiation of halothane-epinephrine arrhythmias in dogs.

Although thiopental is known to potentiate halothane-epinephrine arrhythmias, the precise mechanism of this potentiation is obscure. The authors investigated the comparative role of alpha 1 and beta adrenergic actions in the thiopental-induced potentiation of halothane-epinephrine arrhythmias in dogs. Adult mongrel dogs were anesthetized with halothane alone (1.3%) or thiopental (20 mg kg-1) plus halothane and monitored continuously for systemic arterial pressures and for premature ventricular contractions. The arrhythmogenic doses of phenylephrine and isoproterenol were determined during the two anesthetic methods and the effect of thiopental on the arrhythmogenic action of alpha 1 and beta agonists was examined. Thiopental failed to exert a significant potentiation of arrhythmogenic effect of phenylephrine or isoproterenol, when these agents were administered separately. On the other hand, the potentiation of arrhythmogenicity by thiopental was remarkable in the case of combined administration of both the agonists, that is, thiopental enhanced the synergistic interaction between phenylephrine and isoproterenol for inducing arrhythmias during halothane anesthesia. In addition, the potentiation was more prominent when a low dose of isoproterenol and a high dose of phenylephrine was combined than that when a high dose of isoproterenol and a low dose of phenylephrine was given in combination. The results indicate that thiopental significantly potentiates the arrhythmogenic interaction of alpha 1 and beta adrenergic agonists administered concurrently, although individual potentiation of these agonists is not significant.

Anesthetics↗

The effect of midazolam-thiopental coinduction on recovery in minor surgery.

PURPOSE: The effects of midazolam-thiopental coinduction on recovery were investigated and compared with thiopental induction. METHODS: Fifty patients, ASA 1 or 2, undergoing minor orthopedic surgery, were randomly divided into coinduction and thiopental groups. During preoxygenation, the patients received midazolam 0.1 mg.kg(-1) (coinduction group) or saline (thiopental group) 1 min before induction of anesthesia with thiopental. Isoflurane and nitrous oxide were used to maintain anesthesia. Isoflurane concentration was adjusted to keep blood pressure within +/-20% of the preoperative value. The time to awaken (open eyes, give name and birth-date) and the time to discharge readiness were recorded. Psychomotor tests, including simple light reaction time (SLRT), sedation analogue scale (SAS), and digit span test, were performed pre- and postoperatively. RESULTS: The induction dose of thiopental was significantly lower in the coinduction group. End-tidal isoflurane concentration during surgery was also lower in the coinduction group. There were no significant differences in awakening times and discharge readiness between the two groups. Although SAS values were lower in the coinduction group than in the thiopental group 8 and 24 h after anesthesia, other test results were similar in both groups. The frequency of nausea and vomiting in the recovery period was lower in the coinduction group. CONCLUSION: We conclude that midazolam-thiopental coinduction is a suitable technique when used in conjunction with isoflurane in day-case surgery.

Clinical Trial↗

Effects of thiopental, ketamine, diazepam, xylazine, and nitrous oxide on EEG spike activity and convulsive behavior during enflurane anesthesia in spontaneously breathing atropinized cats. Effect at surgical depth.

The effects of thiopental, ketamine, diazepam, xylazine and nitrous oxide, and combinations of thiopental-nitrous oxide and ketamine-nitrous oxide on electroencephalographic (EEG) spike activity and convulsive behaviors in atropinized cats at surgical depth of enflurane anesthesia were assessed quantitatively for 60 minutes during spontaneous ventilation. Mean inspired enflurane concentrations (MIEC) were reduced 16% to 29% by pretreatment with thiopental, ketamine, diazepam, and xylazine, and were reduced 19% by 66% nitrous oxide. The MIEC of cats anesthetized with thiopental-nitrous oxide-enflurane and ketamine-nitrous oxide-enflurane were 35% to 38% lower than that with nitrous oxide-enflurane. Pretreatment with thiopental, ketamine, diazepam, and xylazine did not reduce the EEG spike frequency during anesthesia but did markedly reduce the spike amplitude. The addition of 66% nitrous oxide did not alter the spike frequency during anesthesia but tended to reduce the spike amplitude. Combinations of thiopental-nitrous oxide and ketamine-nitrous oxide almost abolished the spike activity. The addition of 66% nitrous oxide prevented convulsive responses elicited by photic and auditory stimulation during enflurane anesthesia. Treatment with thiopental, ketamine, diazepam and xylazine, and combinations of thiopental-nitrous oxide and ketamine-nitrous oxide, completely prevented convulsive responses during enflurane anesthesia.

Anesthesia, Inhalation↗

Displacement of thiopental from human serum albumin by associated drugs.

Displacement of thiopental from its binding sites to 4% human serum albumin solution was studied in vitro. Experimental conditions were selected to reproduce a physiological situation. Associations were studied according to the therapeutic conditions of use of the substances (drug and protein concentrations). The unbound fraction of thiopental was obtained by equilibrium dialysis at 37 degrees C and pH 7.4. Eleven drugs were associated with thiopental in 50 combinations of drugs and molar ratios. Bromhexine, citocoline, dextromoramide, dexamethasone, and methotrimeprazine had no effect on thiopental binding. The unbound fraction of thiopental significantly increased with cefamandole, cefazolin, diazepam, desmethyldiazepam, furosemide, and fentanyl. At usual therapeutic drug concentrations, the unbound fraction increase was < 5%. Higher values, however still < 10%, were found with associated drugs that were added at maximal concentrations observed in therapy. The displacement of thiopental from its albumin binding by drugs that are normally associated with the treatment of intracranial hypertension does not modify the pharmacokinetic parameters or pharmacological effect of thiopental.

Binding, Competitive↗

Suppressor cells and increased primary tumor growth rate induced by thiopental.

A single dose of thiopental (37-42 mg/kg) sufficient to achieve anesthesia induction increased the growth rate of a 3-methylcholanthrene-induced syngeneic murine fibrosarcoma in C57B1/6 mice. While no alterations in in vitro growth kinetics of tumor cells cultured with thiopental could explain these data, significant alterations in cell-mediated immunity were observed. Spleen cells from C57B1/6 mice treated with thiopental were impaired in their ability to respond in a mixed leukocyte culture (MLC) to BALB/c stimulator cells. Spleen cells from thiopental-treated mice suppressed the ability of cells from untreated animals to respond in a third-party MLC. The degree of suppression was directly proportional to the number of cells from thiopental-treated mice in the third party. When these cells were added to an MLC at various times during the culture period, suppression of the early phases of the MLC was seen. Removal of plastic adherent cells from the third party resulted in loss of suppression, but treatment of third-party cells with anti-thy 1.2 serum or irradiation did not prevent suppression. Transfer of spleen cells from thiopental-treated mice enhances growth of the B-16 melanoma. Suppressor-cell activity may be one mechanism by which thiopental promotes tumor growth.

Animals↗

The neurologic effects of thiopental therapy after cardiac arrest.

We studied the effect of thiopental loading during resuscitation of 53 patients following cardiopulmonary arrest and compared the outcome with that found in 54 patients treated conventionally in the 30 previous months. Thiopental therapy (10 mg/kg i.v.) was begun within 30 min of the arrest once hemodynamic stability had been established. Thiopental infusion (20 mg/kg over 6 h) was followed by phenobarbital sodium (125 mg every 12 h), tolerance to the initial dose having been assessed. The in-hospital mortality rate for both groups was similar. In patients with ischemic heart disease, the mortality rate within the first 6 h was significantly higher in the thiopental group (p less than 0.05), although for the remaining patients there were more survivors among the thiopental treated patients (p less than 0.05). Excluding the patients who died within the first 6 h, 61% of the patients in the thiopental group survived cardiac arrest with normal cerebral performance, whereas only 37% in the standard treatment group showed normal functional outcome (p less than 0.03). These results suggest a favorable neurologic effect of thiopental loading during resuscitation of patients without ischemic heart disease. In patients with ischemic heart disease, an initial hemodynamic deterioration may contribute to minimising the beneficial effect of barbiturate therapy.

Adult↗

Estimating the rate of thiopental blood-brain equilibration using pseudo steady state serum concentrations.

The equilibration between drug serum concentration and drug effect under non-steady state concentrations has been classically modeled using an effect compartment where the transfer from the serum to the effect compartment is considered to be a first-order process. The purpose of the present study was to examine whether an effect compartment with first-order transfer was adequate for describing thiopental serum concentration-EEG pharmacodynamics. The study has two facets: (i) Successive pseudo steady state serum concentrations of thiopental having a square wave shape were produced and maintained in six human subjects by means of a computer-driven infusion pump. An aperiodic wave form transformation of the electroencephalogram (EEG) was used as a continuous measure of thiopental EEG drug effect. The time course of the EEG effect following each thiopental serum concentration square wave showed an exponential pattern. The first-order rate constant for equilibration of the effect site concentration with the drug serum concentration (keo) was estimated by fitting a monoexponential model to the effect vs. time data resulting from the pseudo steady state thiopental serum concentration profile. (ii) In a second experiment, data were obtained from a classical design, i.e., a zero-order intravenous infusion of thiopental. The same subjects were studied. The keo was estimated by means of a semiparametric iterative method using convolution (effect compartment, transfer of drug from serum to site of action is assumed to be a first-order process). The mean pseudo steady state value for keo of 0.51 min-1 was not different from the mean value of 0.46 min-1 from the semi parametric approach when data from a linear portion of the drug concentration vs. effect curve were examined. The pseudo steady state technique gave inaccurate estimates of keo in the nonlinear portion of the thiopental concentration vs. response curve, i.e., at the peak of the biphasic concentration-effect relationship.

Adult↗

An electroencephalographic comparison of alfentanil with other narcotics and with thiopental.

Using aperiodic analysis, we compared the EEG produced by alfentanil with the EEGs produced by two other opiates--fentanyl and sufentanil--on the one hand and with the EEG produced by a barbiturate--thiopental--on the other hand. Alfentanil and thiopental were injected over 1 minute; fentanyl and sufentanil were injected over 10 to 15 minutes. From the aperiodic analysis we derived up to seven single-number variables computed over 30- or 60-second epochs. All the opiates induced EEGs that were qualitatively similar to each other, although the maximum or minimum values tended to be greater and the time course more rapid with alfentanil than with the other two opiates. This finding may have been related to the fact that we injected relatively more alfentanil and administered it more rapidly. The EEGs produced by alfentanil and thiopental differed markedly, both qualitatively and quantitatively. The total power at 1 Hz and cumulative power at 3 Hz went to higher peak values with alfentanil, the latter tending to decrease with thiopental. The total number of waves per epoch went to lower peak values with alfentanil; there was little change with thiopental. The frequency below which 90% of the power resides went to considerably lower peak values with alfentanil than with thiopental. Finally, total power at 10 to 12 Hz (alpha waves) and average power at 17 to 19 Hz (beta waves) went to very high peak values with thiopental, but decreased with alfentanil.(ABSTRACT TRUNCATED AT 250 WORDS)

Alfentanil↗

Thiopental inhibits migration of human leukocytes through human endothelial cell monolayers in vitro.

OBJECTIVES: The interactions between blood and vascular wall cells are essential for the understanding of pathophysiologic processes, e.g. inflammation. The influence of the anesthetic drug thiopental on leukocyte function is well documented. Recently, an inhibitory effect of thiopental on leukocyte chemotaxis in a Boyden chamber assay (i.e. endothelial cells were not included) was demonstrated. In vivo, leukocytes have to interact with endothelial cell monolayers to invade the tissue. The influence of thiopental on a monolayer of endothelial cells has not yet been investigated. The aim of the current study was to investigate the influence of thiopental on the migration of leukocytes through endothelial cell monolayers (ECM). MATERIAL AND METHODS: Human umbilical vein endothelial cells (HUVEC) were isolated and cultured on microporous membrane filters to achieve a monolayer. Isolated polymorphonuclear leukocytes (PMNL) as well as ECM were preincubated with different concentrations of thiopental. The rate of leukocyte migration against the chemotactic protein formyl-methyl-leucyl-phenylalanine was measured (n = 7). Thiopental was able to reduce the amount of leukocyte migration through ECM significantly. CONCLUSION: In conclusion, we could show that thiopental is able to reduce the migration of PMNL through ECM significantly.

Adult↗

Midazolam potentiates thiopental sodium anesthetic induction in patients.

STUDY OBJECTIVE: To test the hypothesis that midazolam potentiates thiopental sodium-induced unconsciousness. DESIGN: Randomized, double-blind study. SETTING: A university medical center. PATIENTS: Fifty nonpremedicated ASA physical status I and II adult patients scheduled for eye surgery. INTERVENTIONS: Intravenous (IV) injections of thiopental sodium in doses ranging from 1.0 mg/kg to 4 mg/kg with or without the addition of midazolam 0.02 mg/kg. MEASUREMENTS AND MAIN RESULTS: Inability to open eyes on command was used as an end point of anesthesia and the dose-response curves were determined using a probit procedure. A dose of 0.02 mg/kg, which constitutes less than one-tenth of the hypnotic ED50 value for midazolam, potentiated thiopental sodium anesthesia. The thiopental sodium ED50 value was decreased from 2.4 mg/kg to 1.6 mg/kg (p less than 0.001). Midazolam also reduced individual variability in the response to thiopental sodium. As a result, the thiopental sodium dose that reliably induced any nonpremedicated patient decreased from 6 mg/kg (ED99 of 5.57 mg/kg) to 2.5 mg/kg (ED99 of 2.37 mg/kg). CONCLUSIONS: A subhypnotic dose of midazolam potentiates thiopental sodium-induced unconsciousness. This effect suggests the possibility that midazolam enhances barbiturate binding.

Adult↗

The effects of thiopental sodium on fentanyl-induced muscle rigidity in a human model.

STUDY OBJECTIVE: To describe a safe human model in which to study the treatment of fentanyl-induced muscle rigidity and report on the efficacy of thiopental sodium for this purpose. DESIGN: Randomized, observer-blinded comparison of regimens. SETTING: Inpatient surgery at a university-affiliated teaching hospital. PATIENTS: Thirty patients scheduled for elective surgery in whom the administration of high-dose fentanyl was felt to be appropriate and who experienced severe muscle rigidity in the chest, abdomen, and upper extremities after the fentanyl was administered. INTERVENTIONS: One arm was isolated from circulation with a blood pressure (BP) cuff inflated to 100 mmHg above systolic blood pressure (SBP), after which fentanyl 25 to 50 micrograms/kg was administered intravenously (IV) at a rate of 1 mg/min in the contralateral arm. If severe muscle rigidity became apparent in three muscle groups (the chest, abdomen, and arms), patients were either (1) observed for 3.5 minutes without further intervention, (2) given thiopental sodium 1.5 mg/kg IV, followed 120 seconds later by succinylcholine 1 mg/kg IV, or (3) given succinylcholine 1 mg/kg IV, followed 120 seconds later by thiopental sodium 1.5 mg/kg IV. MEASUREMENTS AND MAIN RESULTS: A single observer, blinded to the technique, evaluated and recorded the degree of muscle rigidity present in the chest wall, abdomen, and upper extremities (one isolated from the circulation by a tourniquet) 90 seconds and 3.5 minutes after the onset of muscle rigidity in the control group and 90 seconds after the administration of either thiopental sodium or succinylcholine in the two experimental groups. The observer was the same individual in all instances. The muscle rigidity associated with the administration of high-dose fentanyl was clinically attenuated by the administration of thiopental sodium, especially in the extremities. Succinylcholine was more effective than thiopental sodium in producing muscle flaccidity in all muscle groups not isolated by a tourniquet. In no case did the muscle rigidity compromise our ability to oxygenate the patient adequately. CONCLUSIONS: Thiopental sodium does blunt the degree of muscle rigidity induced by high-dose fentanyl, though not as effectively as does succinylcholine. One can safely isolate an extremity prior to the administration of high-dose fentanyl and a muscle relaxant, intubate the trachea, and ventilate a patient, while retaining the ability to study the effect of centrally acting drugs on fentanyl-induced rigidity in the isolated extremity.

Fentanyl↗

Thiopental induced cerebral protection during ischemia in gerbils.

Temporary interruption or reduction of cerebral blood flow during cerebrovascular surgery may rapidly result in ischemia or cerebral infarction. Thiopental has been shown to have cerebroprotective effects. However, the cerebroprotective dose of thiopental causes burst suppression of the EEG, thus this parameter cannot be used continuously for the detection of metabolic changes in the brain during thiopental anaesthesia. This study was performed in order to examine whether the multiparametric assembly (MPA), which measures energy metabolism CBF and mitochondrial (NADH) as well as extracellular ion concentrations (K+), can shed light on the mechanism of the cerebroprotective effects of thiopental. The MPA was placed on the brain of Mongolian gerbils and burst suppression of the ECoG was induced by thiopental. Cerebral ischemia was induced by occlusion of carotid arteries after burst suppression. Burst suppression of the ECoG was accompanied by a significant decrease in cerebral blood flow. In animals that received thiopental prior to ischemia, NADH increased to a lesser degree and extracellular potassium ion concentration increased to a lesser degree than in the control animals, indicating that thiopental affords protection of the brain under ischemic conditions due to improved energy metabolism. This study also demonstrates that the MPA can monitor changes occurring in the cerebral cortex even after the ECoG can no longer be used. Those findings have a significant value in the development of a new clinical monitoring device.

Animals↗