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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study determined the effect of halothane on arterial and venous propranolol concentrations during a continuous intravenous infusion of propranolol. Arterial and venous concentrations of propranolol remained constant during the experiment in the group of dogs anesthetized only with pentobarbital. However, there was a rapid increase in arterial propranolol concentration from 88 +/- 10 ng/ml (mean +/- SEM) prior to halothane to 116 +/- 12 ng/ml (P less than 0.05) and 130 +/- 7 ng/ml (P less than 0.05) 60 and 120 min, respectively, after starting halothane anesthesia (2.0 MAC 1.74%). The increase in venous propranolol concentration lagged substantially behind that of the arterial concentration, so that, 60 min after starting halothane, the arterial to venous (A/V) concentration ratio increased from 1.13 +/- 0.05 to a maximum of 1.48 +/- 0.08. In contrast to the changes following halothane, no significant change in the A/V ratio occurred following fentanyl. Both halothane and fentanyl administration produced a small but significant increase in the free fraction of propranolol (P less than 0.05). The results from this study emphasize the importance of the choice of sampling sites in pharmacokinetic experiments, as well as excluding subtle pharmacokinetic changes during anesthesia before ascribing changes in drug effect to changes in sensitivity to the drug.
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PMID:Acute effects of halothane anesthesia on arterial and venous concentrations of propranolol in the dog. 360 49

The effect of dezocine, an agonist-antagonist opioid analgesic, on enflurane MAC (EMAC) was measured in dogs and, in a separate study, the hemodynamic effects of IV bolus doses of dezocine in the presence of a stable end-tidal enflurane concentration were measured. Study 1 (n = 8)--EMAC Reduction: Dezocine reduced EMAC in a dose-dependent fashion by a maximum of 58 +/- 3% (mean +/- SEM) after injection of 20 mg/kg. Cardiac toxicity prevented administration of higher doses. Study 2--Hemodynamics: Group 1 (n = 7) received dezocine 0.2, 1.5, 5, and 20 mg/kg IV each as a bolus over 30 sec. Group 2 (n = 5) was studied in exactly the same manner except that instead of dezocine, each dog received drug carrier solution alone (carrier). Significant hemodynamic differences between carrier and drug groups were observed only at the 20 mg/kg dose level, which produced death in one dog and a decrease in mean aortic pressure to 39 +/- 5% of baseline, in cardiac output to 60 +/- 9% of baseline, and in stroke volume to 69 +/- 9% of baseline in the remaining dogs. It is concluded that dezocine produces a dose-dependent reduction in EMAC limited by cardiovascular toxicity. This toxicity appears to be related to direct myocardial depression by high doses of dezocine in the presence of enflurane.
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PMID:Dezocine-MAC reduction and evidence for myocardial depression in the presence of enflurane. 366 62

The authors sought to determine if isoflurane would attenuate effects of three different types of vasoconstrictors on isolated segments of canine epicardial coronary arteries removed from healthy dogs. As the endothelium has a major role in regulating epicardial coronary artery tone, and as it modulates the effect of many vasoactive substances, experiments were conducted both on normal rings and on rings whose endothelium had been mechanically removed. In addition, the endothelium is thought to be damaged in human atherosclerosis. Rings were suspected in organ chambers filled with modified Krebs-Ringer bicarbonate solution, aerated with 95% oxygen and 5% carbon dioxide, and connected to strain gauges for the measurement of isometric tension. Isoflurane 2.3% (1.5 MAC in the dog) was added to the aerating gas mixture in half the preparations, while the other rings served as control. The vasoconstrictors serotonin, phenylephrine, or prostaglandin F2 alpha were added in increasing concentrations to the bath solution. In the presence of endothelium, vasoconstrictor evoked contractions were attenuated by isoflurane. Maximal tension generated by prostaglandin F2 alpha in untreated rings was 114 +/- 18% (mean +/- SEM) of a reference contraction, while, following isoflurane, it was 46 +/- 8% (P less than 0.005). In the absence of endothelium, isoflurane attenuated neither prostaglandin F2 alpha nor serotonin evoked contraction, and had decreased effectiveness against phenylephrine mediated contraction (P less than 0.001). It is concluded that isoflurane attenuates vasoconstrictor-evoked contraction of isolated canine epicardial coronary arteries, and that this effect is mediated by the endothelium.
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PMID:Isoflurane causes endothelium-dependent inhibition of contractile responses of canine coronary arteries. 366 80

Halothane is commonly viewed as a more potent cerebral vasodilator than isoflurane. It was speculated that the lesser vasodilation caused by isoflurane might be the result of the greater reduction in cerebral metabolic rate (CMR) that it causes, and that the relative vasodilating potencies of halothane and isoflurane would be similar if the two agents were administered in a situation that precluded volatile-agent-induced depression of CMR. To test this hypothesis, cerebral blood flow (CBF) and the cerebral metabolic rate for oxygen (CMRO2) were measured in two groups of rabbits before and after the administration of 0.75 MAC halothane or isoflurane. One group received a background anesthetic of morphine and N2O, which resulted in an initial CMRO2 of 3.21 +/- 0.17 (SEM) ml X 100 g-1 X min-1; second group received a background anesthetic of high-dose pentobarbital, which resulted in an initial CMRO2 of 1.76 +/- 0.16 ml X 100 g-1 X min-1. In rabbits receiving a background of morphine sulfate/N2O, halothane resulted in a significantly greater CBF (65 +/- 10 ml X 100 g-1 X min-1) than did isoflurane (40 +/- 5 ml X 100 g-1 X min-1). Both agents caused a reduction in CMRO2, but CMRO2 was significantly less during isoflurane administration. By contrast, with a background of pentobarbital anesthesia, CBF increased by significant and similar amounts with both halothane and isoflurane.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparison of the direct cerebral vasodilating potencies of halothane and isoflurane in the New Zealand white rabbit. 377 75

We determined the heart rate (HR) response to enflurane, halothane, and isoflurane and the effects of narcotics on this response in 81 healthy patients scheduled for elective surgery. Patients were randomly assigned to one of six treatment groups: one of the three anesthetics (approximately 0.9 MAC) in 60% nitrous oxide, and either 0.15 mg/kg of intramuscular morphine 30-60 min before induction or 1 microgram/kg of IV fentanyl 10 min after skin incision. All patients received diazepam, 10 mg orally, 60-90 min before anesthesia, a rapid sequence intravenous induction, and mechanically controlled ventilation. During inhalational anesthesia and the first 10 min of surgery, no significant change in HR occurred in any group (compared to the preinduction HR), although patients given morphine premedication tended to have a decreased HR and those not given morphine premedication tended to have an increased HR. These trends partially account for significant differences that emerged between groups after induction of anesthesia. Patients given morphine premedication and halothane had lower HR (64 +/- 3 SEM) than patients given isoflurane (80 +/- 3) or enflurane (84 +/- 3) and no morphine premedication. Patients anesthetized with enflurane and morphine premedication had lower HR (71 +/- 3) than patients given enflurane without morphine premedication. Administration of fentanyl 10 min after incision (these patients had received no morphine) significantly decreased HR in the presence of any of the vapors. We conclude that inhalational anesthetics used in the clinical setting we employed do not significantly increase heart rate, and that prior administration of morphine or concurrent administration of fentanyl may significantly decrease HR.
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PMID:Narcotics decrease heart rate during inhalational anesthesia. 381 60

To determine whether electrical stimulation of the periaqueductal gray region decreases anesthetic requirement, the authors studied the effect of such stimulation on the MAC of halothane and 60% nitrous oxide in 33 patients. These patients, who were undergoing implantation of a radio-frequency-coupled receiver and connection of that receiver to electrodes previously implanted in the periaqueductal gray area, were assigned randomly to receive (n = 16) or not receive (n = 17) electrical stimulation 1 h before surgery. The mean value (+/- SEM) for the minimum alveolar concentration of halothane combined with 60% nitrous oxide was significantly less (P less than 0.001) for patients who were stimulated preoperatively (0.15 +/- 0.05%) than for those who were not (0.51 +/- 0.02%). The authors conclude that stimulation of the periaqueductal gray region decreases anesthetic requirements and believe that at least three mechanisms are possible: a nonspecific narcotic-like effect, a specific effect on a pain pathway, or an effect on specific neural pathways that affect anesthetic requirements secondary to changes in regional concentrations of neurotransmitters.
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PMID:Reduced anesthetic requirement after electrical stimulation of periaqueductal gray matter. 397 Mar 61

The authors measured resting ventilation, the ventilatory response to added CO2, the VD/VT ratio, the rate of carbon dioxide output, and arterial PCO2 in four healthy volunteers, awake and anesthetized with, in order (I) enflurane 0.4 MAC with nitrous oxide 70 per cent, (II) enflurane 1.1 MAC with nitrous oxide 70 per cent, and (III) enflurane 1.1 MAC alone. Enflurane 1.1 MAC reduced ventilation and the response to added CO2 markedly, increased the VD/VT radio, reduced rate of CO2 output, and elevated values of PaCO2 from 41 +/- 1 to 65 +/- 3 mmHg (mean +/- SEM). Enflurane 1.1 MAC with nitrous oxide 70 per cent had similar effects. Enflurane 1.1 MAC with nitrous oxide 70 per cent had similar effects. Enflurane 0.4 MAC with nitrous oxide 70 per cent caused much smaller changes in each measured respiratory variable, increasing PaCO2 values to only 49 +/- 1 mmHg. The results indicate that enflurane 1.1 MAC alone is too potent a depressant of alveolar ventilation to permit spontaneous breathing, but that the "equi-anesthetic" enflurane 0.4 MAC with nitrous oxide 70 per cent may not be. The magnitude of the beneficial respiratory effects of substituting nitrous oxide for an equivalent amount of vapor is substantially greater with enflurane than with either halothane or isoflurane.
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PMID:Respiratory effects of nitrous during enflurane anesthesia in humans. 680 35

The antiarrhythmic and cardiovascular effects of the slow channel inhibitor, verapamil, were studied during 1.1 MAC halothane anesthesia in the dog. The control epinephrine arrhythmogenic dose to induce ventricular arrhythmias was 2.58 +/- 0.77 microgram . kg-1 . min-1 (mean +/- SEM). Three consecutive doses of 0.2 mg/kg verapamil each elevated the dose of epinephrine required to produce a ventricular arrhythmia to 5.17 +/- 1.27, 8.07 +/- 1.85, and 12.03 +/- 2.76 microgram . kg-1 . min-1, respectively, all of which were significantly elevated above the control value of the preceding values. A second group of dogs, unperturbed by epinephrine, received the same sequence of verapamil doses at similar time intervals for evaluation of effects on cardiovascular function and atrioventricular conduction. Heart rate remained unchanged. Mean arterial pressure decreased maximally by 37 per cent of control, left ventricular dP/dt by 24 per cent, and systemic vascular resistance by 51 per cent. These effects were transient with recovery times up to one hour. Central venous pressure increased by 44 per cent and left ventricular end diastolic pressure by 27 per cent, while PR interval was prolonged by 40 per cent. Thus, verapamil raised the dose of epinephrine required to elicit a ventricular arrhythmia during halothane anesthesia promptly and cumulatively. At the same time verapamil produced transient peripheral vasodilation, direct depression of myocardial contractility, and prolongation of atrioventricular conduction time that was not cumulative at the intervals studied.
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PMID:Epinephrine-induced arrhythmias and cardiovascular function after verapamil during halothane anesthesia in the dog. 727 Sep 49

Arrhythmogenic doses of epinephrine were determined in six mongrel dogs anesthetized at 1.4 MAC halothane initially in the absence of local anesthetics and then at increasing arterial plasma levels of lidocaine, bupivacaine, and etidocaine. The authors gave epinephrine intravenously at 5 microgram/kg/min and calculated the arrhythmogenic dose as a function of time until two or more premature ventricular contractions occurred within a 10-sec period. The control arrythmogenic dose of epinephrine was 4.66 +/- 0.46 microgram/kg (mean +/- SEM). Arrythmogenic doses of epinephrine were increased significantly after each dose of lidocaine, bupivacaine, and etidocaine. With the largest doses studied, local anesthetic plasma levels were frequently in the toxic range. The data show that lidocaine, bupivacaine, and etidocaine equally protect against epinephrine-induced arrhythmias in dogs anesthetized with halothane.
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PMID:Lidocaine, bupivacaine, etidocaine, and epinephrine-induced arrhythmias during halothane anesthesia in dogs. 735 41

Sevoflurane, a new volatile inhalational agent, undergoes biotransformation to fluoride which is potentially nephrotoxic. We compared the effects of sevoflurane or isoflurane anaesthesia on hepatorenal function and serum fluoride concentrations in 50 ASA 1-3 patients undergoing major intra-abdominal surgery. No patient developed renal or hepatic dysfunction. Mean (SEM) peak fluoride concentrations were 23.1 (1.5) mumol.l-1 for sevoflurane and 5.4 (0.4) mumol.l-1 for isoflurane (p < 0.001). There was a significant correlation in the sevoflurane group between the total dose of agent (MAC h), the total fluoride production (r = 0.78, p = 0.0001) and peak fluoride concentration (r = 0.57, p = 0.003). There was no correlation between these variables in the isoflurane group.
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PMID:Circulating fluoride changes and hepatorenal function following sevoflurane anaesthesia. 780 35


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