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PubMed1989

Aminophylline does not attenuate histamine-induced airway constriction during halothane anesthesia.

The effects of aminophylline on the release of endogenous catecholamines and on airway reactivity to aerosol histamine challenge were evaluated during halothane and thiopental/fentanyl anesthesia in basenji-greyhound dogs. Responses to histamine aerosol challenge (0.01, 0.03, 0.1, 0.3, 1.0, and 3.0 mg/ml) were measured during six conditions: 1) thiopental/fentanyl anesthesia (control), 2) thiopental/fentanyl with aminophylline infusion, 3) halothane anesthesia (1.5 MAC), 4) halothane anesthesia with aminophylline infusion, 5) thiopental/fentanyl anesthesia after pretreatment with iv propranolol, and 6) thiopental/fentanyl anesthesia with aminophylline infusion after pretreatment with iv propranolol. Prior to aerosol challenge baseline pulmonary resistance (RL) did not differ in the six groups. Aminophylline significantly attenuated the pulmonary response to histamine and increased catecholamine concentrations during thiopental/fentanyl anesthesia. Although halothane itself significantly attenuated the pulmonary response to histamine, the administration of aminophylline during halothane anesthesia produced no additional protective effect and no increases in catecholamines were noted. Moreover, no protective effect was seen after aminophylline administration during thiopental/fentanyl anesthesia in the same dogs pretreated with propranolol. These data suggest that the protective effect of aminophylline on histamine reactivity results from release of endogenous catecholamines and that the use of aminophylline during halothane anesthesia, which blocks this release, is not warranted.

Aminophylline↗
PubMed1990

Synergistic interaction of morphine and halothane in the guinea pig ileum: effects of pertussis toxin.

The effects of pertussis toxin on the actions of morphine and halothane in the guinea pig ileum are described. Both morphine and halothane produce a dose-related inhibition of electrically induced muscle contraction. The IC50 of morphine was unchanged by the toxin (2.1 and 2.2 X 10(-7) M in control and toxin-pretreated animals). However, the IC50 of halothane was increased from 2.1 to an extrapolated value of 9.1 vol/vol% by pertussis toxin. At high levels of inhibition the interaction between morphine and halothane was synergistic and was converted to additive in the presence of the toxin. These results demonstrate that in the myenteric longitudinal muscle preparation the effects of halothane, but not those of morphine, are mediated by the substrate for pertussis toxin, possibly a Gi membrane protein. The present study provides significant evidence that the effects of halothane on neuronal tissue are dependent upon an interaction with a specific membrane protein.

Animals↗
PubMed1990

Direct and neurally mediated effects of halothane on pulmonary resistance in vivo.

It has been suggested that halothane inhibits contraction of airway smooth muscle in vivo mainly by reducing reflex activity in nerves innervating the muscle with only minimal direct effects on the muscle itself. To examine possible mechanisms of action of halothane at clinically relevant concentrations the authors studied the effect of halothane on increases in pulmonary resistance (RL) produced by either vagus nerve stimulation (VNS, which caused neurally mediated constriction) or the inhalation of nebulized acetylcholine (ACh, which directly stimulated the smooth muscle cell) in nine mongrel dogs. The frequency of bilateral VNS and the dose of nebulized ACh were adjusted to produce approximately equal increases in RL. Halothane reduced the response to both types of stimulation in a dose-dependent fashion. At halothane concentrations greater than or equal to 0.4 MAC, the VNS response was significantly less than the ACh response. When tetrodotoxin was given to block neural activity, the ACh response was unchanged, confirming that neural activation did not contribute significantly to smooth muscle contraction in response to ACh. The authors conclude that in addition to neurally mediated effects, halothane at clinically used concentrations has significant direct effects on airway smooth muscle stimulated by ACh. The relative importance of each factor in vivo should depend on the stimulus that causes contraction of airway smooth muscle.

Acetylcholine↗
PubMed1990

Isoflurane and halothane attenuate coronary artery constriction evoked by serotonin in isolated porcine vessels and in intact pigs.

Serotonin is a vasoconstrictor thought to cause coronary artery constriction in humans. The purpose of this study was to determine if isoflurane and halothane each attenuated coronary artery constriction evoked by serotonin in pigs. Both in vitro and in vivo experimental methods were used. Isolated coronary arteries with an without endothelium were studied in organ chambers in the presence and absence of 2.5% concentrations of the anesthetics. In intact pigs serotonin was infused directly into the left anterior descending coronary arteries to induce constriction. The vasodilator effects of 0.5%, 1.25%, and 2.0% isoflurane and halothane were determined using quantitative angiography. Contractile responses of isolated coronary arteries were depressed by the two anesthetics. Maximum contractile responses to serotonin were as follows: rings with endothelium 45 +/- 5% untreated versus 29 +/- 5% with isoflurane 2.5% (difference between dose-response curves, P less than 0.01) and without endothelium 67 +/- 5% untreated versus 51 +/- 6% with isoflurane 2.5% (P less than 0.001); with endothelium 52 +/- 7% untreated versus 28 +/- 7% with halothane 2.5% (P less than 0.001) and without endothelium 65 +/- 5% untreated versus 40 +/- 6% with halothane 2.5% (P less than 0.001). In intact pigs isoflurane and halothane dilated constricted coronary arteries with and without endothelium at all anesthetic concentrations tested, including concentrations as low as 0.5%. Isoflurane 1.25% increased diameter of vessels with endothelium from 1.5 +/- 0.1 mm to 1.7 +/- 0.1 mm (P less than 0.02) and halothane 1.25% increased diameter from 1.6 +/- 0.1 mm to 1.7 +/- 0.1 mm (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

The minimum alveolar concentration (MAC) and hemodynamic effects of halothane, isoflurane, and sevoflurane in newborn swine.

To determine the minimum alveolar concentration (MAC) and hemodynamic responses to halothane, isoflurane, and sevoflurane in newborn swine, 36 fasting swine 4-10 days of age were anesthetized with one of the three volatile anesthetics in 100% oxygen. MAC was determined for each swine. Carotid artery and internal jugular catheters were inserted and each swine was allowed to recover for 48 h. After recovery, heart rate (HR), systemic systolic arterial pressure (SAP), and cardiac index (CI) were measured awake and then at 0.5, 1.0, and 1.5 MAC of the designated anesthetic in random sequence. The (mean +/- SD) MAC for halothane was 0.90 +/- 0.12%; the MAC for isoflurane was 1.48 +/- 0.21%; and the MAC for sevoflurane was 2.12 +/- 0.39%. Awake (mean +/- SD) measurements of HR, SAP, and CI did not differ significantly among the three groups. Compared to the awake HR, the mean HR decreased 35% at 1.5 MAC halothane (P less than 0.001), 19% at 1.5 MAC isoflurane (P less than 0.005), and 31% at 1.5 MAC sevoflurane (P less than 0.005). Compared to awake SAP, mean SAP measurements decreased 46% at 1.5 MAC halothane (P less than 0.001), 43% at 1.5 MAC isoflurane (P less than 0.001), and 36% at 1.5 MAC sevoflurane (P less than 0.005). Mean SAP at 1.0 and 1.5 MAC halothane and isoflurane were significantly less than those measured at equipotent concentrations of sevoflurane (P less than 0.005). Compared to awake CI, mean CI measurements decreased 53% at 1.5 MAC halothane (P less than 0.001) and 43% at 1.5 MAC isoflurane (P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1990

Halothane decreases the release of neuropeptide Y and 3,4-dihydroxyphenylglycol from superfused segments of dog pulmonary artery.

Neuropeptide Y (NPY), norepinephrine (NE), and 3,4-dihydroxyphenylglycol (DOPEG), the metabolite of NE that arises intraneuronally, were measured in superfusates before, during, and after nerve stimulation and in extracts of dog pulmonary artery after superfusion and electrical stimulation (ES) at 12, 6, and 1 Hz. NE and DOPEG were quantified by high-pressure liquid chromatography with electrochemical detection; peptides were quantified by radioimmunoassay. The rate of overflow of NPY, NE, and DOPEG into superfusate was measured over time. The overflow of DOPEG into superfusate during basal conditions was 3.0 times that of NE. Efflux of DOPEG and NPY increased during ES; peak effluxes were not reached, however, until after cessation of stimulation. NE efflux peaked during ES. Effluxes of NE, NPY, and DOPEG were frequency-dependent at 12 and 6 Hz; at 1 Hz efflux of only NE was greater than basal. Halothane decreased significantly the rates of NPY and DOPEG efflux during and after 12 Hz ES; DOPEG efflux evoked by 6 Hz stimulation was also decreased by halothane. The percentage of the total tissue content of NPY that overflowed was decreased by halothane. Halothane did not affect the molar ratios of NE:DOPEG or NE:NPY during basal conditions or ES. These studies provide evidence that halothane slows efflux of NPY that is released along with NE from dog pulmonary artery during high frequencies of stimulation. Halothane also reduces the metabolism of NE to DOPEG.

Animals↗
PubMed1990

Differential protective effects of halothane and isoflurane against hypoxic and reoxygenation injury in the isolated guinea pig heart.

The authors investigated the effects of halothane (HAL) and isoflurane (ISO) on cardiac depression produced by global hypoxia and the recovery of function following reoxygenation is isolated guinea pig hearts perfused with Krebs' solution at constant pressure. Isovolumetric left ventricular systolic (LVSP) and end-diastolic pressures (LVEDP) were measured by placing a saline filled, latex balloon into the left ventricle. Bipolar electrodes were placed in the right atrium and right ventricle for measurements of heart rate (HR), atrioventricular conduction time (AVCT), and determination of the incidence and severity of dysrhythmias occurring during hypoxia and reoxygenation. Hearts were divided into three groups: control (n = 20), halothane (n = 12), and isoflurane (n = 13). All hearts were exposed in sequence to oxygenated perfusate (PO2, 530 mmHg), moderately hypoxic perfusate (PO2, 91 mmHg) for 30 min, and then to oxygenated perfusate for 40 min. Halothane (1%, 0.4 mM) or isoflurane (1.5%, 0.5 mM) were administered 10 min before hypoxia, during hypoxia, and during the first 10 min of reoxygenation. Exposure to halothane and isoflurane before hypoxia produced a 14 and 11% decrease in heart rate, a 32 and 23% increase in AVCT, and a 47 and 28% decrease in LVSP (all P less than or equal to 0.001) for halothane and isoflurane, respectively, and no significant change in LVEDP. During hypoxia, HR decreased and AVCT increased similarly in both groups. Left ventricular systolic pressure (LVSP) decreased sharply with a narrowing of the prehypoxic differences among the groups. In the control and isoflurane groups, LVEDP increased during hypoxia but remained unchanged in the halothane group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Kinetics of desflurane, isoflurane, and halothane in humans.

The low solubility of desflurane in blood and tissues suggests that the partial pressures of this agent in blood and tissues should approach the inspired partial pressure more rapidly than would the blood and tissue partial pressures of other potent inhaled anesthetics. We tested this prediction, comparing the pharmacokinetics of desflurane with those of isoflurane, halothane, and nitrous oxide in eight volunteers. We measured the rate at which the alveolar (endtidal) (FA) concentration of nitrous oxide increased towards an inspired (FI) concentration of 65-70%, and then measured the concurrent increase in FA and mixed expired concentrations (FM) of desflurane, isoflurane, and halothane at respective FI values of 2.0%, 0.4%, 0.2%. Minute ventilation (VE) was measured concurrently with the measurements of anesthetic concentrations. The potent vapors were administered for 30 min; administration of nitrous oxide continued throughout the period of anesthesia. For the potent agents, we also measured VE, FA, and FM for 5-7 days of elimination. We used FA/FI and FA/FA0 (FA0 = the last FA during the administration of each anesthetic) to define the rate of increase of anesthetic in the lungs and the rate of elimination of anesthetic, respectively. FA/FI values at 30 min of administration were: (mean +/- SD) nitrous oxide 0.99 +/- 0.01, desflurane 0.90 +/- 0.01, isoflurane 0.73 +/- 0.03, and halothane 0.58 +/- 0.04. FA/FA0 values after 5 min of elimination were: desflurane 0.14 +/- 0.02, isoflurane 0.22 +/- 0.02, and halothane 0.25 +/- 0.02. Recovery (volume of anesthetic recovered during elimination per volume taken up) of desflurane (105 +/- 25%) equalled recovery of isoflurane (102 +/- 13%) and exceeded recovery of halothane (64 +/- 9%). Time constants for a five-compartment mammillary model for halothane and isoflurane differed for the lungs, fat group, and hepatic metabolism, and exceeded those for desflurane for all compartments. In summary, we found that FA/FI of desflurane increases more rapidly and that FA/FA0 decreases more rapidly in humans than do these variables with other available potent anesthetics. We also found that desflurane resists biodegradation in humans and so may have little or no toxic potential.

Adult↗
PubMed1991

Alteration of left ventricular diastolic function by desflurane, isoflurane, and halothane in the chronically instrumented dog with autonomic nervous system blockade.

The effects of the new volatile anesthetic desflurane on three indices of left ventricular diastolic function were examined and compared to those produced by equianesthetic concentrations of isoflurane and halothane. Diastolic function has been shown to significantly influence systolic performance, but the effects of volatile anesthetics on diastolic function have not been extensively examined. Since autonomic nervous system function may significantly influence hemodynamic actions of anesthetics in vivo, experiments were performed in the presence of pharmacologic blockade of the autonomic nervous system. Three groups comprising a total of 23 experiments were performed using 11 dogs instrumented for measurement of aortic and left ventricular pressure, rate of increase of left ventricular pressure (dP/dt), subendocardial segment length, and cardiac output. Systemic hemodynamics were recorded in the conscious state and after 30 min equilibration at 1.0 and 1.5 MAC desflurane, isoflurane, or halothane. Ventricular relaxation was described using invasively derived time constants of isovolumetric relaxation with zero (To) or nonzero (Tn) assumptions of asymptotic decay. Chamber and myocardial stiffness the viscoelastic properties of the ventricle, were described using exponential relationships relating ventricular pressure to segment length and end-diastolic pressure to Lagrangian strain, respectively. Desflurane produced a significant (P less than 0.05) and dose-dependent increase in isovolumetric relaxation as a evaluated by both time constants (To, 22.2 +/- 2.0 during control to 33.9 +/- 3.5 ms at 1.5 MAC; Tn, 33.1 +/- 1.6 during control to 45.1 +/- 4.3 ms at 1.5 MAC). Similar degrees of prolongation of isovolumetric relaxation were produced by isoflurane (Tn, 35.6 +/- 1.5 during control to 47.1 +/- 2.9 ms at 1.5 MAC) and halothane (Tn, 31.7 +/- 2.2 during control to 42.3 +/- 3.9 ms at 1.5 MAC). Halothane also caused an increase in regional passive chamber stiffness (Kp, 0.46 +/- 0.07 during control to 0.88 +/- 0.17 mm-1 at 1.5 MAC) indicating a decrease in ventricular compliance. No changes in chamber stiffness were observed with desflurane or isoflurane. In addition, no significant changes in myocardial stress-strain relationships as evaluated by nonlinear elastic coefficients, alpha (gain) and beta (myocardial stiffness), were observed with any anesthetic. Although the effects of volatile anesthetics on systolic function could not be entirely excluded from the analysis, the results indicated that desflurane, isoflurane, and halothane produce equivalent degrees of prolongation of isovolumetric relaxation. Halothane also caused a decrease in compliance during passive filling as evaluated by chamber stiffness, but no change in compliance was observed at end diastole as assessed by stress-strain relationships.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

The electrophysiologic effects of amiodarone and halothane on canine Purkinje fibers.

Amiodarone may cause serious complications in patients receiving general anesthetics. Potentially adverse electrophysiologic interactions between amiodarone and halothane were studied with the use of standard microelectrode techniques to record intracellular action potentials (APs) from excised canine Purkinje fibers. A second dog (support dog) was anesthetized and a femoral arteriovenous bypass circuit created in which arterial blood from the support dog superfused the Purkinje fiber in a tissue bath. The applicability of this model was established by first comparing the AP effects of halothane during blood perfusion with those in Tyrode's solution. Halothane reduced AP duration (APD; P less than 0.05) during Tyrode's solution superfusion and blood cross-perfusion. After the blood perfusion-Purkinje fiber model was validated, the interaction between halothane and amiodarone was studied using Purkinje fibers from dogs chronically treated with oral amiodarone, superfused with blood from chronically amiodarone-treated support dogs. Amiodarone reduced resting membrane potential and prolonged APD. Depression of AP amplitude and reduction of the maximum rate of increase of phase 0 of the AP (Vmax) by halothane (both P less than 0.05) suggested risk of conduction defects if halothane is administered to patients receiving chronic amiodarone therapy.

Action Potentials↗
PubMed1991

Comparative effects of halothane, isoflurane, and sevoflurane on the liver with hepatic artery ligation in the beagle.

Recently, there has been increasing interest in the alterations in splanchnic and hepatic circulation and preservation of hepatic oxygenation and function during anesthesia and surgery. However, the effects of volatile anesthetics under a condition of marginal hepatic oxygen supply are not well understood. Using a crossover design, we therefore studied the effects of equianesthetic concentrations (1.5 MAC) of halothane, isoflurane, and sevoflurane on hepatic oxygenation and function in nine beagles in which the hepatic artery had been ligated. Portal blood flow was measured by an electro-magnetic flow meter. Hepatic function was assessed by indocyanine green elimination kinetics. While cardiac output and mean arterial pressure were greater during halothane anesthesia than during isoflurane and sevoflurane anesthesia, portal blood flow and hepatic oxygen supply were significantly less during halothane and sevoflurane anesthesia than during isoflurane anesthesia. With regard to hepatic oxygen uptake, there was a significant difference between halothane (2.7 +/- 1.2 ml.min-1 x 100 g-1) and sevoflurane (3.7 +/- 2.0 ml.min-1 x 100 g-1; P less than 0.05). Consequently, the hepatic oxygen supply/uptake ratio and the hemoglobin oxygen saturation and oxygen partial pressure in hepatic venous blood during sevoflurane anesthesia were significantly less than they were with the other anesthetics. Indocyanine green clearance was better preserved during sevoflurane anesthesia (39.7 +/- 12.0 ml.min-1) than during halothane anesthesia (30.9 +/- 8.4 ml.min-1; P less than 0.05). We conclude that sevoflurane is accompanied by a smaller oxygen supply/uptake ratio than is halothane and isoflurane, while it preserves hepatic function.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics↗
PubMed1991

The effect of halothane on thermosensitive neurons in the preoptic region of the anterior hypothalamus in acutely instrumented cats.

Normal thermoregulatory processes are significantly impaired by halothane anesthesia. However, the direct effects of halothane on thermosensitive neurons in the preoptic region of the anterior hypothalamus, a major thermoregulatory site, have not been previously investigated. Thirty-eight cats were anesthetized with alpha-chloralose (60 mg/kg) and urethane (600 mg/kg) and placed in stereotactic restraint. Stainless steel thermodes for highly selective local heating and cooling were stereotactically placed into the preoptic region with thermocouples used to monitor regional temperature. Using tungsten microelectrodes, 148 single neurons in the preoptic region were identified and subjected to local heating (to 42 degrees C) and cooling (to 30 degrees C). Eighteen percent (n = 27) in 15 different cats were classified as thermosensitive by accepted criteria (change in firing rate per degree centigrade of greater than 0.8 spikes.s-1.degrees C-1 or less than -0.6 spikes.s-1.degrees C-1). Thermosensitve units were then subjected to graded concentrations of halothane (0.25-1.0% end-tidal), and local heating and cooling were repeated. The spontaneous firing rate (spikes per second) at 37 degrees C of 21 warm-sensitive neurons was significantly (P less than 0.05) reduced, to 65.5 +/- 8.3, 42.6 +/- 10.7, 28.0 +/- 9.5, and 18.1 +/- 6.0% of control at 0.25, 0.50, 0.75, and 1% halothane, respectively. Spontaneous firing rate returned to 99.5 +/- 19.8% of control within 30 min after discontinuation of halothane. Thermosensitivity (change, per degree centigrade, in spikes per second) was also significantly reduced, to 33.3 +/- 5.6, 28.5 +/- 14.6, and 13.9 +/- 6.6% of control at 0.50, 0.75 and 1.0% halothane (all P less than 0.05 compared to control).(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1991

Halothane depresses D600 binding to bovine heart sarcolemma.

Volatile anesthetics exert their negative inotropic effects by interfering with Ca2+ homeostasis in the myocardial cell. The mechanism of this dose-dependent action is uncertain. 3H-D600 (3H-Gallopamil), a Ca(2+)-channel antagonist, binds to the voltage-dependent Ca2+ channels (VDCC) in a specific, saturable, and reversible manner. We used this ligand to study the effect of halothane on the binding characteristics of the VDCC in purified bovine heart sarcolemma. Cardiac sarcolemmal vesicles were isolated from fresh bovine heart by differential centrifugation and filtration. 3H-D600 equilibrium binding assays were performed in the presence or absence of 1.0 mM unlabeled D600 to determine total and nonspecific binding in room air and at 0.7, 1.3, and 2.5% (vol/vol) halothane. Halothane produced a significant dose-dependent and reversible depression of 3H-D600 specific binding in bovine heart sarcolemma. Depression was completely reversed when halothane had evaporated from the samples prior to filtration. Halothane 1.3% (vol/vol) produced a 40% reduction in the maximum binding capacity. The dissociation constant was not affected by any concentration of halothane. One mechanism by which the volatile anesthetics may induce negative inotropism is through the reduction of functional VDCCs in the heart, leading to reduction of Ca2+ entry. The results of this study support this hypothesis.

Animals↗
PubMed1992

The effects of sevoflurane, halothane, enflurane, and isoflurane on hepatic blood flow and oxygenation in chronically instrumented greyhound dogs.

Inhalational anesthetics produce differential effects on hepatic blood flow and oxygenation that may impact hepatocellular function and drug clearance. In this investigation, the effects of sevoflurane on hepatic blood flow and oxygenation were compared with those of enflurane, halothane, and isoflurane in ten chronically instrumented greyhound dogs. Each dog randomly received enflurane, halothane, isoflurane, and sevoflurane, each at 1.0, 1.5, and 2.0 MAC concentrations. Mean arterial blood pressure and cardiac output decreased in a dose-dependent fashion during all four anesthetics studied. Heart rate increased compared to control during enflurane, isoflurane, and sevoflurane anesthesia and did not change during halothane anesthesia. Hepatic arterial blood flow and portal venous blood flow were measured by chronically implanted electromagnetic flow probes. Hepatic O2 delivery and consumption were calculated after hepatic arterial, portal venous, and hepatic venous blood gas analysis. Hepatic arterial blood flow was maintained with sevoflurane and isoflurane. Halothane and enflurane reduced hepatic arterial blood flow during all anesthetic levels compared to control (P less than 0.05), with marked reductions occurring with 1.5 and 2.0 MAC halothane concomitant with an increase in hepatic arterial vascular resistance. Portal venous blood flow was reduced with isoflurane and sevoflurane at 1.5 and 2.0 MAC. A somewhat greater reduction in portal venous blood flow occurred during 2.0 MAC sevoflurane (P less than 0.05 compared to control and 1.0 MAC values for sevoflurane). Enflurane reduced portal venous blood flow at 1.0, 1.5, and 2.0 MAC compared to control. Halothane produced the greatest reduction in portal venous blood flow (P less than 0.05 compared to sevoflurane).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics↗
PubMed1992

Dose-response relationship of isoflurane and halothane versus coronary perfusion pressures. Effects on flow redistribution in a collateralized chronic swine model.

The authors studied the redistribution of myocardial blood flow in a collateral-dependent (CD) zone as a function of coronary perfusion pressure (CPP) during isoflurane and halothane anesthesia. A swine model with CD myocardium distal to a chronically occluded left anterior descending coronary artery was developed and studied. Sixteen piglets were allowed to grow for 8-10 weeks after banding of the left anterior descending coronary artery. They were randomly anesthetized with either isoflurane (n = 8) or halothane (n = 8) as the sole anesthetic, which was used to regulate specific CPP. The resultant regional myocardial blood flows were measured using radiolabeled microspheres. Four randomly allocated CPPs, of 30, 40, 45, and 55 mmHg, were studied in each animal. Four additional collateralized animals were anesthetized with alpha-chloralose, and the same CPPs were obtained using an intravenous adenosine infusion (1-5 microM kg-1) to validate this model. There was a proportional decrease in heart rate and blood pressure in both the isoflurane and and the halothane group with CPP. Cardiac output was significantly decreased in the halothane group at 30 mmHg when compared to 55-mmHg CPP, but it was maintained in the isoflurane group. Systemic vascular resistance was significantly lower in the isoflurane group at 30 and 40 mmHg when compared to 55-mmHg CPP. Both the isoflurane and the halothane group showed a proportional and significant decrease in endo-, mid-, and epicardial blood flows at 30-mmHg CPP when compared to baseline. In both CD and normal perfusion zones, isoflurane consistently sustained a higher endocardial blood flow than halothane (5.7-41.1%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

The inhibitory effect of halothane on mesenteric venoconstriction and related reflex responses during acute graded hypoxia in rabbits.

Systemic hypoxia is a common abnormality encountered frequently in the clinical setting that produces compensatory cardiopulmonary changes affecting heart rate, blood pressure, peripheral vascular resistance, and respiratory drive. These changes are known to be inhibited or reversed by inhaled anesthetics. More recently, chemoreflex-mediated constriction of capacitance veins has been identified as a mechanism that contributes significantly to the hemodynamic adjustments during hypoxia. However, the effects of anesthetics on this response have not been clarified. The current study was designed to quantify sympathetically mediated mesenteric venoconstriction as well as heart rate and blood pressure responses to acute graded hypoxia; to identify the inhibitory effects of inhaled halothane on these responses; and to estimate the contribution of the peripheral chemoreceptors in mediating these changes. Changes in mesenteric vein diameter were measured in alpha-chloralose anesthetized rabbits in situ with simultaneous changes in heart rate and blood pressure during 40-s periods of 10%, 5%, 2.5%, and 0% inspired O2 administered sequentially before, during, and after 1% or 1.25% inhaled halothane. Sympathetic efferent nerve activity also was measured, and, in a separate group of animals, measurements were preceded by carotid chemoreceptor denervation. Hypoxia-mediated venoconstriction, bradycardia, and hypertension were attenuated almost equally by both 1% and 1.25% inhaled halothane (the higher dose produced only slightly greater inhibition). These responses were inhibited significantly in chemoreceptor-denervated animals, and the subsequent 1% inhaled halothane added only minimal additional attenuation. Increases in chemoreflex-mediated sympathetic efferent nerve activity also were reduced significantly by (1.25%) inhaled halothane. These results indicate that halothane impairs capacitance vein responses and other hemodynamic adjustments during hypoxia. Inhibition of these compensatory changes appears to be mediated, at least in part, via attenuation of peripheral chemoreflex responses and suppression of the resultant reflex increases in sympathetic efferent nerve activity.

Acute Disease↗
PubMed1993

Effects of nifedipine with isoflurane, halothane, or enflurane on automaticity, conduction, and contractility in isolated guinea pig hearts.

BACKGROUND: Calcium channel blockers and volatile anesthetics have depressant effects on cardiac function. Both groups of drugs appear to exert both qualitatively and quantitatively different effects on electrophysiologic and mechanical function. The aim of this study was to compare the direct cardiac effects of the calcium channel blocker nifedipine in the absence and presence of isoflurane, halothane, or enflurane. METHODS: Guinea pig hearts (N = 36) were isolated and perfused with oxygenated Krebs-Ringer solution (pH 7.4, 37 degrees C). Recording electrodes were placed in the right atrium and ventricle to measure heart rate and atrioventricular (AV) conduction time. Isovolumetric left ventricular pressure (LVP) was measured via a latex balloon and transducer. Hearts were randomly assigned to one of three anesthetic groups at 0.7 and 1.4 minimum alveolar concentration (MAC) and treated with 15 and 30 nM nifedipine. RESULTS: Nifedipine alone significantly decreased atrial rate and left ventricular pressure, without prolonging AV conduction. Nifedipine plus isoflurane, halothane, or enflurane did not significantly prolong AV conduction compared with the respective anesthetic agent alone, but nifedipine plus isoflurane, halothane, or enflurane significantly decreased atrial rate compared with the effect of the anesthetic alone. Halothane or enflurane plus nifedipine significantly decreased atrial rate more than nifedipine alone or isoflurane plus nifedipine. Isoflurane, halothane, or enflurane plus nifedipine significantly depressed LVP more than the respective anesthetic agent alone. Halothane or enflurane plus nifedipine also significantly depressed LVP more than isoflurane plus nifedipine or nifedipine alone. CONCLUSIONS: This study demonstrates that the combined treatment of nifedipine and volatile anesthetics, especially enflurane, additively depresses atrial rate and contractility, but not AV conduction in vitro. In comparison with results reported previously, these effects appear less pronounced than those of the combination of volatile agents with diltiazem and, especially, verapamil.

Animals↗
PubMed1994

Effects of isoflurane on ouabain toxicity in canine Purkinje fibers. Comparison with halothane.

BACKGROUND: Although halothane reduces digitalis toxicity, other anesthetics, notably cyclopropane, increase toxicity. This study determined the effects of isoflurane on digitalis toxicity in isolated cardiac tissue and compared these effects with those of halothane. METHODS: Standard microelectrode techniques were used to record action potentials from excised canine Purkinje fibers. Fibers were paced at cycle lengths between 1,000 and 250 ms for 20 beats to induce delayed afterdepolarizations, which are membrane potential oscillations indicative of intracellular Na+ and Ca2+ overload, produced in these experiments by digitalis toxicity. The digitalis glycoside ouabain, 2 x 10(-7) M, was added to the Tyrode's solution superfusate to induce delayed after-depolarizations. Action potential variables and the coupling interval and amplitude of afterdepolarizations were then measured. Isoflurane (0.5%, 1%, or 2%) was added with a calibrated vaporizer (n = 8). In a second set of experiments (n = 10), isoflurane 1.25% or halothane 0.75% was added to the superfusate. After measurements had been made, the other agent was substituted. RESULTS: Ouabain produced primary and secondary delayed afterdepolarizations, which were reduced in amplitude by isoflurane in a dose-related manner (P = 0.0002). Action potential duration to 90% repolarization was shortened by ouabain (P = 0.009) and remained shortened during isoflurane administration. Action potential duration to 50% repolarization was shortened by isoflurane 2%. Halothane and isoflurane were equally effective in reducing the amplitude of delayed afterdepolarizations (both P = 0.0002). In three fibers, triggered extrasystoles appeared. Halothane and isoflurane each abolished extrasystoles. In two fibers, sustained triggered activity appeared. Isoflurane abolished the arrhythmia in each fiber. CONCLUSIONS: Isoflurane and halothane are equally effective in reducing delayed afterdepolarizations induced by ouabain toxicity.

Action Potentials↗