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PubMed1989

Effects of halothane, isoflurane and enflurane on isolated rat heart muscle.

Since the effects in the intact organism are complicated by central as well as peripheral effects, we compared the direct cardiac effects of three commonly used inhalational anaesthetics--halothane, isoflurane and enflurane--on isolated heart muscle. Concentration-response curves for inotropic, chronotropic and ventricular automaticity effects of halothane, isoflurane and enflurane (0.1-2% v/v) on electrically stimulated left atria, right atria and right ventricles of the rat were obtained. All three inhalational anaesthetics significantly decreased contractile force; the inhibitory concentration 50 (IC50) of enflurane was 0.55 +/- 0.06% v/v, significantly lower than halothane (0.96 +/- 0.08% v/v) and isoflurane (0.67 +/- 0.05% v/v). Similar results were obtained on atrial nomotopic rate. Halothane, isoflurane and enflurane produced negative chronotropic effects in this preparation. On the other hand, halothane and isoflurane significantly reduced the ventricular ectopic automaticity. However enflurane (0.3, 0.5, 1% v/v) increased ventricular rate. There were statistically significant differences between the IC50 values of atrial and ventricular rate for halothane and isoflurane. These results indicate: (a) direct negative inotropic and chronotropic effects for the three inhalational anaesthetics tested; (b) anti-dysrhythmic actions for halothane and isoflurane; and (c) dysrhythmogenic effects of enflurane.

Animals↗
PubMed1988

Halothane decreases calcium channel antagonist binding to cardiac membranes.

The effect of halothane concentration on the binding of the calcium antagonist, [3H] nitrendipine (3HNTP), to rat and rabbit heart membranes was examined in vitro because it has been hypothesized that one mechanism by which halothane depresses cardiac contractility is by interfering with Ca2+ channel function. Membranes were incubated for 90 minutes in a closed system with 3HNTP and increasing concentrations of halothane. The amount of 3HNTP bound to membranes was quantified by radioligand binding technique and liquid scintillation counting. It was found in both the rat and rabbit cardiac membranes that halothane (0.4-2.0%) caused a dose-dependent decrease in specific 3HNTP binding (P less than 0.0001). The decrease in 3HNTP binding caused by halothane was also found to be reversible. These results indicate that halothane interferes with one property of the Ca2+ channel and suggest that this may be one possible mechanism for the negative inotropic action of halothane.

Animals↗
PubMed1988

Anesthetic and hemodynamic effects of the stereoisomers of medetomidine, an alpha 2-adrenergic agonist, in halothane-anesthetized dogs.

The anesthetic-sparing and hemodynamic effects of the stereoisomers of the highly selective alpha 2-adrenergic agonist medetomidine were studied in halothane-anesthetized dogs. Male beagles were anesthetized with halothane in oxygen. After a 2-hour equilibration period, halothane MAC and baseline hemodynamic functions were determined. DL-(n = 7), D- (n = 5), or L-medetomidine (n = 5) at 1, 3, and 10 micrograms/kg was administered via a right atrial port over 15 minutes while each dog was given halothane at the MAC dose for that animal. Twenty minutes after the end of infusion (when the hemodynamic variables were stable), hemodynamic function was reassessed. Halothane MAC was then redetermined. MAC for halothane significantly decreased after DL-medetomidine administration in a dose-dependent fashion to the extent that at the highest dose (10 micrograms/kg) the halothane MAC was less than 0.1%. This effect could be mimicked by the D-isomer, whereas the L-isomer was without effect. Neither isomer changed the mean arterial pressure, whereas only the D-isomer significantly decreased heart rate and cardiac output. Medetomidine, the highly selective alpha 2-adrenergic agonist, reduces the MAC for volatile anesthesia by a greater degree than with any other physiologic, pharmacologic, or pathologic intervention thus far reported. The fact that this effect is stereospecific suggests a structure activity relation that can be accounted for by a homogeneous receptor population. The role of medetomidine as a supplemental anesthetic agent appears promising and requires further investigation.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

Metabolic activation of the halothane metabolite, [14C]2-chloro-1,1-difluoroethene, in hepatic microsomes.

Halothane is reduced to 2-chloro-1,1,1-trifluoroethane (CTE) and 2-chloro-1,1-difluoroethene (CDE) by cytochrome P-450. These compounds may potentially undergo secondary metabolism in vivo, but their capacity to undergo metabolic activation and bind to macromolecules is unknown. This study, therefore, compared the abilities of CDE and CTE to bind to microsomal components in relation to that of halothane in hepatic microsomes. The results show that CDE, in addition to halothane, binds to microsomes under conditions of cytochrome P-450 activity. While halothane bound predominantly to lipids under nitrogen, CDE bound mainly to protein under oxygen. No CTE binding under any conditions could be detected. On an equimolar basis, CDE binding to protein was approximately one-third of that of halothane under oxidative conditions, however, CDE binding was enhanced in the presence of halothane. The results support the hypothesis that CDE metabolism may contribute to the metabolic binding due to halothane exposures.

Anaerobiosis↗
PubMed1986

Effect of halothane on brain 2',3'-cyclic nucleotide 3'-phosphodiesterase during neurodevelopment in the rat.

Chronic exposure to anesthetic concentrations of halothane during the prenatal and early postnatal periods inhibits the incorporation of the leucine into myelin subcellular fractions in the rat. The enzyme 2',3' - cyclic nucleotide 3' - phosphodiesterase (CNPase) has been widely used as a myelin marker. To determine the effect of halothane on the developmental profile of CNPase, two groups of pregnant Sprague Dawley rats were exposed to 500 p.p.m. or 250 p.p.m. halothane, eight hours per day, five days per week from the third day after conception through postnatal day ten. Control animals were exposed to air alone. CNPase activity was significantly decreased by 500 p.p.m. halothane (34%) and by 250 p.p.m. halothane (29%) at postnatal day 17. Brain and body weights in both halothane treated groups were also less than control animals throughout the measurement period. The data indicates that chronic pre- and postnatal halothane exposure at low levels delays myelination in the rat.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗
PubMed1988

Minimum anesthetic dose and cardiopulmonary dose response for halothane in chickens.

The minimum anesthetic dose (MAD) and the cardiopulmonary dose-response for halothane were determined in male chickens. The MAD for halothane was 0.85 +/- 0.09% (mean +/- SD), with a range of 0.75% to 0.98%. There was a significant (P less than 0.002) positive correlation between increasing concentrations of halothane and PaCO2, and significant negative correlations of halothane concentration with respiratory rate (P less than 0.04), arterial blood pH (P less than 0.008), and mean arterial blood pressure P less than 0.008). A significant correlation was not found between halothane concentration and heart rate or arterial blood bicarbonate concentration. It was concluded that the MAD for halothane in chickens is similar to values for minimum alveolar concentrations of halothane in mammalian species, and that there is substantial dose-dependent depression of cardiopulmonary function in chickens.

Anesthesia, General↗
PubMed1988

Altered hepatic calcium homeostasis in guinea pigs with halothane-induced hepatotoxicity.

Exposure of guinea pigs to 1% halothane in air for 4 hr resulted in extensive centrizonal hepatic necrosis in 70% of animals examined 2 to 3 days later. In contrast, confluent hepatic necrotic lesions were not present in animals studied 24 hr after halothane exposure; only microvascular fatty change of hepatocytes with occasional necrotic cells was observed at that time (in 84% of animals). This delayed onset of lesion development afforded the opportunity to study microsomal membrane composition and indices of Ca++ homeostasis before and after the onset of halothane-induced hepatic necrosis. Hepatic microsomal cytochrome P-450 levels were unaltered 24 hr after halothane exposure, but fell to approximately 50% of control values at 72 hr. This indicates that such changes were most likely the result of hepatocellular necrosis. Microsomal lipid composition, including the relative proportions of individual phospholipids, was unaltered during halothane-induced hepatotoxicity. In contrast, microsomal Ca++ sequestration, as assessed by 45Ca uptake, was reduced 24 hr after halothane exposure compared with controls (2.76 +/- 1.32 nmol/mg of protein per min, vs. 6.63 +/- 2.88 nmol/mg of protein per min, P less than .001). This early change in microsomal Ca++ uptake was associated with a 10-fold increase in total hepatic Ca++ content at 24 hr. Subsequent changes in hepatic Ca++ content were proportionate to the severity of liver necrosis. The observation that abnormalities of hepatic Ca++ homeostasis antedate the presence of liver cell necrosis is consistent with a role for altered Ca++ fluxes in the mechanism of halothane-induced liver injury.

Alanine Transaminase↗
PubMed1987

Hepatic circulation during surgical stress and anesthesia with halothane, isoflurane, or fentanyl.

Hepatic blood flow and the oxygen supply/uptake relation were studied in 19 miniature pigs using labeled microspheres. Changes in hepatic arterial blood flow and portal blood flow, as well as total hepatic blood flow during halothane anesthesia were more closely associated with changes in mean arterial pressure (MAP) and cardiac output than during anesthesia with isoflurane or fentanyl. Halothane or isoflurane administered in concentrations that decreased MAP by approximately 30% were accompanied by decreases in hepatic oxygen delivery (DO2th) averaging 46% during halothane and 31% during isoflurane anesthesia and parallel decreases in hepatic blood flow. In concentrations that decreased MAP by 50%, halothane and isoflurane decreased DO2th 61 and 37%, respectively. DO2th was maintained (statistically insignificant, 23% increase) during both doses of fentanyl administered (20 micrograms/kg followed by 0.17 microgram . kg-1 . min-1, and 50 micrograms/kg followed by 0.42 microgram . kg-1 . min-1). Hepatic oxygen uptake increased 50% during fentanyl and was maintained at baseline levels during both doses of halothane and isoflurane anesthesia. Oxygen content in hepatic venous blood was maintained at baseline levels during fentanyl and isoflurane administration and was decreased by both concentrations of halothane anesthesia. The hepatic oxygen supply demand ratio was maintained at baseline levels after both doses of fentanyl and during isoflurane administered in a concentration that decreased blood pressure 30%; the ratio decreased during isoflurane administered in a concentration decreasing blood pressure by 50% and during both doses of halothane anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1987

[Is halothane obsolete? An illustration of measurement with two standards].

In 1986 the discussion on the further use of halothane broke out anew, especially after the Bristol symposium and the European Congress of Anesthesiology in Vienna. Everywhere there is great uncertainty on whether or not halothane should continue to be used. A critical analysis of the literature shows that there are two standards applied to halothane. When judged by the same stringent criteria as halothane other anesthetic techniques are also dubious, e.g. neuroleptanesthesia or epidural block. Finally, experience with isoflurane, the strongest rival of halothane, is not adequate to warrant abandoning halothane, especially as long as the question of coronary steal is still open. At present there is no solid scientific basis for vanishing halothane.

Anesthesia, General↗
PubMed1987

Pulsed Doppler and two-dimensional echocardiography: comparison of halothane and isoflurane on cardiac function in infants and small children.

The combination of two-dimensional and pulsed Doppler echocardiography was used to measure determinants of cardiac function in 20 ASA physical status I infants and small children (9 days-32 months of age) during equipotent halothane (n = 10) or isoflurane (n = 10) anesthesia in oxygen. Five sets of cardiovascular data were recorded in each patient. In the awake, unmedicated state prior to induction, at three different anesthetic levels, 0.75, 1.0, and 1.25 MAC (corrected for age) and a final measurement repeated at 1.25 MAC after the intravenous infusion of 15 ml X kg-1 of Lactated Ringers solution. The study was completed prior to intubation and surgery. Results are expressed as mean +/- SEM. Isoflurane and halothane decreased mean blood pressure from the awake level (isoflurane 76.6 +/- 2.3 to 60.6 +/- 3.1 mm, halothane 72.2 +/- 3.9 to 60.6 +/- 3.1 mm at 1.25 MAC). Isoflurane increased heart rate at all anesthetic levels (128.7 +/- 4.2 to 142.5 +/- 6.0 beats/min at 0.75 MAC). Halothane decreased heart rate at 1.25 MAC (124.6 +/- 4.6 to 119.4 +/- 3.5 beats/min). Isoflurane and halothane decreased cardiac index at 1.25 MAC. Stroke volume index decreased at 1.0 and 1.25 MAC with both isoflurane (36.9 +/- 3.8 to 30.2 +/- 3.5 ml/m2) and halothane (32.7 +/- 2.5 to 28.9 +/- 2.5 ml/m2). Ejection fractions also decreased significantly at 1.0 and 1.25 MAC in both groups of patients (22 +/- 6% at 1.25 MAC halothane and 28 +/- 8% at 1.25 MAC isoflurane).(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1986

Ketamine and the arrhythmogenic dose of epinephrine in cats anesthetized with halothane and isoflurane.

Epinephrine-induced arrhythmias were studied in 4 cats (group A), using a 4 X 4 Latin square design. Each cat was anesthetized 4 times, 1 week apart, with halothane (1.5% end expired), isoflurane (2.0% end expired), and halothane or isoflurane preceded by ketamine administered IM (8.8 mg/kg). Lead II of the ECG and femoral artery pressure were recorded. Epinephrine was infused in progressively doubled rates (initial rate = 0.125 micrograms/kg/min) for a maximum of 2.5 minutes or until at least 4 ventricular premature depolarizations occurred within 15 s of each other. The arrhythmogenic dose of epinephrine (ADE; micrograms/kg) was calculated as the product of infusion rate and time to arrhythmia. The ADE (means +/- SD) during anesthesia with halothane alone and with ketamine-halothane anesthesia were 1.33 +/- 0.65 and 1.37 +/- 0.59 micrograms/kg, respectively; during anesthesia with isoflurane alone and ketamine-isoflurane anesthesia, the ADE were 9.34 +/- 1.29 and 16.16 +/- 3.63 micrograms/kg, respectively. The ADE was significantly greater (P less than 0.05) during isoflurane anesthesia and ketamine-isoflurane anesthesia than during halothane anesthesia. The percentages of change in systolic blood pressure (means +/- SD) at the ADE during halothane, ketamine-halothane, isoflurane, and ketamine-isoflurane were 31 +/- 34, 41 +/- 17, 127 +/- 27, and 148 +/- 57, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1987

Halothane hepatotoxicity in guinea pigs.

A recently reported animal model of halothane-associated hepatotoxicity in males of a colored strain of guinea pig was further characterized as to possible sex and strain specificity in outbred albino Amana, inbred albino Hartley, inbred colored strain 2, and inbred colored strain 13 guinea pigs. Exposure to 1% halothane for 4 hr in 21% O2 proved to be hepatotoxic in both sexes. Forty-eight hours after halothane exposure fatty vacuolization of hepatocytes was present in all animals. Histologically identifiable hepatic necrosis occurred in 60% of the guinea pigs exposed, along with concomitant increases in SGPT. Approximately one half of these responding animals had extensive centrilobular necrosis, which was still present 96 hr after halothane exposure. Females of the inbred strain 2 and males and females of strain 13 were the most susceptible to halothane-induced hepatic necrosis whereas the inbred Hartley strain was almost totally refractory to necrosis. Outbred Amana and male inbred strain 2 animals exhibited an intermediate hepatotoxic response. Comparison of the halothane-associated hepatic lesion with that induced by anoxic/ischemic mechanisms, (exposure to low (8%) oxygen during 1.7% enflurane anesthesia) showed obvious differences in the morphology of the hepatic necrosis and the apparent time course of lesion development. This guinea pig model of halothane-associated hepatotoxicity appears to be superior to previous animal models in that no pretreatment of the guinea pigs is required, both sexes are affected, and the resulting hepatic lesion is more persistent.

Animals↗
PubMed1986

Pulmonary macrophage mobilization in cigarette smoke-exposed mice after halothane anesthesia.

The effects of halothane anesthesia on pulmonary tissue and lung macrophage population were evaluated in normal and in C57BL/6 mice exposed to cigarette smoke twice daily for one year. Morphologic assessment of pulmonary tissue revealed no lung abnormalities that could be attributed solely to halothane anesthesia. However, in animals that were exposed to smoke and subsequently halothane anesthesia, airways cilia were shorter in stature and fewer in number. Disorientation of ciliary basal bodies was also observed. Airway macrophages in smoke-exposed animals subjected to halothane anesthesia were, for the most part, larger in size and contained more lysosomes and inclusions than phagocytes in airways of all other animals. Smoke inhalation alone caused a significant increase in number of lung parenchymal macrophages when compared to the number of these cells in sham-treated and control animals. However, the total macrophage population was significantly greater in lungs of smoke-exposed mice 48 hr after anesthesia than in lungs of smoke-exposed mice not subjected to halothane anesthesia and to those of sham-treated and control animals that were or were not exposed to the anesthetic. Airway macrophage numbers were significantly elevated in smoke-exposed mice 48 hr after halothane when compared to those of all other groups. Conversely, the number of parenchymal macrophages decreased in lungs of these mice. It was proposed that in smoke-exposed mice subjected to halothane anesthesia, ciliary function is impaired and phagocytes are mobilized from alveoli into the airways.

Animals↗
PubMed1985

Effect of halothane on rat liver adenylate cyclase: role of cytosol components.

Halothane, in a number of tissues, alters the activity of adenylate cyclase, the enzyme that catalyzes the formation of cyclic 3',5'-adenosine monophosphate, an important intracellular regulator. The present studies demonstrate that in rat liver whole homogenates, basal and glucagon-stimulated adenylate cyclase activity is increased by halothane. In isolated rat liver membranes, halothane does not increase basal activity and it decreases activity stimulated by glucagon. Suspension of membranes in the cytosol fraction restores the halothane-induced increase of basal and glucagon-stimulated activity. When cytosol denatured by trypsin or heat was used, the halothane-induced increase in glucagon-stimulated activity was lost, but the increase of basal activity was still observed. Suspension of membranes in albumin solution restored the effect of halothane on basal activity only. These results suggest that presence of heat-labile proteins in the cytosol fraction that modulate the halothane interaction with rat liver adenylate cyclase.

Adenylyl Cyclase Inhibitors↗
PubMed1985

Epinephrine-induced ventricular arrhythmias in dogs anesthetized with halothane: potentiation by thiamylal and thiopental.

Epinephrine-induced ventricular arrhythmias were studied in 8 dogs anesthetized at weekly intervals with halothane (1.09% end-tidal concentration) preceded by thiamylal or thiopental (20 mg/kg of body weight). Lead II, bundle of His and high right atrial electrograms, and femoral artery and airway pressures were recorded. Epinephrine was infused in logarithmically spaced increasing rates (initial rate = 0.25 micrograms/kg/min) for a maximum of 2.5 minutes. The maximal (greater than or equal to 4 ventricular premature depolarizations within 15 s of each other) and minimal (all other ventricular or junctional rhythms) arrhythmogenic doses were calculated (infusion rate X time to arrhythmia). The mean (+/- SD) minimal arrhythmogenic dosages for the thiamylal-halothane, thiopental-halothane, and halothane-only groups were 1.84 +/- 0.66, 1.83 +/- 0.64, and 3.69 +/- 1.32 micrograms/kg, respectively; the mean (+/- SD) maximal arrhythmogenic dosages were 2.32 +/- 0.77, 3.37 +/- 1.30, and 8.86 +/- 4.40 micrograms/kg, respectively, with no change after 4 hours of anesthesia. During infusion of the maximal arrhythmogenic dosages, the mean infusion of the maximal arrhythmogenic dosages, the mean percentage increase in serum K+ for thiamylal-halothane, thiopental-halothane, and halothane-only groups was 33 +/- 14%, 31 +/- 13%, and 38 +/- 18%, respectively.

Anesthesia, General↗
PubMed1985

Cerebral, renal, adrenal, intestinal, and pancreatic circulation in conscious ponies and during 1.0, 1.5, and 2.0 minimal alveolar concentrations of halothane-O2 anesthesia.

Blood flow to the brain, kidneys, adrenal glands, pancreas, and small intestine was studied in 8 healthy ponies while awake (control) and during 1.0, 1.5, and 2.0 minimal alveolar concentrations (MAC) of anesthesia produced, using halothane vaporized in oxygen. During the anesthesia steps, intermittent positive-pressure ventilation was used to ensure isocapnia. Organ blood flow was determined with 15-micron (diameter) radionuclide-labeled microspheres, after allowing 30 minutes of equilibration at each of the 3 preestablished end-tidal halothane concentrations. The sequence of 1.0, 1.5, and 2.0 MAC levels of anesthesia (0.90, 1.35, and 1.80% end-tidal halothane) was randomized for every animal. In the awake ponies, cerebral blood flow in the cortical (106 +/- 15 ml/min/100 g) and deep gray (103 +/- 12 ml/min/100 g) matter was approximately 5-fold of that in the white matter (22 +/- 3 ml/min/100 g). In the brain stem, there was a decreasing gradient of blood flow from the cranial (thalamohypothalamus: 65 +/- 8 ml/min/100 g) to caudal regions (medulla: 34 +/- 5 ml/min/100 g). Vasodilatation occurred in all regions of the brain with halothane-O2 anesthesia; the decrease in vascular resistance reached its nadir at 1.5 MAC. In the medulla and pons, blood flow increased above control values, with each of the 3 concentrations of halothane, but in the midbrain and thalamohypothalamus, it remained similar to the control value. In the cerebral white matter and cerebellum, blood flow increased with 1.0 and 1.5 MAC of halothane anesthesia, whereas mean aortic pressure decreased to 91% and 74% of the control value. Blood flow in the cerebral cortex was not different from the control value, even at 2.0 MAC of halothane, despite a 49% reduction in perfusion pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1979

Recovery rate of the cardiovascular system in rabbits following short-term halothane anesthesia.

Mean arterial pressure, cardiac output and heart rate were determined in eight male New Zealand white rabbits while conscious and after being anesthetized with halothane plus nitrous oxide for 15 minutes. Delivery of the anesthetic agent was stopped and the measurement repeated at 15, 30, 60 and 210 minutes. In a separate experiment blood samples were obtained for plasma renin activity in six rabbits before anesthesia, after 15 minutes of halothane plus nitrous oxide administration, and again 210 minutes after cessation of the anesthesia. Later, this experiment was repeated with the same rabbits except that they were allowed to breathe room air instead of the anesthesia. The halothane anesthesia resulted in decreased mean arterial pressure and cardiac output, but these returned to the preanesthetic levels by 15 minutes after stopping the anesthesia. Heart rate increased during halothane administration, and although it tended to return toward control levels after cessation of the halothane, heart rate was still elevated 210 minutes later. Halothane plus nitrous oxide produced an increase in plasma renin activity, which then subsided to normal by 210 minutes following anesthesia; breathing room air did not result in increases in plasma renin activity. These studies revealed that although short-term anesthesia with halothane plus nitrous oxide resulted in cardiovascular changes in rabbits, after cessation of the anesthetic agent the cardiovascular system quickly returned to normal.

Animals↗
PubMedDate not supplied

Effects of exposure concentrations on distribution of halothane metabolites in the body.

The effect of exposure concentration on halothane metabolism was studied in rats exposed to subanesthetic concentrations of halothane in air. Concentrations of halothane, total nonvolatile fluorine, and volatile metabolites (CF3CH2Cl and CF2 = CHCl) were determined in liver, kidneys, muscles, and brains excised at the end of a 3-hr exposure. It was observed that concentrations of all halothane metabolites in tissues rose less than exposure concentrations, that nonvolatile fluorine was present in all tissues in approximately the same concentrations, and that concentrations of volatile metabolites in liver were much higher than in any other tissues. A simulation model was used to support the following conclusions. Metabolism of halothane by all metabolic pathways is flow limited at small exposure concentrations and is capacity limited at high exposure concentrations. Volatile metabolites formed in livers are efficiently removed from circulation by pulmonary clearance, but trifluoroacetic acid is accumulated in the body. Halothane is most susceptible to biodegradation to trifluoroacetic acid, but this pathway is saturated at very small exposure concentrations. Susceptibility to biodegradation of volatile metabolites is small, but the pathways are not saturated even at anesthetic concentrations. The contribution of each of the three metabolites to total metabolic clearance depends on exposure concentrations. Trifluoroacetic acid was the major metabolite during exposure to small halothane concentrations; formation of more toxic, volatile metabolites increased during exposure to high concentrations. Postmortem formation of metabolites was studied in order to prevent its interference with tissue analysis. The method for determination of volatile metabolites is described.

Animals↗