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PubMed1987

Respiratory and cardiovascular effects of halothane, isoflurane and enflurane delivered via a Jackson-Rees breathing system in temperature controlled and uncontrolled rats.

We studied the respiratory and cardiovascular effects of 1.25 MAC halothane, isoflurane and enflurane in oxygen delivered via the Jackson-Rees breathing system in 10 rats. Mean arterial pressure, heart rate and respiratory rate were depressed significantly (P less than 0.05) in rats (n = 5) whose body temperature was not controlled after 2 hr of anesthesia regardless of the inhalational agent. Respiratory and metabolic acidosis developed. The respiratory and cardiovascular depression was most marked under enflurane anesthesia. In normothermic rats (n = 5) the initial cardiovascular depression stabilized after 30 min of halothane and isoflurane anesthesia. Moderate respiratory depression developed (PCO2 48.42 +/- 2.48 torr with halothane vs. 41.02 +/- 1.68 torr with isoflurane). Because the cardiovascular and respiratory changes caused by halothane and isoflurane were far less than changes produced by enflurane, halothane or isoflurane is preferable to enflurane for maintaining anesthesia in rats. Maintenance of constant temperature minimizes the cardiovascular and respiratory disturbances.

Anesthesia, Inhalation↗
PubMed1986

Halothane-cooling contractures of mammalian muscles.

Mouse soleus and extensor digitorum longus muscles exposed to halothane concentrations (0.3-2.0%) that, at room temperature, have no effect on either resting or twitch tension, develop transient contractures when cooled to 2-10 degrees C. The halothane-cooling contractures (HCC) are reproducible and their amplitudes can be graded by both the halothane concentration and the temperature of cooling. Under identical conditions the HCC is significantly larger in soleus as compared to extensor digitorum longus muscles. The maximal HCC in soleus muscles (1-2% halothane, 2 degrees C) reaches 42% of the tetanic tension recorded at 24 degrees C; in extensor digitorum longus the maximum is 12% of tetanic tension. This difference is ascribed to the predominance of slow-twitch fibers in the soleus muscle. Neither membrane depolarization with high [K]0 solutions nor a short (2 min) exposure to Ca-free media inhibits the HCC. The contractures are depressed, however, when the muscles are preequilibrated for 30 min with Ca-free solutions; under these conditions, the muscle twitches and the caffeine-cooling contractures are also depressed. These effects are ascribed to partial depletion of the Ca content of the sarcoplasmic reticulum. The HCC is abolished by 4 mM procaine, partially inhibited by 4 to 10 mM procainamide and potentiated by 4 mM lidocaine, but it is not significantly affected by dantrolene (40 microM). It is proposed that the HCC results from synergistic interaction of halothane and low temperature inhibiting Ca-sequestration by the sarcoplasmic reticulum of the muscle fibers.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics, Local↗
PubMed1986

Oxygen concentrations required for reductive defluorination of halothane by rat hepatic microsomes.

The free oxygen concentrations required for reductive defluorination of halothane by rat hepatic microsomes from control and phenobarbital- (PB) and polychlorinated biphenyl-(PCB) treated animals were determined. Halothane-exposed microsomes from treated rats generated measurable levels of fluoride ion after 30 min incubations with oxygen concentrations of 5% or less. Microsomes from control animals produced fluoride only if the free oxygen concentration was 2% or less. During anoxic (0% oxygen) incubations, defluorination rates of 2.10 +/- 0.17, 5.55 +/- 0.38, and 5.46 +/- 0.30 nmol fluoride X mg protein-1 X 30 min-1 were observed for microsomes from control, PB, and PCB rats, respectively. Normalizing the maximal rates of defluorination to the microsomal cytochrome P-450 content yielded values of 5.14 +/- 1.40, 3.70 +/- 0.15, and 2.38 +/- 0.26 nmol fluoride X nmol cytochrome P-450-1 X 30 min-1 for control, PB, and PCB microsomes, respectively. Oxygen concentrations required for reductive metabolism of halothane by isolated rat hepatic microsomes are close to normal physiologic free oxygen concentrations of 4-5% reported for centrilobular areas of the rat liver. Thus even slight reductions in hepatic oxygenation during anesthetic exposure could lead to enhanced reductive biotransformation, an observation found in rat models of halothane-associated hepatic injury. The large differences among the treatment groups in the rates of fluoride ion generated per nanomole cytochrome P-450 indicate that enzyme induction regimens disproportionately increase those isozymes of hepatic cytochrome P-450 that are not involved with the reductive defluorination of halothane.

Animals↗
PubMed1986

[Effects of halothane on sensory evoked potentials].

Intraoperative monitoring of central nervous system functions is useful for safe neurosurgical operations. For such a purpose, some kinds of sensory evoked potentials play significant roles, but their reliability during general anesthesia have not yet been established. The authors conducted experimental and clinical studies to reveal effects of halothane, a most popular anesthetic, on sensory evoked potentials. Eight adult cats, weighing 2.8-4.0 kg, were induced to anesthesia with thiopental and ether, and after tracheostomy and venous cannulation, they were immobilized with succinylcholine and artificially ventilated with mixture of oxygen, nitrous oxide halothane. The concentration of halothane was increased up to 4.0% by 0.5% steps. The body temperature, systemic blood pressure and carbon dioxide concentrations in expires gas were monitored continuously, and maintained within normal ranges as much as possible. The hypotension induced by halothane was easily corrected by dopamine infusion initially, but later became difficult to be controlled as the halothane concentration increased. In each concentration, short latency somatosensory evoked potentials by median nerve stimulations (SL-SEP), and brain stem auditory evoked potentials (BAEP) were recorded. Active electrode was placed on the bregma, and reference electrodes were placed on a hindlimb for SL-SEP, on the tongue for BAEP recordings. Peak amplitudes of SL-SEP were gradually decreased and finally disappeared without apparent dose dependency. Relatively the peaks with longer latencies were more affected than those with shorter latency such as P1 and N1. In BAEP, decrement of the amplitude was apparent in the peaks with longer latencies with an obvious dose dependency.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed1986

Genetic predisposition to liver damage after halothane anesthesia in guinea pigs.

Three 4-hr normoxic (21% oxygen) exposures to 1% halothane administered 3 days apart were associated with elevations in serum alanine aminotransferase (ALT) activity in four of 20 guinea pigs after the initial and third exposures. Serum alanine aminotransferase values were not measured after the second anesthetic. Susceptibility was defined as an ALT level greater than 300 IU/L after halothane. Nonsusceptible animals, that is, animals without significant increases in ALT values after halothane, remained nonsusceptible after reexposure. Serum alanine aminotransferase values after the first and third anesthesias were significantly correlated (rs = 0.86, P less than 0.001). Two exposures of another 30 guinea pigs at a 5-week interval resulted in high elevations of ALT in the same eight animals after both anesthetics. In contrast, after an initial exposure nonsusceptible animals remained nonsusceptible upon reexposure. Serum alanine aminotransferase levels after the first and second anesthetics were significantly correlated (rs = 0.85, P less than 0.001). The proportion of first generation (F1) males with elevated ALTs whose parents were susceptible to halothane hepatotoxicity (HH) was significantly higher than the proportion of males with elevated ALTs in a random group of 90 males (P less than 0.005). First generation males and females of nonsusceptible parents had ALTs within the normal range after halothane exposure. These studies suggest that in the guinea pig genetic predisposition is an important determinant of susceptibility to HH, although other contributing factors are not excluded.

Alanine Transaminase↗
PubMed1986

[Comparative echocardiographic studies on the negative inotropic effect of halothane, enflurane and isoflurane].

Using the afterload-independent end-systolic pressure-dimension-relationship a study was performed in order to investigate whether there are differences in the negative inotropic effects of halothane, enflurane and isoflurane at 1 MAC in 70% N2O. 30 patients of ASA-groups I and II were studied. Using transoesophageal 2d- and m-mode echocardiography the end-systolic-pressure-dimension-relationship was established and the slope (parameter of contractility) determined. The slope decreased significantly (paired Wilcoxon-test 2 alpha less than 0.01) with halothane (68.5/46.5 mmHg/cm), enflurane (56/48 mm Hg/cm) and isoflurane (63/35 mmHg/cm). There is no difference between the three groups (Kruskal-Wallis-test 2 alpha greater than 0.05). The negative inotropic effects of halothane, enflurane and isoflurane at 1 MAC in 70% N2O are the same. The vasodilation caused by isoflurane enables better pump function compared to halothane and enflurane, but may cause severe hypotension. We conclude that for cardiac risk patients isoflurane has no outstanding advantages in comparison to halothane and enflurane.

Adult↗
PubMed1985

Choline uptake, acetylcholine synthesis and release, and halothane effects in synaptosomes.

Synaptosomes isolated from rat cerebra were used as a model to study the effects of halothane on choline uptake and acetylcholine synthesis and release processes. Synaptosomes are membrane-bound particles that are formed by gentle disruption of brain tissue. These particles include the presynapse, cleft, portions of postsynaptic membrane, and all other components contained in brain nerve terminals necessary for neurotransmitter synthesis, storage, and release. Halothane (3% in air, vol/vol) caused a "competitive-like" inhibition of choline uptake in synaptosomes but had no effect on the enzymatic activity of choline acetyl-transferase (ChAT). Three percent halothane depressed synaptosomal acetylcholine (ACh) synthesis by 86% while ACh release from synaptosomes was inhibited 50%. It is suggested that halothane inhibits ACh synthesis by directly interfering with the carrier-mediated transport system of choline. Since halothane also inhibits ACh release, as well as choline uptake, it is probable that the anesthetic is acting upon more than one site in these cholinergic nerve terminals. These data require an interpretive evaluation that cannot fit the "unitary" hypothesis as the mechanism of action of general anesthetics.

Acetylcholine↗
PubMed1985

Hormonal and hemodynamic responses to halothane and enflurane in spontaneously hypertensive rats.

Forty-two spontaneously hypertensive rats (SHR) and 42 normotensive Wistar-Kyoto rats (WKY) were anesthetized with either halothane or enflurane. Blood pressure, heart rate, cardiac output, distribution of blood flow, plasma renin activity, and plasma catecholamines were measured to determine in what manner the hypertensive animal responded to these two anesthetics. Major findings of the study were that plasma renin activity did not increase in the SHR despite a 25% reduction in MAP. The infusion of saralasin, an angiotensin II antagonist, resulted in a further decrease in blood pressure in SHR anesthetized with halothane but not with enflurane. Plasma catecholamine concentrations were elevated in the awake SHR and were decreased in SHR anesthetized with enflurane. Both halothane and enflurane anesthesia resulted in similar alterations in blood flow in the SHR. The normotensive WKY responded to halothane and enflurane in a different manner than the SHR. Plasma renin activity increased with the decrease in blood pressure with both agents. A further decrease in blood pressure occurred with saralasin infusion in WKY anesthetized with halothane or enflurane. Significant blood flow alterations occurred in the WKY anesthetized with both agents, but enflurane caused the greatest changes. The SHR may prove useful in examining the effects of anesthetic agents and other drugs so that we may have a better understanding of the perioperative management of the patients with essential hypertension.

Anesthesia, Inhalation↗
PubMed1985

Effect of halothane-oxygen anesthesia on the pharmacokinetics of diazepam and its metabolites in rats.

Inhalation anesthetics have been shown to substantially diminish the clearance of several drugs eliminated by hepatic routes. The purpose of the present study was to determine the influence of halothane-oxygen anesthesia on the hepatic metabolism of diazepam and its proximate metabolites in anesthetized rats whose physiologic status was monitored and maintained. The portal vein, femoral artery and bile duct of male Sprague-Dawley rats 370 to 395 g, were cannulated under pentobarbital anesthesia. After a 2-hr recovery period, [14C]diazepam was administered in to the portal vein as a 0.25-mg/kg bolus followed immediately by a 0.25-mg/kg/hr infusion by the same route. After the attainment of steady state, the halothane group (seven rats) received 1% halothane in oxygen whereas the control group (six rats) continued to breathe room air. The diazepam infusion was maintained for an additional 3 hr. Concentrations of diazepam, N-desmethyldiazepam, 4-hydroxyphenyldiazepam and 3-hydroxydiazepam were determined in plasma; these metabolites as well as oxazepam and N-desmethyl-4-hydroxyphenyldiazepam were also determined in bile. Radioactivity in bile was approximately 98% conjugated; radioactivity in plasma was approximately 30% conjugated. Halothane anesthesia caused an increase in the concentrations of diazepam and its metabolites in plasma, but the steady-state ratios of the concentration of the individual metabolites in plasma to diazepam concentration were not changed. The intrinsic clearance of diazepam was decreased by 42%, P less than .01, and the ratio of formation to elimination clearance of the metabolites measured in plasma was not changed. Halothane anesthesia also decreased the excretion rate of 14C into bile.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1985

Nitrous oxide does not hinder the repair of halothane-induced hepatic injury in the rat.

Nitrous oxide administration may limit DNA synthesis by inactivating methionine synthetase, and may thus hamper the repair of an injured organ such as the liver. To test this possibility, we pretreated rats with phenobarbital and exposed them to 0.3 MAC halothane in 9% oxygen for 46 min, followed immediately and again 24 hr later by 70% nitrous oxide (0.25 MAC) at an FIO2 of 0.30 for 2 hr. The results from this group were compared with an anesthetic control group in which 0.35% isoflurane (0.25 MAC) was substituted for the nitrous oxide. Additional groups were given a third exposure to nitrous oxide or isoflurane 48 hr after the halothane exposure. All rats were killed 24 hr after their last anesthetic exposure. A second (nonanesthetic) control group of phenobarbital-pretreated rats received 0.3 MAC halothane in 9% oxygen for 46 min and no anesthetic thereafter. They were killed 24, 48, or 72 hr later. Histologic changes in the livers of rats did not differ among the groups given nitrous oxide, isoflurane, or no additional anesthetic after exposure to halothane alone. Thus neither nitrous oxide nor isoflurane appears to hinder the repair of hepatic injury produced by halothane in the hypoxic rat model.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1985

Halothane effects on subendocardial oxygen supply-demand balance: estimation from intramyocardial tissue pressure and left ventricular pressure.

We evaluated the effect of halothane on the balance of subendocardial oxygen supply and demand in six dogs by estimating the endocardial viability ratio (EVR) based on the pressure generated within the subendocardium (ENDO-IMP). Concurrently, the conventional EVR based on left ventricular pressure (LVP) was estimated and compared with the EVR based on ENDO-IMP. The subendocardial oxygen supply-demand ratio based on ENDO-IMP (IMP-EVR) was significantly less than EVR based on LVP (LVP-EVR) (0.87 +/- 0.03 vs 1.07 +/- 0.06, P less than 0.05) during the control period. With 0.5% halothane administration, IMP-EVR improved significantly (1.04 +/- 0.07, P less than 0.05) while LVP-EVR remained unchanged (1.08 +/- 0.09). No further changes in EVR (either IMP-EVR or LVP-EVR) were observed with increasing halothane concentrations up to 2%. The relationship between the two indices was weak (r2 = 0.44, P less than 0.001) but statistically significant. Because an estimate of EVR based on direct measurement of subendocardial tissue pressure (IMP-EVR) would reflect more accurately the oxygen supply-demand balance of this region than the LVP-EVR, our results suggest that the oxygen balance of the subendocardium improves with halothane administration. The use of LVP-EVR as a hemodynamic index of subendocardial oxygen balance during halothane anesthesia, therefore, is questionable.

Anesthesia↗
PubMed1979

[Halothane-pentazocine interaction in dogs (author's transl)].

It is known that narcotics reduce the alveolar concentration of inhalation anesthetics in man and animals. However the magnitude and duration of narcotic effect on inhalation anesthesia is not known. Accordingly, I determined in dogs the temporal effect of various doses of pentazocine, a commonly used anesthetic adjuvant, on the minimum alveolar concentration (MAC) of halothane. In addition, I compared plasma pentazocine concentrations in dogs both awake and during halothane anesthesia using an identical intramuscular dose of pentazocine. Intramuscular injection of pentazocine, group II (2.5 mg/kg), group III (5 mg/kg), group IV (10 mg/kg) reduced MAC of halothane required for anesthesia. The magnitude of MAC depression were 19.3% of control halothane MAC in group II, 36.4% of control in group III and 41.7% of control in group IV. Postinjection plasma concentration was fitted by computer with a 2-compartment open pharmacokinetic model. Plasma pentazocine concentration for awake (group I) and anesthetized (group II) dogs given the same dose (2.5 mg/kg) did not differ significantly on biological half-life, total apparent volume of distribution and body clearance. Halothane minimum alveolar concentration (MAC) was correlated to plasma pentazocine concentration (r= -0.60) and cerebrospinal fluid pentazocine concentration (r= -0.74).

Anesthesia↗
PubMedDate not supplied

Electroencephalographic abnormalities following halothane anesthesia.

In 7 subjects, serial EEGs, serum bromide determinations, and psychological tests were done prior to and following 13.83 +/- 0.74 (SEM) MAC-hours of halothane anesthesia. Significant psychological impairment demonstrated 2 days following anesthesia in these subjects was absent 2 weeks following exposure to halothane. Nonspecific postanesthetic slowing of the EEG was found, qualitatively similar to but more marked than that following exposure to enflurane. Generalized EEG slowing, with a tendency toward posterior delta activity and significant reduction of frequency and amplitude of the alpha rhythm, persisted for 6 to 8 days following anesthesia. Rare sharp-wave activity developed in 3 subjects in the 1st week after halothane. A potentially psychoactive postanesthetic serum bromide level of 2.97 +/- 0.17 mEq/L (SEM) was found 5 days following anesthesia. Electroencephalographic changes characteristic of mild bromide intoxication were absent, suggesting that the psychological impairment noted after halothane anesthesia is probably not due to this metabolite; these psychological changes are probably due instead to persistence in the circulation of unchanged halothane.

Adult↗
PubMedDate not supplied

Impairment of tracheal ring ciliary activity by halothane.

The effects of varying concentrations of halothane on tracheal ciliary activity were studied using a ferret tracheal organ culture technique. Using 1% and 2% halothane produced no impairment of ciliary activity, while 3% halothane caused some ciliostasis; 4% and 5% halothane produced rapid cessation of ciliary activity. Recovery was prompt and complete after exposure to 4% halothane for as long as 3 days, but after 4 days of exposure recovery was incomplete and after a week of exposure death of ciliary cells occurred.

Anesthesia, Inhalation↗
PubMed1978

Metabolism of halothane after its repeated administration in man.

Metabolism of halothane following its repeated administration, was studied in three patients by estimating the blood bromide concentrations before, during and after halothane anaesthesia. In one patient, the blood halothane concentration was measured during and after its administration. The fraction of halothane metabolised was found to be increased after its repeated administration. This was proved by the rapid clearance of halothane and the increased blood bromide concentration.

Anesthesia, General↗
PubMed1982

Reduction in halothane anesthetic requirement by clonidine, an alpha-adrenergic agonist.

The effects of clonidine, a potent central alpha-adrenergic agonist, and of tolazoline, an alpha-adrenergic antagonist, on the minimal anesthetic concentration (MAC) of halothane were studied in male mongrel dogs. Control halothane MAC was 0.8 +/- 0.04 vol% (determined in each dog by gas chromatography of arterial blood, n = 30). Clonidine, 5 microgram/kg (n = 10) and 20 microgram/kg (n = 10), give slowly intravenously, maximally reduced MAC by 42% (at 2.3 hours after clonidine) and 48% (at 2.6 hours after clonidine) for each dose. In another set of animals (n = 5) an alpha-adrenergic antagonist, tolazoline, 5 mg/kg IV, reversed the clonidine-induced reduction in halothane MAC rapidly and completely. Tolazoline alone, 5 mg/kg, (n = 5) had no significant effect on halothane MAC. Thus, the administration of the central alpha-adrenergic agonist clonidine decreased the required anesthetic concentration of halothane, as defined by MAC, by almost half. This effect, as it is reversed by tolazoline, is likely to be mediated through a central alpha-adrenergic receptor mechanism.

Adrenergic alpha-Agonists↗
PubMed1984

Renovascular hypertension: effect of halothane and enflurane.

Male Wistar rats were anesthetized at 6 weeks of age and a silver clip placed around the renal artery to produce renovascular hypertension. The rats were allowed to grow on a normal sodium diet for the next 6-9 weeks. Using diethyl ether anesthesia, arterial and venous cannulae were placed and the animals allowed to awaken in restraining cages. The group of rats was divided into three groups: awake (n = 7), halothane 1.3 vol% (n = 9), and enflurane 2.2 vol% (n = 8). The protocol consisted of a 1-h control awake period, 1 h of stable anesthesia (one group received no anesthesia), and 30-min iv infusion of saralasin, a competitive inhibitor of angiotensin II. Plasma renin activity (PRA) and plasma catecholamines were measured after 1 h of stable anesthesia and after the saralasin infusion. In additional rats treated identically, radiolabelled microspheres were used to measure cardiac output and regional blood flows during halothane (n = 7) or enflurane (n = 6) anesthesia. Principal responses were as follows: mean arterial pressure (MAP) was 193 +/- 4 mmHg awake and decreased to 114 +/- 3 mmHg and 135 +/- 3 mmHg with halothane and enflurane, respectively. Saralasin decreased MAP in the awake group to 176 +/- 3 mmHg and to 69 +/- 3 mmHg and 96 +/- 5 mmHg with halothane and enflurane, respectively. PRA in the awake rats was 7.24 +/- 1.3 ng X ml-1 X h-1. PRA increased with halothane but decreased with enflurane. Plasma catecholamines were decreased markedly by saralasin and by both anesthetic agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1984

Effects of halothane anesthesia on equine liver function.

Effects of halothane anesthesia were investigated in ponies prepared surgically with chronic external biliary fistulas (T tubes) to determine the effects on liver function and biliary excretion during 2 hours of anesthesia. Four studies were performed on 2 ponies, 2 to 6 months after surgery with the enterohepatic circulation held intact between studies. Intravenous bile acid infusion was used to maintain steady-state bile flow, bilirubin, and bile acid excretion during each study. Compared with the immediate 2-hour preanesthesia values (base line), halothane caused a 138% increase in bilirubin excretion, a 60% increase in biliary bilirubin concentration, and a 43% increase in PCV. Halothane anesthesia also caused a 16% reduction in plasma bilirubin, a 46% reduction in biliary bile acid concentration, and a 27% reduction in bile acid excretion. The bile acid independent fraction of bile flow appeared to increase. Plasma aspartate transaminase concentration did not change during anesthesia. The ratio of conjugated bilirubin fractions in bile [82% to 83% disconjugates of glucuronide and glucoside (2 forms) and 17% to 18% monoconjugates of glucoside, glucuronide, and xyloside] did not change during anesthesia and less than 1% was excreted unconjugated. Halothane anesthesia did not appear to affect adversely the activity of the transferase-conjugating enzymes in the presence of an increased bilirubin load. Seemingly, greatly increased conjugated bilirubin excretion observed during halothane anesthesia was most likely the result of a combination of increased hepatic clearance from plasma and increased hepatic bilirubin production from turnover of free hepatic heme or heme from the induced cytochrome P-450 system.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗