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PubMed1990

[Halothane hepatitis in the differential diagnosis of postoperative jaundice].

Based on a case report the necessity of including halothane hepatitis in differential diagnosis of postoperative jaundice is described. Even in this case report, the diagnosis is a synopsis of the case history, clinical and biochemical findings and exclusion of other causes of disease. The detection of antibodies to halothane-altered hepatocyte components is at present only possible in a few special laboratories and does not succeed in all cases. Confirmation of the connection between halothane exposure and liver damage is of vital importance for the patient because a second exposure to halothane may result in fulminant hepatic failure. In choosing the appropriate anaesthetic method, other halothane anaesthesias carried out a short time ago should be considered.

Chemical and Drug Induced Liver Injury↗
PubMed1990

[Hemo- and cardiodynamic action of halothane or isoflurane following peroral long-term pretreatment with nifedipine. An animal experimental study].

This study investigated the influence of chronic oral nifedipine on the hemodynamic effects of halothane or isoflurane anesthesia in dogs. Under general anesthesia with fentanyl 0.3 microgram/kg/min i.v. and 3:1 N2O/O2 inhalation mixture a left thoracotomy was performed and two needle force probes were placed in the left ventricular wall to measure myocardial force of contraction. In the halothane group (n = 12) a Hall-effect sensor was placed on the anterior surface of the left ventricle, which in combination with a magnet on the posterior surface allowed measurements of left ventricular diameter. In the isoflurane group (n = 15) a Widney gauge was placed around the left ventricle to measure left ventricular circumference changes. The dogs were also monitored with left ventricular tip manometers, pulmonary arterial thermodilution catheters, and femoral arterial and venous catheters. Prior to surgery, in the halothane group 6 dogs were pretreated with nifedipine 6 mg/kg p.o. for 10 days; the other 6 served as controls. In the isoflurane group, 8 dogs were pretreated with nifedipine in the same way and 7 served as controls. Three hours after instrumentation baseline hemodynamic measurements were performed and repeated 15 min after adding 1 MAC and then 2 MAC halothane or isoflurane. Oral pretreatment with nifedipine caused vasodilation with a significant decrease in systemic vascular resistance (SVR) and mean arterial pressure (MAP); heart rate (HR) and dp/dt max were unchanged in comparison to the control group. The cardiac output (CO) increased. Halothane (1 MAC/2 MAC) had a dose-related circulatory depressant effect. This occurred to the same extent in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1990

[Difference in the effect of halothane on regional oxygen demand-supply relationship depending on the severity of coronary artery stenosis].

We examined the effect of halothane on myocardial oxygen balance and hemodynamics in three groups of canine heart. We measured regional subendocardial oxygen tension before and after 30 minute inhalation of 0.8% and 1.5% halothane in the mixture of nitrogen and oxygen (FIO2 not equal to 0.5). In moderate and severe stenosis group, left circumflex coronary artery flow was reduced to 66% and 31% respectively, at buprenorphine-anesthetized basal condition. In occlusion group, left circumflex coronary artery was ligated at its origin. Both concentrations of halothane decreased heart rate, aortic pressure and LV dp/dt max in all groups. Subendocardial oxygen tension increased in moderate stenosis group. But it was unchanged in severe stenosis group, and it rather decreased in occlusion group with 1.5% halothane inhalation. Halothane might improve endocardial oxygen demand-supply relation in the myocardium with mild to moderate coronary stenosis, while it will possibly deteriorate endocardial oxygen demand-supply balance in ischemic myocardium after coronary artery occlusion.

Animals↗
PubMed1990

Effects of the calcium antagonist, TMB-8 on halothane and on caffeine contractures of malignant hyperthermia susceptible skeletal muscle.

This investigation sought to determine if the Ca2+ antagonist, TMB-8, alters the contracture responses of malignant hyperthermia susceptible (MHS) skeletal muscle to halothane and to caffeine. Muscle fiber bundles were excised from both MHS and normal pigs and exposed to TMB-8 (100 microM), halothane (3%) and caffeine (0.5-8.0 mM), administered alone and in combination. TMB-8 depressed tension developed during isometric twitches in both MHS and normal muscle but had no effect on resting tension (RT). Halothane, however, increased RT in MHS but not in normal muscle. TMB-8 failed to reduce the halothane contracture of MHS muscle but hastened its onset. Caffeine concentrations of greater than or equal to 2 mM increased RT in MHS whereas only 8 mM evoked contracture of normal muscle. These effects were also unaltered by TMB-8. Results suggest that TMB-8 does not inhibit halothane nor caffeine contractures of MHS muscle.

Animals↗
PubMed1989

The effects of vasoactive drugs on halothane inhibition of contractions of rat mesenteric lymphatics.

The effects of halothane on alpha-adrenergic receptors, beta-adrenergic receptors, and the process of Ca++ dependent contractions on rat mesenteric lymphatics were examined. Halothane depressed the contraction rate of mesenteric lymphatics but did not effect the increase in lymphatic contraction rate caused by noradrenaline (an alpha-agonist). The depressant effect of halothane on the contraction rate was also not antagonized by propranolol (a beta-blocker), but was partly reversed by CaCl2. These findings suggest that the depressant effect of halothane on the lymphatic contraction rate derives not from blocking lymphatic alpha-receptors or stimulating lymphatic beta-receptors but rather by halothane inhibition on the process of Ca++ dependent lymphatic contractions.

Animals↗
PubMed1989

Dexmedetomidine decreases halothane anesthetic requirements in rats.

alpha 2-Adrenergic agonists, such as clonidine, reduce the dose requirements for halothane. Medetomidine is more selective as a full agonist for central alpha 2-adrenoceptors than clonidine and is available as both an active (d) and an inactive (l) isomer. We have used the d-isomer to probe the mediating mechanism for the MAC-sparing effect of this alpha 2-agonist in rats. The dose of halothane which rendered 50% of animals insensitive to a painful stimulus (halothane MAC) was determined in rats (150-200 g) before and after d- or l-medetomidine, 10, 30 and 100 micrograms/kg or saline i.p. To determine whether alpha 2-adrenoreceptors mediated the MAC-sparing effect of dexmedetomidine (d-medetomidine), cohorts of rats (n = 6 for each dose) were pretreated with idazoxan, 10 mg/kg i.p., the highly selective alpha 2-antagonist. To determine whether dexmedetomidine's MAC-reducing action was mediated in part through either opiate or adenosine receptors, groups of rats were pretreated with either naltrexone, 5 mg/kg i.p., an opiate antagonist; or 8-phenyltheophylline (8-PT), 2.5 mg/kg i.p., an A1 adenosine antagonist. To determine whether postsynaptic mechanisms mediate the anesthetic-sparing effect of dexmedetomidine, rats were depleted of central norepinephrine stores with 6-OHDA and 4 days later MAC was determined before and after each dose of dexmedetomidine. Dexmedetomidine dose-dependently decreased MAC for halothane such that at the highest dose, halothane could be discontinued for up to 30 min without eliciting a response to tail-clamping. Idazoxan completely prevented the MAC-reducing action of dexmedetomidine, while naltrexone and 8-PT were without effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Adjuvants, Anesthesia↗
PubMed1989

Effects of halothane and isoflurane on baroreflex sensitivity in horses.

Baroreflex sensitivity (BS) was used to quantitatively assess the effects of halothane and isoflurane on the heart rate/arterial pressure relationship during steady-state (10 minutes) and dynamic pressure changes in adult horses. Arterial pressure was decreased in response to nitroglycerin or sodium nitroprusside and increased in response to phenylephrine HCl. Mean (+/- SEM) BS in awake horses was 28.9 +/- 2.6 and 13.2 +/- 2.0 ms/mm of Hg during steady-state decreases and increases in systolic arterial pressure (SAP), respectively. Halothane and isoflurane either significantly (P less than 0.05) decreased or eliminated BS during steady-state decreases in SAP, with no significant differences detected between anesthetic agents. During steady-state decreases in SAP, significant (P less than 0.05) correlation between R-R interval and arterial pressure was not observed for 6 of 10 and 4 of 11 halothane and isoflurane anesthesia periods, respectively. Halothane significantly (P less than 0.05) decreased BS during steady-state increases in SAP to 7.9 +/- 0.6 and 6.5 +/- 1.1 ms/mm of Hg during low and high minimal alveolar concentration (MAC) multiples, respectively. Isoflurane decreased BS during steady-state increases in SAP to 9.6 +/- 1.5 and 6.6 +/- 1.1 ms/mm of Hg during low and high MAC anesthesia, respectively, with high MAC of isoflurane decreasing BS significantly (P less than 0.05), compared with awake and low MAC values. Plasma catecholamine (epinephrine and norepinephrine) concentrations increased significantly (P less than 0.05), compared with baseline values during steady-state vasodilator infusions in halothane- and isoflurane-anesthetized horses.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Inhibitory effect of paraquat on biotransformation of halothane in rabbit liver microsomes.

Microsomal fractions were prepared from the liver of rabbits to investigate the effects of paraquat (methyl viologen) on generation of metabolites of halothane under the optimal aerobic and anaerobic conditions. Halothane (CF3CHClBr) is known to undergo oxidative and reductive biotransformation in the hepatic mixed function oxidase system including cytochrome-P450 reductase and cytochrome P450. The results showed that paraquat inhibited generation of metabolites of halothane under these conditions. Generation of the aerobic metabolite, trifluoroacetic acid (CF3COOH), and anaerobic metabolites, 2-chloro-1, 1, 1-trifluoroethane (CF3CH2Cl) and 2-chloro-1, 1-difluoroethylene (CF2CHCl), were inhibited 50% by 4.96 mM and 35.3 mM paraquat, respectively. Possible mechanisms were speculated on to account for the inhibitory effects: one being the impaired formation of halothane-cytochrome P450 complex by addition of paraquat, and the other the diversion of electrons from cytochrome-P-450 reductase to generate active paraquat radicals. It is concluded that paraquat inhibits NADPH-dependent biotransformation of halothane catalyzed in mixed function oxidase system.

Animals↗
PubMed1989

[Protective effects of ulinastatin on hepatic oxygen metabolism during halothane anesthesia in the presence of graded hypoxic hypoxemia].

Hepatic oxygen metabolism and the hepatic energy charge were assessed in mongrel dogs receiving 40,000 U.kg-1 of ulinastatin intra-portally during 2 MAC halothane anesthesia combined with graded hypoxic hypoxemia (21-6% oxygen) for the purpose of evaluating the role of ulinastatin in protecting the liver against the deprivation of the hepatic energy charge resulting in halothane-induced hepatotoxicity. Hepatic blood flow was measured using electromagnetic flowmetry; hepatic oxygen delivery and consumption were calculated from measured hepatic blood flow and oxygen content in hepatic arterial, portal venous and hepatic venous blood. In the animals who received ulinastatin during halothane anesthesia (the UST group), nine out of ten survived even at 8% oxygen, whereas six out of eight died in the halothane-alone group. There was no significant difference in total hepatic blood flow between the two groups. PaO2 was higher in the UST group than the halothane-alone group at 15 and 12% oxygen. Therefore hepatic oxygen delivery was significantly higher in the UST group at 15 and 12% oxygen. Hepatic oxygen consumption and the delivery/consumption ratio were also higher in the UST group at the various inspired oxygen levels. The arterial ketone body ratio, which indicates the mitochondrial energy charge level, significantly decreased with the progress of hypoxia in both groups, but it was significantly higher in the UST group at 8% oxygen.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1989

Cerebral blood flow and metabolism in patients undergoing anesthesia for carotid endarterectomy. A comparison of isoflurane, halothane, and fentanyl.

The effects of isoflurane, halothane, and fentanyl on cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) during anesthesia prior to carotid endarterectomy were compared using the intravenous method of 133-Xenon CBF determination. Patients, mean (+/- SE) age 68 +/- 2, received either isoflurane (N = 16), 0.75% in O2 and N2O, 50:50; halothane (N = 11), 0.5% in O2 and N2O, 50:50; or fentanyl (N = 10), 5-6 micrograms/kg bolus and then 1-2 micrograms.kg-1.h-1 infusion in addition to O2 and N2O, 40:60. Measurements were made immediately before carotid occlusion. Mean (+/- SE) CBF (ml.100 g-1.min-1) was 23.9 +/- 2.1 for isoflurane, 33.8 +/- 4.8 for halothane, and 19.3 +/- 2.4 for fentanyl. CMRO2 (ml.100 g-1.min-1) was available from 22 patients and was 1.51 +/- 0.28 for isoflurane (N = 7), 1.45 +/- 0.24 for halothane (N = 6), and 1.49 +/- 0.21 for fentanyl (N = 9). Although CBF was greater during halothane than during isoflurane or fentanyl anesthesia (p less than 0.05), there were no demonstrable differences in CMRO2 among the 3 agents. We conclude that choice of anesthetic agent for cerebrovascular surgery with comparable anesthetic regimens should not be made on the basis of "metabolic suppression." During relatively light levels of anesthesia, vasoactive properties of anesthetics are more important than cerebral metabolic depression with respect to effects on the cerebral circulation.

Aged↗
PubMed1989

Comparative effects of halothane and isoflurane anesthesia on the ultrastructure of human hepatic cells.

The effects of halothane and isoflurane on the ultrastructure of the liver cells in adult patients with normal liver-function tests were compared. After induction of anesthesia with thiopental, fentanyl, and pancuronium, 18 patients were randomly divided into three groups of six each. Anesthesia was maintained with droperidol (droperidol group), with halothane (1.7 MAC, halothane group), or with isoflurane (1.7 MAC, isoflurane group). During the surgical procedure, 1 hr after the induction, a liver biopsy was performed in each patient and processed for light and electron microscopy. All biopsies were normal on light microscopy. On electron microscopy, no mitochondrial abnormalities were found. In all three groups, irregular nuclear membranes, dilation of the rough endoplasmic reticulum, and vesiculation of the smooth endoplasmic reticulum were seen, without any significant differences between the groups. There were significantly more lysosomes in the hepatocytes of patients receiving halothane than in the hepatocytes of patients receiving isoflurane or droperidol. This study shows that halothane can induce ultrastructure abnormalities very early after the beginning of its administration while, under the same conditions, isoflurane does not.

Adult↗
PubMed1989

[A case of fulminant hepatitis after reexposure to halothane six years later].

We reported a case of halothane-induced fulminant hepatitis with acute renal failure which developed 6 days after reexposure to halothane. The patient was a 58-year-old female. She had a history of liver dysfunction after exposure to halothane 6 years previously. She had surgical treatment of clubfoot under halothane anesthesia in other hospital. Preoperative physical examination and laboratory data were normal. On the 6th post-operative day she abruptly developed high fever and general fatigue. Next day, she was transferred to our hospital. At admission, fulminant hepatitis complicated with acute renal failure was diagnosed with severe liver and renal damage. She was immediately treated with plasma exchange, glucose-insulin therapy, and hemodialysis. Serum transaminase level returned to normal value within a week. However, despite repeated hemodialysis, renal function did not improve, and she died of P. aeruginosa sepsis on 28th day after the operation. It may be suggested that in this patient hypersensitivity to halothane has persisted during the six years.

Acute Kidney Injury↗
PubMed1988

Comparison of cardiopulmonary effects of isoflurane and halothane after atropine-guaifenesin-thiamylal anesthesia for rumenotomy in steers.

Cardiopulmonary effects were assessed in 12 yearling steers anesthetized with guaifenesin and thiamylal sodium, intubated, and allowed to breathe isoflurane or halothane in oxygen spontaneously. Light surgical anesthesia, determined using eye position as a clinical indication of anesthetic depth, was maintained during surgical placement of a rumen cannula. Heart rate and respiratory rate were measured while the steers were standing quietly (baseline). Atropine (0.06 mg/kg of body weight, IM) was given after baseline measurements were taken. Heart rate, respiratory rate, arterial blood pressures, pHa, PaCO2, PaO2, arterial [HCO3-], esophageal temperature, and end-tidal anesthetic concentration were measured every 15 minutes for 90 minutes after induction of anesthesia. Mean heart rate increased significantly (P less than 0.05) above baseline in the isoflurane group at 15 and 30 minutes. Mean respiratory rate increased significantly (P less than 0.05) above baseline in the halothane group at 45 minutes. At 45 minutes, mean respiratory rate was lower (P less than 0.05) in the isoflurane group, compared with that in the halothane group. Mean values for arterial blood pressures and arterial gases were similar for both agents at comparable times. Mean end-tidal isoflurane concentrations were less than mean end-tidal halothane concentrations at each comparable time during maintenance of similar anesthetic depth. Maintenance of anesthesia with isoflurane resulted in higher heart rates and lower respiratory rates, compared with maintenance of anesthesia with halothane in these steers.

Anesthesia, General↗
PubMed1988

Effects of halothane and isoflurane on isolated human ventricular myocardium.

Segments of viable human left ventricular trabeculae were obtained at the time of endocardial resection for intractable ventricular ectopy. Muscle segments which showed suitable and reproducible contractions in 26 mM K Tyrode solution with 1 microM isoproterenol were electrically stimulated after rest, and at frequencies of 0.1, 0.25, 0.5, and 1 Hz. Effects of 0.75% halothane and 1.3% isoflurane on peak tension, maximum rate of tension development (dT/dt-max), and on slow (calcium dependent) action potential (AP) characteristics were studied. Halothane depressed peak tension, dT/dt-max, and slow AP maximum rate of depolarization (Vmax) at all frequencies, and caused a significantly greater depression of peak tension and dT/dt-max at 0.5-1 Hz than after rest and at 0.1-0.25 Hz. Isoflurane did not significantly depress slow AP Vmax, showed no frequency dependent contractile depression, and depressed dT/dt-max less than halothane at 0.5 and 1 Hz. Halothane and isoflurane caused differing depression in the pattern of developed tension. The differential depression by halothane and isoflurane of human ventricular myocardium was similar to that previously observed in isolated animal ventricular tissue.

Action Potentials↗
PubMed1988

Respiratory mechanics and intrinsic PEEP during ketamine and halothane anesthesia in young children.

Static compliance of the respiratory system (Crs) was measured by the interrupter technique in 18 anesthetized children to compare the effects of ketamine on Crs with those of halothane. Crs was the slope of the pressure-volume (P-V) curve obtained by repeated brief airway occlusions throughout relaxed expiration, and the intercept of the P-V curve on the pressure axis was the intrinsic positive end-expiratory airway pressure (PEEPi). Expiratory time (Te) was measured during a period of quiet breathing, and the passive expiratory time constant (tau) was measured during the relaxed expiration after an end-inspiratory occlusion. Nine children were anesthetized with a continuous infusion of ketamine and a matching group of nine children inhaled halothane in oxygen. Crs was significantly greater in the ketamine group (22.8 +/- 6.2 ml/cm H2O) than in the halothane group (15.7 +/- 5.5 ml/cm H2O). The tau value was also significantly greater in the ketamine group. Mean PEEPi in the ketamine group was 2.3 +/- 1.8 cm H2O and in the halothane group was 0.4 +/- 0.8 cm H2O. PEEPi correlated inversely with Te/tau according to a logarithmic function. It was concluded that, in children anesthetized with ketamine, Crs is significantly greater than that in children anesthetized with halothane, and the resultant prolongation of tau and decreased Te/tau with ketamine anesthesia lead to increased PEEPi.

Airway Resistance↗
PubMed1988

Renin-angiotensin-aldosterone system and plasma vasopressin in surgical patients anaesthetized with halothane or isoflurane.

The effects of halothane and isoflurane anaesthesia on plasma renin activity and plasma concentrations of aldosterone and vasopressin were investigated in 20 cholecystectomy patients. Plasma renin activity rose significantly during both halothane and isoflurane anaesthesia without surgery, and increased further after the commencement of operation. Plasma aldosterone increased slightly during halothane and isoflurane anaesthesia, but the highest concentrations, three times the control values, were measured during surgery in both groups. Plasma vasopressin decreased during halothane and isoflurane anaesthesia to half of the control values, but rose significantly during cholecystectomy. During anaesthesia and surgery there were no significant differences in the mean arterial pressures of the groups. The results demonstrate that isoflurane stimulates the renin-angiotensin system to a similar extent as halothane, although it causes hypotension by a different mechanism. The activation of the renin-angiotensin-aldosterone system may be an essential compensatory mechanism, which antagonizes the decrease of blood pressure. Plasma vasopressin probably has no role in regulating blood pressure during anaesthesia.

Adolescent↗
PubMed1988

Increasing halothane concentration abolishes anesthesia-associated arrhythmias in cats and dogs.

Fifteen cats and 6 dogs developed ventricular arrhythmias during halothane anesthesia. Halothane was administered by precision vaporizer, using a semiclosed anesthetic system. Cardiac arrhythmias were diagnosed within 5 to 10 minutes after a surgical plane of anesthesia was achieved. Arrhythmias in 9 of 15 cats and 3 of 6 dogs were converted to sinus rhythm by increasing the inspired halothane concentration. Conversion to sinus rhythm occurred within 4 minutes. Cardiac arrhythmias were reestablished in 8 of 9 cats and 2 of 3 dogs, after decreasing the inspired halothane concentration to its original value. Increasing the inspired halothane concentration can convert anesthetic-associated ventricular arrhythmias to sinus rhythm in dogs and cats.

Anesthesia↗
PubMed1987

Effect of halothane on sinus rhythm of dog heart in situ.

Effect of halothane on sinus rhythm was investigated using a direct perfusion technique of the canine SA node artery in situ. Halothane was dissolved in a fat emulsion and administered to the SA node artery in doses between 148.8 micrograms and 2976 micrograms. Both the solvent itself and a stabilizer of halothane produced no change in the heart rate. Halothane induced a biphasic chronotropic response in all doses: an initial sinus acceleration of 2 to 5 sec duration followed by a long-lasting sinus deceleration. Both responses were dose-related. The positive response was not substantially affected by prior administration of propranolol or tetrodotoxin or in reserpinized dogs. Atropine or tetrodotoxin also failed to cause any change in the negative response. Therefore, both responses were assumed to have resulted from a direct action of halothane on the SA node, but the detailed mechanism underlying the positive response remains to be further clarified.

Animals↗