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PubMed1985

Laudanosine (a metabolite of atracurium) increases the minimum alveolar concentration of halothane in rabbits.

The authors hypothesized that laudanosine, a metabolite of atracurium and a central nervous system stimulant, might increase the minimum alveolar concentration (MAC) of halothane. An initial study in five rabbits anesthetized with halothane used a two-compartment model to produce estimates of pharmacokinetic variables for laudanosine. These estimates were used to determine the rates of infusion that would produce steady state plasma concentrations of laudanosine of approximately 200, 400, and 800 ng . ml-1. Subsequent infusion of laudanosine in eight rabbits produced mean (+/- SD) steady state plasma concentrations of laudanosine of 234 +/- 56, 457 +/- 66, and 873 +/- 105 ng . ml-1. The control value for MAC of halothane was 1.08 +/- 0.28%. At the lowest steady state plasma laudanosine concentration, MAC did not significantly differ from control (MAC = 1.15 +/- 0.23%, P less than 0.1). However, at 457 and 873 ng . ml-1, laudanosine significantly increased the MAC of halothane by 23% and 30%, respectively. Infusion with saline in two additional rabbits did not affect MAC. Therefore, at the plasma concentrations of laudanosine found in humans after administration of atracurium, laudanosine increased the MAC of halothane in rabbits.

Animals↗
PubMed1985

The cerebral effects of pancuronium and atracurium in halothane-anesthetized dogs.

Pancuronium decreases the minimal alveolar anesthetic concentration (MAC) of halothane in humans, while atracurium has a metabolite, laudanosine, which is a known cerebral stimulant. To determine if these muscle relaxants significantly alter cerebral function, their effects on cerebral metabolic rate (CMRo2), cerebral blood flow (CBF), intracranial pressure (ICP), EEG, and the cerebral energy state were studied in halothane-anesthetized dogs. Group A dogs (n = 6) were maintained at 0.86% end-expired (1.0 MAC) halothane. Thereafter, a sequence of 1) pancuronium 0.1 mg . kg-1; 2) reversal of neuromuscular blockade with neostigmine plus glycopyrrolate; and 3) pancuronium 0.2 mg . kg-1 produced no changes in CMRo2, CBF, ICP, or EEG. Group B dogs (n = 6) also were maintained at 0.86% end-expired halothane and received the following in sequence: 1) atracurium 0.5 mg . kg-1; 2) reversal of neuromuscular blockade with neostigmine plus glycopyrrolate; 3) atracurium 1.0 mg . kg-1; and 4) atracurium 2.5 mg . kg-1. There were no changes in CMRo2, CBF, or ICP; EEG evidence of cerebral arousal occurred in only one dog with the final dose of atracurium. Group C dogs (n = 6) received tetracaine spinal anesthesia and the minimal halothane concentration (mean +/- SE = 0.69 +/- 0.03% end-expired) that would maintain an "anesthetic" EEG pattern. Each Group C dog received the following in sequence: 1) atracurium 1.0 mg . kg-1, and 2) atracurium 2.5 mg . kg-1. EEG evidence of cerebral arousal occurred in all six Group C dogs. Arousal was not accompanied by significant increases in CBF, CMRo2, or ICP.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1986

A comparison of the direct cerebral vasodilating potencies of halothane and isoflurane in the New Zealand white rabbit.

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

Anesthesia↗
PubMed1987

Hepatic oxygen supply and consumption in rats exposed to thiopental, halothane, enflurane, and isoflurane in the presence of hypoxia.

Hepatic oxygen supply and uptake were assessed in phenobarbital-pretreated male Sprague-Dawley rats receiving subanesthetic doses of thiopental, halothane, enflurane, or isoflurane combined with hypoxia (approximately 0.5 MAC and 12% oxygen) for the purpose of evaluating the role of these combinations in hepatic blood flow alterations and the concomitant hepatic oxygen supply and uptake. Hepatic blood flow was measured using microspheres; hepatic oxygen supply and consumption was calculated from measured hepatic blood flow and oxygen content in hepatic arterial, portal venous, and hepatic venous blood. In all anesthetic groups, total hepatic blood flow did not change from the control value. Oxygen supply to the liver was decreased from air control values in all anesthetic groups, but there were no significant differences among anesthetic groups. Hepatic oxygen consumption was significantly lower in animals exposed to halothane and isoflurane versus air controls, whereas it was not significantly decreased in animals receiving thiopental or enflurane. The hepatic oxygen supply/consumption ratio was higher in the air control and the isoflurane groups than in other groups; however, no significant differences in this ratio were observed among the thiopental, halothane, and enflurane groups. Oxygen content in hepatic venous blood correlated well with hepatic oxygen supply/consumption ratio in all five groups. These results show that, during exposure to mild hypoxia, a sub-MAC dose of isoflurane maintains the relationship of hepatic oxygen supply to uptake better than thiopental, halothane, or enflurane. However, a subanesthetic dose of halothane did not aggravate liver hypoxia specifically, compared with thiopental or enflurane.

Animals↗
PubMed1987

Inhibition of d-tubocurarine-induced histamine release by halothane.

To determine whether anesthetics modify mediator release, the authors measured the amount of histamine released by d-tubocurarine (dTC) in human foreskin preparations in the presence of high (2.0%) and low (0.5%) halothane concentrations and nitrous oxide (10%). Freshly excised human foreskins were divided into four matched pieces. Two matched pieces were aerated with oxygen, and the other two with an oxygen-anesthetic gas mixture. One chamber of each served as a control, while the other was stimulated with 3 X 10(-5) M d-tubocurarine for 30 min. Supernatant histamine concentrations were measured by automated fluorometry. Percent histamine release was determined by dividing the experimentally released histamine concentration by the total histamine released after the tissue was sonicated and boiled. Neither halothane nor N2O alone altered spontaneous histamine release. Histamine release by d-tubocurarine was significantly reduced by 2% halothane compared to d-tubocurarine alone (2.8% +/- 0.9 vs. 13.9% +/- 3.7, mean + SEM) (P less than 0.05) in the in vitro preparation. Histamine release was reduced in the preparations pretreated with 0.5% halothane group, but this was not statistically significant (P greater than 0.05) when compared to d-tubocurarine alone. N2O (10%) did not reduce d-tubocurarine-induced histamine release. The authors conclude that halothane, in clinically used concentrations, significantly impairs histamine release from human neonatal foreskin preparations.

Anaphylaxis↗
PubMed1987

Halothane relaxes previously constricted isolated porcine coronary artery segments more than isoflurane.

Coronary vasodilation by halothane and isoflurane were compared using in vitro tension recording. Porcine left anterior descending coronary arterial segments (1.5-2.0 mm o.d.) were constricted with either K+ (30 mM) or prostanoid U44069 (6 X 10(-7) M) in the absence of other drugs or anesthetics. Following stabilization of constriction, arteries were exposed to halothane or isoflurane at 0.5, 1.0, 1.5, 2.0, and 3.0% concentrations. K+ (30 mM) induced constriction was reduced by halothane at 1.5, 2.0, and 3.0% and U44069 (6 X 10(-7) M) induced constriction was reduced at 0.5, 1.0, 1.5, 2.0, and 3.0%. K+ (30 mM) induced constriction was reduced by isoflurane only at 3.0% and U44069 (6 X 10(-7) M) induced constriction was reduced by isoflurane only at 2.0 and 3.0%. U44069 induced constriction was more susceptible than K+ induced constriction to relaxation by halothane or isoflurane. Halothane was more potent than isoflurane as a direct relaxant of porcine epicardial left anterior descending arterial segments previously constricted with K+ (30 mM) or U44069 (6 X 10(-7) M).

Animals↗
PubMed1987

Isoflurane when compared to enflurane and halothane decreases the frequency of cerebral ischemia during carotid endarterectomy.

Data from the records of patients who underwent 2223 carotid endarterectomies at the Mayo Clinic between January 1, 1972, and December 31, 1985, were abstracted to compare the effects of isoflurane, enflurane, and halothane on the critical cerebral blood flow (CBF) (i.e., the CBF below which the majority of patients develop EEG ischemic changes within 3 min of carotid occlusion), the incidence of EEG ischemic changes, and the neurologic outcome. In a total of 2196 of these procedures, the patient received one of the three volatile anesthetics and, in 2010 of these, both the EEG and the CBF were monitored. Chronologically, halothane was the primary agent from 1972-1974; enflurane progressively replaced halothane during 1975-1981; and isoflurane was used almost exclusively since 1982. This analysis confirmed a previous study that the critical CBF during isoflurane anesthesia (703 procedures) was approximately 10 ml X 100 g-1 X min-1, as contrasted to that of approximately 20 ml X 100 g-1 X min-1 during halothane anesthesia (467 procedures). This analysis also established that the critical CBF during enflurane anesthesia (840 procedures) was approximately 15 ml X 100 g-1 X min-1. The incidence of EEG ischemic changes was significantly less (P less than 0.001) during isoflurane anesthesia (18%) than during either enflurane (26%) or halothane (25%) anesthesia. This difference occurred despite the fact that the preoperative risk status was greater in the patients given isoflurane. There was no difference in neurologic outcome between the three anesthetics, and none was expected, since all patients with EEG changes were immediately shunted, if possible.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1987

The intracranial pressure effects of isoflurane and halothane administered following cryogenic brain injury in rabbits.

The intracranial pressure (ICP) responses to administration of either halothane or isoflurane were compared in New Zealand white rabbits following a standardized cryogenic brain injury. Animals were tracheally intubated and paralyzed, and background anesthesia was maintained with morphine sulfate and nitrous oxide. Following injury and attainment of an elevated and stable ICP, animals were divided into four groups. Animals in groups I and III were maintained normocapnic throughout the experiment and administered 1 MAC halothane or isoflurane, respectively. Group II and IV animals were made hypocapnic (PaCO2 = 20 mmHg) prior to the administration of either 1 MAC halothane or isoflurane, respectively. Monitored variables were mean arterial blood pressure, ICP (ventriculostomy), end-tidal (ET) CO2, ET volatile anesthetic, the electroencephalogram, temperature, and arterial blood gases. Prior to producing the lesion, ICP was approximately 5 mmHg in all animals with no differences among groups. Sixty to ninety minutes after injury, ICP increased significantly to approximately 20 mmHg in all animals. Introduction of either halothane or isoflurane was associated with significant increases in ICP in all groups to approximately 30 mmHg. These data suggest that further significant increases in ICP may occur following introduction of either halothane or isoflurane in the presence of acute brain injury and elevated ICP. Furthermore, these ICP increases may not be altered by the prior establishment of hypocapnia.

Animals↗
PubMed1987

Effects of isoflurane and halothane on coronary vascular resistance and collateral myocardial blood flow: their capacity to induce coronary steal.

Some coronary vasodilators, paradoxically, may endanger patients with coronary artery disease by causing "coronary steal." To determine the capacity of isoflurane and halothane to cause coronary steal, the authors studied their effects on coronary vascular resistance (CVR), diastolic coronary artery pressure, and collateral myocardial blood flow. Using ameroid constrictors, chronic occlusions of the left anterior descending (LAD) coronary artery were created in ten dogs. Six to eight weeks after implantation, the dogs were anesthetized with fentanyl and pentobarbital, and a stenosis was created on the circumflex (Cx) coronary artery. Isoflurane and halothane were each administered in doses of 0.5 and 1.5 MAC. Diastolic aortic pressure was held constant. Using small catheters in the circumflex and LAD coronary arteries, the authors measured diastolic coronary artery pressures. Collateral myocardial blood flow was measured by the microsphere method. In this model, halothane and isoflurane minimally affect CVR. The maximum change in CVR, which was found during 1.5 MAC isoflurane, was -8% (not significant). Diastolic coronary pressures distal to the Cx stenosis (54.5 +/- 11.5 mmHg) and distal to the LAD occlusion (44.5 +/- 5.2 mmHg) did not change significantly with either isoflurane or halothane. Transmural collateral blood flow distal to the LAD occlusion (0.51 +/- 0.11 cc.g-1.min-1) was unaltered by either drug. There was no evidence of coronary steal. Epicardial ECG S-T segments showed no evidence of ischemia. The finding of minimal direct effects of halothane and isoflurane on CVR, diastolic coronary pressure, and collateral myocardial blood flow suggest that, under the conditions of this study, neither agent, when used as an adjuvant to high-dose narcotic anesthesia, is likely to cause myocardial ischemia by a coronary "steal" mechanism.

Animals↗
PubMed1987

The effects of halothane and pentobarbital on the threshold of transpulmonary passage of venous air emboli in dogs.

The influence of halothane, pentobarbital, and their interaction on the passage of air across the pulmonary circulation was studied in 12 dogs using transesophageal M-mode echocardiography for air detection in the left atrium and/or aorta. Air was detected in the left atrium and/or aorta after pulmonary artery air injection of 0.04 ml/kg during 1% halothane anesthesia (n = 5). Addition of pentobarbital changed the threshold to 1.0 ml/kg. During pentobarbital anesthesia with and without halothane (n = 7), the thresholds were 1.1 and 1.2 ml/kg, respectively. The authors conclude that the threshold for transpulmonary passage of venous air is higher during anesthesia with pentobarbital with or without halothane than during anesthesia with halothane alone.

Anesthesia, General↗
PubMed1988

Effects of halothane, enflurane, and isoflurane on coronary blood flow autoregulation and coronary vascular reserve in the canine heart.

To investigate the effects of volatile anesthetics on coronary blood flow (CBF) autoregulation and coronary vascular reserve, studies were performed on chronically instrumented dogs, awake and during the administration of 1.0 MAC halothane, enflurane, and isoflurane. Coronary pressure-flow plots were generated by measuring left anterior descending coronary artery blood flow while varying coronary inflow pressure with a hydraulic occluder. Autoregulation was quantitated by two measures: the slope of the horizontal "autoregulated" portion of the pressure-flow relationship and the autoregulation index (ArI) of Norris. Slope values (ml.min-1.mmHg-1 +/- SD) were: awake, 0.243 +/- 0.043; halothane, 0.414 +/- 0.044; enflurane, 0.587 +/- 0.187; and isoflurane, 0.795 +/- 0.246. The increase in slope was statistically significant only for halothane and isoflurane (P less than .05). The ArI approaches 1.0 when autoregulation is perfect, and approaches zero or is a negative number when autoregulation is absent. The authors found ArI values of: awake, 0.55; halothane, -0.08; enflurane, -0.01; isoflurane, -0.02. These values indicate good autoregulation while awake, but impaired autoregulation with all three anesthetics (P less than .05). Coronary vascular reserve was calculated, at a diastolic coronary pressure of 40 mmHg, as the difference between resting flow and flow during maximal coronary vasodilation induced by intracoronary adenosine. Coronary vascular reserve, maximal coronary conductance, and coronary zero-flow pressure were not significantly altered by these anesthetics. The authors conclude that 1.0 MAC enflurane, halothane, and isoflurane mildly disrupt CBF autoregulation, increasing CBF out of proportion to myocardial demands. Under the conditions of this study, these anesthetics do not affect maximal CBF or coronary vascular reserve.

Animals↗
PubMed1988

Myocardial tolerance to total ischemia in the dog anesthetized with halothane or isoflurane.

Myocardial tolerance to total ischemia was compared in animals anesthetized with halothane or isoflurane by measuring the time required for development of cardiac rigor in the absence of coronary circulation or wall stress. Sixteen dogs, eight in each group, were anesthetized with equally potent inspired concentrations of either halothane (2 MAC) or isoflurane (2 MAC), intubated, and ventilated. Thirty minutes later, the heart was rapidly excised. A left ventricular slab was prepared and maintained at 37 degrees C. A portion of each slab was placed in a compressibility gauge that detects rigor onset by an abrupt increase in resistance to tissue deformation. Subendocardial tissue pressure was continuously measured in a second slab using needle-tipped Millar pressure transducers. A third slab was used for intermittent tissue sampling and HPLC assay of high-energy nucleotide levels. There were no differences in pre-ischemic heart rate, mean arterial pressure, glucose, lactate, PO2, PCO2, pH, plasma epinephrine, or norepinephrine levels between the two groups. The onset of rigor as measured by the compressibility gauge was delayed in the halothane group (68 +/- 7.2 vs. 60 +/- 5.0 min; P less than .05). Tissue ATP and ADP levels declined throughout the period of ischemia, with a trend towards preservation in the halothane group. The data show that myocardial tolerance to total normothermic ischemia is improved in animals anesthetized with halothane compared to isoflurane, independent of the effects on hemodynamics or collateral coronary circulation.

Adaptation, Physiological↗
PubMed1988

Neurologic outcome in rats following incomplete cerebral ischemia during halothane, isoflurane, or N2O.

Using rats in which incomplete cerebral ischemia was induced, the authors evaluated the effects of halothane (H) and isoflurane (I) on neurologic outcome compared to nitrous oxide (N2O) controls. Incomplete cerebral ischemia was produced by right carotid artery occlusion combined with hemorrhagic hypotension. Neurologic outcome was evaluated using a graded deficit score from 0 to 5 (0 = normal, 5 = death associated with stroke). Two levels of cerebral ischemia were tested. At moderate ischemia with hypotension of 30 mmHg, an FIO2 of 0.3, and ischemic periods of 30 or 45 min, N2O produced a deficit of 4.7-5.0 and a mortality rate of 90-100%. In contrast, halothane (1 MAC) and isoflurane (1 MAC) resulted in similar deficit scores (H = 1.1-1.8, I = 1.4-1.6) and mortality rates (H = 17-30%, I = 17-20%). Cerebral blood flow (CBF) measured with radioactive microspheres showed a 60-65% decrease in the ischemic hemisphere at this level of hypotension. With severe ischemia with hypotension = 25 mmHg, FIO2 = 0.2, and a 30-min period of ischemia, deficit scores increased to 3.0 and 3.9 with 1 MAC halothane and 1 MAC isoflurane, respectively. Mortality rates also increased to 40% with halothane and 70% with isoflurane. Increasing the concentration of halothane or isoflurane to 2 MAC did not significantly improve outcome. Brain histology demonstrated extensive neuronal damage in striatal, hippocampal, and neocortical regions of N2O control treated rats, and less damage with little difference between H- and I-treated rats at each level of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1988

Effects of halothane on acetylcholine release and sympathetic ganglionic transmission.

Depression of synaptic transmission is one of the actions common to many general anesthetics. They appear to act primarily on the chemical transmission process itself without affecting the conduction of impulses in nerve axons. The objective of the present study was to directly examine the effects of halothane on the release of acetylcholine and overall ganglionic transmission. The effects of halothane on ganglionic transmission were studied in the stellate ganglion of the cat in vitro. The preganglionic nerves of the stellate ganglion were stimulated electrically to generate threshold and suprathreshold evoked potentials in the postganglionic nerves. The picomole levels of released acetylcholine in the superfusate were determined with a radioenzymatic method using 32P-ATP following a 5-min preganglionic stimulation before and after the addition of 0.28 and 0.59 mM halothane (vaporizer settings of 1% and 2%, respectively). Halothane at both concentrations: 1) depressed sympathetic ganglionic transmission induced by either threshold or suprathreshold stimulation of the preganglionic nerves; and 2) caused a dose-dependent decrease in acetylcholine release during threshold stimulation with no change in neurotransmitter release during suprathreshold stimulation. In summary, the interruption of synaptic transmission by halothane involves at least two mechanisms: 1) decrease in acetylcholine release during low level of synaptic transmission; and 2) postsynaptic decrease in sensitivity to acetylcholine during low and high levels of synaptic transmission.

Acetylcholine↗
PubMed1989

Alterations of alpha 1 and alpha 2 adrenoceptor-mediated pressor responses by halothane and isoflurane anesthesia.

The mechanism by which halothane and isoflurane interfere with catecholamine-mediated vasoconstriction was investigated, utilizing selective agonists of postjunctional alpha1 and alpha2 adrenoceptors in chronically instrumented dogs. After ganglionic, cholinergic, and beta adrenergic blockade, dose responses to phenylephrine (0.3-1.2 micrograms/kg, iv), a selective alpha1 adrenoceptor agonist, and azepexole [B-HT 933] (5-20 micrograms/kg, iv), a selective alpha2 adrenoceptor agonist, were obtained in conscious dogs. Each dog was subsequently anesthetized with either halothane (1.7%) or isoflurane (2%) in oxygen in equihypotensive concentrations. After a 1 h equilibration period, the dose response curves were repeated. Twenty experiments in ten chronically instrumented dogs were completed. Halothane and isoflurane produced significant (P less than 0.05) attenuation of both the increase in systolic and diastolic arterial pressure after bolus administration of all doses of phenylephrine and azepexole. No specific selectivity of either volatile anesthetic for alpha1 or alpha2 mediated pressor responses was found. Therefore, in chronically instrumented dogs, alpha1- and alpha2-mediated pressor responses were similarly influenced by halothane and isoflurane. The present results suggest that both halothane and isoflurane act as functional antagonists to alpha adrenergic mediated vasoconstriction.

Adrenergic alpha-Agonists↗
PubMed1989

Metabolism of halothane in obese Fischer 344 rats.

Halothane is metabolized by an oxidative pathway to stable, nonvolatile end products, trifluoroacetic acid (TFAA) and bromide (Br-), and by reductive pathways to Br-and inorganic fluoride (F-). There is evidence that both oxidatively and reductively formed intermediates may produce hepatotoxicity, although the exact etiology of the fulminant hepatic necrosis seen in humans is unproven. Obese patients receiving volatile anesthetics exhibit higher serum anesthetic metabolite concentrations than do normal-weight patients, and thus might be at greater risk of hepatotoxicity because of higher concentrations of reactive intermediates from halothane metabolism. To eliminate the variables inherent in human clinical studies leading to confounding interpretation of data, this study determined the contributions of oxidative and reductive pathways to halothane metabolism in an animal model of human hypertrophic obesity, the most common form of human obesity. Eight pairs of obese (high-fat diet) and normal-weight (standard chow), male Fischer 344 rats were anesthetized with halothane for 4 h at an inspired concentration of 0.78%. Serum and urinary concentrations of TFAA, Br-, and F-were measured. Thirty-six hours following halothane anesthesia, mean serum TFAA concentrations peaked at 7.3 +/- 1.1 mM in obese rats and 4.7 +/- 0.7 mM in nonobese rats. TFAA urinary excretions during the 180-h period postanesthesia were 519 +/- 69 and 336 +/- 22 mumol, respectively. Peak serum Br- concentrations were 9.1 +/- 1.0 and 6.9 +/- 0.6 mM for obese and nonobese rats, respectively, and Br-urinary excretions were 127 +/- 30 and 79 +/- 14 mumol, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

The effect of halothane, isoflurane, or sufentanil on the hypertensive response to cerebellar retraction during posterior fossa surgery.

The blood pressure (BP) response to cerebellar retraction during microvascular decompression of the fifth cranial nerve was investigated in 26 ASA physical status 2 or 3 patients with trigeminal neuralgia. One surgeon performed all operations. To determine the effect of three anesthetic techniques on the BP response, patients were randomly assigned to receive halothane, isoflurane, or sufentanil in sufficient doses with 60% nitrous oxide to achieve a precerebellar retraction systolic BP that was 10-20% below the average ward systolic BP (as per standard clinical practice). The resultant doses were halothane 1.65 +/- 0.27 (mean +/- SD) MAC, isoflurane 1.56 +/- 0.17 MAC (P greater than 0.05), and sufentanil 2.7 micrograms/kg (MAC values include 0.6 MAC contribution from 60% nitrous oxide). In all patients BP increased during the cerebellar retractor placement period compared with the preretractor placement period (P less than 0.05). The peak increase in systolic BP in response to cerebellar retraction was 17 +/- 6 mmHg for halothane, 38 +/- 20 mmHg for isoflurane, and 26 +/- 19 mmHg for sufentanil. The difference between halothane and isoflurane was significant (P less than 0.05). Mean and diastolic BP showed similar significant differences. The authors conclude that halothane attenuates the hypertensive response to cerebellar retraction more than isoflurane when administered in approximately 1.6 MAC concentrations (MAC value includes contribution from nitrous oxide).

Aged↗
PubMed1990

Cardiovascular effects of acute changes in extracellular ionized calcium concentration induced by citrate and CaCl2 infusions in chronically instrumented dogs, conscious and during enflurane, halothane, and isoflurane anesthesia.

To study the cardiovascular effects of low blood ionized calcium ion concentrations [Ca2+] induced by citrate infusion followed by high [Ca2+], induced by CaCl2 infusion awake and during enflurane (2.5% ET), halothane (1.2% ET), and isoflurane (1.6% ET) anesthesia, dogs were chronically instrumented to measure heart rate, aortic, left atrial, and left ventricular (LV) blood pressures, and cardiac output. In conscious dogs low [Ca2+] (decreased 0.35 mM); increased heart rate (HR) and mean aortic pressure (MAP) and decreased stroke volume (SV) and LV dP/dtmax. Low [Ca2+] increased HR during all three anesthetics and decreased LV dP/dtmax except during isoflurane anesthesia. Low [Ca2+] produced more hemodynamic depression during enflurane anesthesia than during anesthesia with halothane or isoflurane increasing left atrial pressure and decreasing MAP and SV. The differences seen were partially related to decreased systemic vascular resistance during halothane and isoflurane anesthesia. In conscious dogs following high [Ca2+] (increased 0.37 mM); only MAP and LV dP/dtmax increased. LVdP/dtmax was also increased by high [Ca2+] during all three anesthetics without a change in MAP. Cardiac output increased during halothane and isoflurane anesthesia but was unchanged during enflurane. It would appear that the hemodynamic sensitivity for the effects of changing [Ca2+] was enflurane greater than halothane greater than isoflurane greater than awake. The results suggest that the effects of changes in [Ca2+] induced by citrate and CaCl2 infusion are modified by the three volatile anesthetics.

Anesthesia, Inhalation↗