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PubMed1979

Left ventricular function and compliance in swine during halothane anesthesia.

Halothane (0.05--1.7 vol per cent end-tidal) in nitrous oxide (N2O), 60 per cent: oxygen (O2), 40 per cent was administered to nonmedicated, closed-chest pigs. Ventricular function was analyzed from cardiac output (thermodilution) and left ventricular (LV) pressure indices. Ventricular volumes and compliance were estimated from single and biplane LV angiography. In separate experiments, the effects of N2O, time, and the angiographic dye injections were shown to be minimal. Halothane caused dose-dependent decreases in aortic blood pressure, cardiac output, peak first derivative of left ventricular pressure (LV dP/dt), the in-vivo maximum velocity of fiber shortening (Vmax), and ejection fraction; non-dose-dependent decreases in heart rate and circumferential fiber shortening rate. Although a pronounced dose-related negative inotropic effect of halothane in the pig heart was demonstrated, there was no definite effect on ventricular pressure-volume relationships (compliance). If there was any such effect of halothane, it was obscured by the cardiac depression produced.

Animals↗
PubMed1979

Fetal morphology in mice exposed to halothane.

The teratogenic potential of subanesthetic and anesthetic exposure to halothane was studied in Swiss/ICR mice. Two treatment regimens were employed: daily exposure of males and females for nine weeks prior to conception and on days 1 through 17 of pregnancy; and exposure of females only on days 6 through 15 of pregnancy. Mice were exposed to subanesthetic concentrations of halothane for 0.025, 0.1, 0.4, and 1.2 MAC hours/day; anesthetic exposure was 4.0 MAC hours/day. Fetal morphologic development was normal at the two lowest exposures. Exposures of 0.4 MAC hours/day and more were associated with decreased fetal ossification. At the 1.2 MAC hour/day exposure, renal pelvic masturation was retarded and the incidence of skeletal variants was increased. The incidences of major malformations and minor anomalies were not increased following exposure to subanesthetic concentrations of halothane. Anesthetic exposure to 4.0 MAC hours/day was lethal to both dams and embryos, and resulted in major developmental malformations in surviving fetuses. These effects were probably due to altered maternal physiologic status. It is concluded that exposure of mice to subanesthetic concentrations of halothane does not result in important morphologic abnormalities in their offspring.

Abnormalities, Drug-Induced↗
PubMed1980

Cerebral metabolic effects of naloxone administered with anesthetic and subanesthetic concentrations of halothane in the dog.

An abrupt significant increase in cerebral oxygen consumption when narcotic anesthesis is reversed by a narcotic antagonist has been reported. Since naloxone has also been reported partially to reverse nonnarcotic anesthesia, a similar effect might be expected were maloxone admininistered during exposure to inhalational anesthetics. To determine whether such a cerebral response should occur, naloxone, 1 and 10 mg/kg, was administered to eight dogs receiving an anesthetic concentration of halothane (0.87 per cent) or a subanesthetic concentration (0.3 per cent). Both naloxone doses failed to alter cerebral oxygen consumption at either halothane concentration. A transient EEG "reversal" was observed only after naloxone, 10 mg/kg, in animals breathing halothane, 0.87 per cent. These results would argue against any appreciable reversal of halothane anesthesia by naloxone. A significant increase in mean arterial blood pressure of 12 to 16 per cent followed naloxone administration at each condition. This is consistent with a previous report that interaction with specific receptors near the cardiovascular control center is responsible for this effect of naloxone.

Anesthesia, Inhalation↗
PubMed1981

Interactions among ventilation, the circulation, and the uptake and distribution of halothane--use of a hybrid computer multiple model: II. Spontaneous vs. controlled ventilation, and the effects of CO2.

The authors have described a basic hybrid computer multiple model of the circulation, ventilation, and uptake and distribution of halothane in a companion paper. A multiple model consists of two or more submodels, each of which is complete in itself and could operate independently. In a multiple model, however, each submodel interacts with the others. The present paper describes the addition of a CO2-control loop (submodel), through which the partial pressure of CO2 modulates ventilation, as well a myocardial "contractility," arterial pressure, cardiac output, and regional vascular resistances. The concentration of halothane modifies these CO2-induced modulations. The CO2- and halothane-induced changes in ventilation and circulation in turn modify the uptake and distribution of halothane. Thus, a complex set of interrelationships among the submodels and compartments exists.

Anesthesia, Inhalation↗
PubMed1982

Halothane biotransformation in obese and nonobese patients.

Serum levels of inorganic fluoride, trifluoroacetic acid, and bromide ion were measured at various time intervals following two hours of halothane anesthesia in 17 morbidly obese and eight nonobese patients. Ionic fluoride, a marker of reductive halothane metabolism, increased in the obese but not the nonobese patients. This is of concern since reductive halothane metabolism is associated with hepatoxicity in animals. In addition, serum bromide levels were higher after 48 h in the obese patients compared to the nonobese patients (mean +/- SE, 1,311 +/- 114 vs. 787 +/- 115 microM, P less than 0.01). Sedative levels of bromide were not attained in any patient. Peak trifluoroacetic acid levels were similar in the two patient groups. Sex age, medication intake, and smoking history had no influence on the halothane metabolite levels found in this study.

Adult↗
PubMed1982

Free radical formation in vivo and hepatotoxicity due to anesthesia with halothane.

In vivo studies were undertaken to determine whether free radical formation in the liver during administration of various halogenated anesthetics is associated with hepatotoxicity of these agents in an animal model. In addition to the anesthetics halothane, enflurane, and isoflurane, carbon tetrachloride was studied as an example of a hepatotoxic halogenated compound acting by a free radical mechanism. Free radicals were trapped in vivo during anesthesia as stable adducts using the spin trap, alpha-phenyl-t-butyl nitrone. These adducts were extracted from the liver and studied by electron spin resonance spectrometry. Free radicals were detected after administration of halothane or carbon tetrachloride, compounds which were hepatotoxic under the conditions of the experiment, but were not found after anesthesia induced with enflurane or isoflurane, anesthetics which were not hepatotoxic under identical conditions. The free radical trapped after alpha-phenyl-t-butyl nitrone treatment of halothane-anesthetized rats appeared to be a metabolic intermediate of halothane.

Animals↗
PubMed1983

Halothane-induced ATP depletion in platelets from patients susceptible to malignant hyperthermia and from controls.

Since the cellular defect of malignant hyperthermia (MH) may occur in tissues other than muscle and since platelets share certain contractile characteristics with muscle cells, testing platelets has been suggested as a way to diagnose susceptibility to MH. In analogy to the in vitro depletion of muscle adenosine triphosphate (ATP), the authors compared platelet basal nucleotide levels and halothane-induced depletion of ATP from 10 MH-susceptible patients and from 12 unrelated nonsusceptible controls. A rapid and simple isocratic high-pressure liquid chromatography technique was used to analyze acid-extracted platelet nucleotides. Halothane added to platelet-rich plasma at 37 degrees C significantly decreased ATP in platelets in a dose-dependent as well as a time-dependent manner. In contrast, adenosine diphosphate (ADP) and adenosine monophosphate (AMP) were not changed significantly. Other volatile anesthetic agents also depleted ATP in platelets. Although ATP in platelets exposed to halothane was depleted significantly, there was no difference between platelets from MH-susceptible patients and nonsusceptible controls. Therefore, halothane-induced ATP depletion in platelets is not a reliable test for diagnosing MH susceptibility.

Adenosine Diphosphate↗
PubMed1983

Comparison of isoflurane and halothane safety margins in rats.

In rat experiments, the dose-effect curves for three different end points of anesthesia [loss of righting reflex (RR), prevention of movement (PM), and heart rate response (HR) to noxious stimuli] and for the lethal effect (LE) due to cardiovascular depression were determined with isoflurane and halothane. The obtained data were used to calculate LD50/ED50 ratios and standard safety margins (SSM) for assessment of each agent's safety. It was found that isoflurane provides an equal degree of separation between dose-effect curves for different end points of anesthesia as halothane does. However, isoflurane provides greater margins of safety. The margin between the highest of anesthetic doses--the loss of HR response--and the lethal dose for isoflurane was twice that for halothane (LD50/HR ED50 4.3 vs. 2.2, P less than 0.01). The standard safety margin for the loss of HR response was also greater with isoflurane (142 vs. 43, P less than 0.05). These results agreed that isoflurane may provide greater cardiovascular safety for anesthesia than halothane does.

Anesthesia, Inhalation↗
PubMed1983

Pressure reversal of halothane's antiviral effect.

The authors have studied the effects that hyperbaric pressure and halothane had on measles virus replication. Two per cent halothane at one atmosphere of air (ATA) reduced the number of infectious measles virus particles produced in cultured Vero cells by greater than four orders of magnitude (P less than 0.001) relative to virus produced in untreated cultures at 1 ATA. The same concentration of halothane at 100 ATA still reduced the amount of virus synthesized but only by 1 1/2 orders of magnitude (P less than 0.01) as compared with control cultures. Pressure (100 ATA) alone reduced virus production insignificantly. Thus, it appears that the antiviral effects of halothane on measles virus replication in cultured Vero cells is reversible at least partially by pressure.

Animals↗
PubMed1983

Identification of receptor mechanism mediating epinephrine-induced arrhythmias during halothane anesthesia in the dog.

The adrenergic receptor mechanism by which halothane sensitizes the myocardium to the ventricular arrhythmogenic properties of catecholamines is unknown. The new generation of selective adrenergic receptor antagonists have been used to determine which receptor blockade causes the greater increase in the dose of epinephrine needed to achieve a threshold for ventricular arrhythmias. Dogs anesthetized with 1.2 MAC halothane had an arrhythmogenic dose of epinephrine (ADE) of 2.2 micrograms X kg X min-1 that significantly increased (P less than 0.01) to 27 micrograms X kg-1 X min-1 after alpha 1 blockade with prazosin. beta 1 blockade with metoprolol also significantly increased the ADE to 12 micrograms X kg-1 X min-1 (P less than 0.05) but was less than the effect noted after prazosin treatment (P less than 0.05). The dramatic increase in the threshold for arrhythmias noted after prazosin could not be ascribed solely to its hemodynamic properties because treatment with sodium nitroprusside did not change the ADE (2.7 micrograms X kg-1 X min-1) significantly; yet nitroprusside treatment resulted in a similar drop in mean arterial pressure (59 mmHg) to that of prazosin treatment (51 mmHg) when compared with the control group. Thus postsynaptic myocardial alpha 1 adrenergic receptors mediate most of the sensitization by halothane to the ventricular arrhythmogenic effects of catecholamines, while a lesser contribution is conferred by the beta 1 adrenoceptors. These results have implications for the treatment and identification of patients particularly at risk from halothane-epinephrine interactions.

Adrenergic alpha-Antagonists↗
PubMed1984

Vecuronium-induced neuromuscular blockade during enflurane, isoflurane, and halothane anesthesia in humans.

To determine the effect of the commonly used volatile anesthetics on a vecuronium-induced neuromuscular blockade, the authors studied 54 patients anesthetized with 1.2 MAC or 2.2 MAC enflurane, isoflurane, or halothane (MAC value includes contribution from 60% nitrous oxide). During 1.2 MAC enflurane, isoflurane, and halothane, the ED50S (the doses depressing twitch tension 50%) for vecuronium were 12.8, 14.7, and 16.9 micrograms/kg, respectively. During 2.2 MAC enflurane, isoflurane, and halothane, the ED50S for vecuronium were 6.3, 9.8, and 13.8 micrograms/kg, respectively (P less than 0.05). Time from injection to peak effect was the same for each anesthetic group (6.5 +/- 0.5 min, mean +/- SD), except for the group given 2.2 MAC enflurane (9.7 +/- 0.6 min) (P less than 0.05). The duration of a 50% block from injection to 90% recovery was the same for each group (mean 20 +/- 4 min), except for the group given 2.2 MAC enflurane (46.5 min) (P less than 0.05). The authors conclude that enflurane is the most potent volatile anesthetic, followed by isoflurane and then halothane, in augmenting a vecuronium-induced neuromuscular blockade. Increasing the concentration of volatile anesthetic has less effect on a neuromuscular blockade produced by vecuronium than on one produced by other nondepolarizing relaxants (e.g., pancuronium and d-tubucurarine).

Dose-Response Relationship, Drug↗
PubMed1985

The influence of halothane and isoflurane on pulmonary collateral ventilation.

The effects of halothane and isoflurane on hypocapnic increases in pulmonary collateral resistance were studied in dogs. A bronchoscope with a double lumen catheter in the suction port obstructed a peripheral airway and allowed gas to flow out of the isolated segment of lung only via collateral channels. The collateral gas flow (Vcoll) was measured with a flowmeter and delivered through one lumen of the catheter, while the other lumen measured distal pressure (Pb). At FRC, the resistance to collateral ventilation (Rcoll) was calculated as Rcoll = Pb/Vcoll. The rest of the lung was ventilated with air, while air (hypocapnia), 10% CO2 in air, or air and halothane or isoflurane were delivered to the isolated segment. A measurement of resistance was made after 4 min of test gas flow. For each segment, when air replaced 10% CO2, the average increase in Rcoll was calculated and called Rmax. When 10% CO2 in air was infused into segments the mean Rcoll (n = 50) was 0.0196 +/- 0.0022 cmH2O X ml-1 X min. This increased to 0.0285 +/- 0.0031 cmH2O X ml-1 X min (mean +/- E) when air was infused, a mean increase in resistance of 52 +/- 3%. When halothane or isoflurane was added to air the hypocapnic increase in Rcoll was attenuated with a 50% decrease at 1.3% (1.4 MAC and 0.8 MAC, respectively). These two inhalational anesthetics reduce active changes in the flow resistance to collateral ventilation. When collateral resistance acts to adjust ventilation perfusion deviations, this action of halothane and isoflurane may make this regulation less effective.

Airway Resistance↗
PubMed1985

Ventilatory responses to acute metabolic acidemia in humans awake, sedated, and anesthetized with halothane.

The authors produced metabolic acidemia acutely in human subjects awake, sedated with halothane (0.1 MAC), and anesthetized with halothane (1.0 MAC) by infusing L-arginine hydrochloride, 5-6 mmol X kg-1, over 3 h. Ventilation was recorded at resting arterial hydrogen ion concentration [( H+]a) and at 2-4 isocapnic increments of [H+]a, in each case, while end-tidal oxygen tension (PETO2) was varied between greater than 300 mmHg and 45 mmHg. Total increments of [H+]a in awake, sedated, and anesthetized subjects were 13 +/- 4, 12 +/- 2, and 12 +/- 3 nmol X 1(-1) (means +/- SD). In the awake state, metabolic acidemia increased ventilation (VI) in proportion to [H+]a. The magnitude of response increased with reduced PETO2, such that the response to acidemia and hypoxemia combined was synergistic. The delta VI/delta [H+]a slopes at PETO2 values of greater than 300, 100-120, and 45 mmHg were 0.47 +/- 0.27, 0.85 +/- 0.24, and 3.01 +/- 1.30 1 X min-1 X nmol-1 X 1, respectively (means +/- SD). Halothane sedation reduced the responses to added [H+]a determined at PETO2 values of 100-120 and 45 mmHg, as well as the response to hypoxemia and to the interaction of acidemia and hypoxemia, each to less than half awake values. Halothane anesthesia further impaired the responses to [H+]a and virtually abolished the response to hypoxemia and to acidemia-hypoxemia interaction. A small residual response to added [H+]a during anesthesia could be accounted for by a slight concurrent increase of PaCO2, leaving no response attributable to metabolic [H+]a itself.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1985

Neuromuscular effects of atracurium during halothane-nitrous oxide and enflurane-nitrous oxide anesthesia in humans.

To compare the effect of halothane and enflurane on an atracurium-induced neuromuscular blockade, the authors studied 40 patients during elective surgery. During 1.25 MAC enflurane-nitrous oxide (n = 20) or halothane-nitrous oxide (n = 20) (MAC value includes contribution from 60% nitrous oxide), the doses depressing twitch tension 50% (ED50S) for atracurium were 70 and 77 micrograms/kg, respectively. The difference was not significant. Time from injection to peak effect did not differ between groups. However, the duration of action of atracurium (expressed as duration 50 or the duration of a 50% blockade) was longer during enflurane-nitrous oxide anesthesia (34.2 min) than during halothane-nitrous oxide anesthesia (25.5 min) (P less than 0.05). The authors conclude that the potency of atracurium does not differ during halothane-nitrous oxide and enflurane-nitrous oxide anesthesia. Combining the results of this study with a previous study (atracurium ED50 = 68 micrograms/kg and 83 micrograms/kg during isoflurane-nitrous oxide and fentanyl-nitrous oxide anesthesia respectively), the potency of atracurium does not differ by more than 20% among the four anesthetic techniques studied. The background anesthetic appears to have less effect on an atracurium-induced neuromuscular blockade than on one produced by other longer-acting nondepolarizing muscle relaxants (e.g., pancuronium and d-tubocurarine).

Adult↗
PubMed1985

Cardiovascular actions of nitrous oxide or halothane in hypovolemic swine.

During normovolemia, nitrous oxide causes mild sympathetic stimulation and direct myocardial depression; these effects offset each other, resulting in only minimal cardiovascular changes. To test the hypothesis that during hypovolemia this balance would change and depression predominate, 10 swine were made hypovolemic (30% blood loss) and then were given 70% N2O (0.25 MAC in swine) or an equipotent concentration of halothane, an agent that does not cause sympathetic stimulation. The alternate anesthetic was given to the same hypovolemic swine on another day. Five minutes after induction of anesthesia during hypovolemia, both N2O and halothane caused significant, physiologically important deterioration of compensation for hemorrhage. Halothane decreased systemic vascular resistance (SVR); N2O was more variable in its action, and SVR did not decrease significantly. Both agents caused similar decreases in cardiac output, mean aortic blood pressure, stroke volume, oxygen consumption, and left ventricular minute work, despite increases in plasma epinephrine concentration and plasma renin activity. No differences were found between groups for any of these variables (P greater than 0.05). Plasma norepinephrine concentration increased only in the N2O group and was greater in that group than in the halothane group. The deterioration of cardiovascular compensation for hemorrhage was expressed metabolically by similar decreases in the two groups in partial pressure of oxygen of mixed venous blood and by increases in blood lactate concentration. Thirty minutes after induction of anesthesia, with stable end-tidal anesthetic concentrations, both groups had some cardiovascular, but no metabolic, recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1985

Halothane anesthesia attenuates cardiopulmonary baroreflex control of peripheral resistance in humans.

The effects of halothane anesthesia on cardiopulmonary (low pressure) baroreflex control of peripheral resistance were studied in 10 ASA class I young men. Graded (-5, -7.5, -10, -12.5 mmHg) lower body negative pressure (LBNP) was used to produce progressive decreases in thoracic blood volume and central venous pressure. These stimuli activate reflexes from cardiopulmonary baroreceptors. Volunteers were studied while awake and during 1 MAC (0.75%) and 1.25 MAC (0.93%) halothane anesthesia. Hetastarch (6%) in 0.9% normal saline was infused into patients before baseline recordings were initiated. Blood pressure, stroke volume, cardiac output, and systemic and forearm vascular resistance decreased and forearm blood flow increased during halothane anesthesia. In awake subjects, LBNP did not alter heart rate or blood pressure, but stroke volume and cardiac output decreased. Blood pressure was maintained by cardiopulmonary baroreflex-mediated increases in peripheral resistance. In anesthetized subjects, decreases in stroke volume and cardiac output during LBNP were similar to awake responses, however, hypotension occurred because reflex resistance increases were markedly attenuated. The authors conclude that halothane anesthesia blunts cardiopulmonary baroreflex resistance responses provoked by mild decreases in thoracic blood volume in humans.

Adult↗
PubMed1986

Cell proliferation in developing brain after brief exposure to nitrous oxide or halothane.

Several inhalant anesthetics, including nitrous oxide and halothane, are known to be antimitotic in a variety of developing tissues, but none has been tested for antimitotic activity in developing brain. Concern about the safety of these agents has centered around behavioral effects reported in humans and animals after early exposure. Because interference with cell production during CNS development is a sufficient cause for later behavioral abnormalities, it is important to know whether cell production in the nervous system is altered by these agents. Mice were exposed to either nitrous oxide (75% N2O and 25% O2) or halothane (0.5% halothane in 75% N2 and 25% O2) or a mixture of 75% N2 and 25% O2. Prenatal treatment groups were exposed for 6 h on the 14th day of gestation, while postnatal treatment groups were exposed for 4 h on the second day after birth. Treated and control animals were then killed immediately after exposure, or 12, 24, or 48 h later, to be evaluated for CNS mitotic activity. Each of the four anesthetic-exposed groups showed some deviations from normal mitosis, but only the postnatal nitrous oxide group showed the pattern of reduced cell proliferation followed by a rebound that is characteristic of many antimitotic teratogens. Although prenatal nitrous oxides' effects on the fetal brain were not clearly interpretable, it did delay development of blood, as has been reported by other investigators. Both nitrous oxide and halothane significantly reduced body weight of fetuses in utero, but did not reduce body weight of neonates. The pattern of the body-weight effects suggests that they occur by some mechanism other than reduced cell production.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1987

Determinants of end expiratory volume in young children during ketamine or halothane anesthesia.

The expiratory time (Te) and the rate of lung emptying in expiration are important determinants of functional residual capacity (FRC) in infants. In order to determine whether these factors also influence FRC in children during anesthesia, 20 preschool children were studied, 10 while receiving ketamine, and 10 during halothane anesthesia. Te was measured during quiet breathing and the passive expiratory time constant (tau) was determined from the passive expiratory flow volume (V/V) curve following a brief end inspiratory airway occlusion. The number of time constants available for expiration, Te/tau, was then calculated. The difference between FRC and the relaxation volume of the respiratory system (Vrs) (FRC-Vrs) was measured by extrapolating the linear segment of the V/V curve to zero flow, and measuring FRC-Vrs. During ketamine anesthesia, tau was markedly prolonged (1.15 s, range 0.73-2.29 s), with the result that Te/tau was, in all subjects, less than 2. Children anesthetized with halothane had shorter tau (0.38 s, range 0.24-0.65 s), and Te/tau was more than 2 in most subjects. FRC-Vrs was significantly greater in the subjects from the ketamine group (203 ml, range 115-392 ml) than in those from the halothane group (32 ml, range 1-71 ml). For the 20 subjects, there was a significant relationship between FRC-Vrs (ml) and Te/tau described by the equation. FRC-Vrs = 845.0e-1.28(Te/tau) The authors conclude that, in children during ketamine anesthesia, tau is prolonged and, in these children, the relationship of Te to tau is an important determinant of FRC-Vrs. Te/tau was not related causally to FRC-Vrs in the halothane group.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗

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