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PubMed1990

Halothane inhibits hypoxic pulmonary vasoconstriction in the presence of cyclooxygenase blockade.

Using an isolated lung the effects of halothane on hypoxic pulmonary vasoconstriction (HPV) were studied in the presence of cyclooxygenase blockade. The pulmonary vasculature can be divided into arterial, middle and venous segment resistances. Analysis of the vascular pressure-flow relationship further separates resistance into a flow dependent resistance (1/slope) and a zero-flow pressure intercept (PCRIT). We ventilated six lobes with control (35 per cent O2) and hypoxic (three per cent O2) gas mixtures with the addition of either 0, 0.5, 1.0, or 2.0 per cent halothane. We found that after addition of indomethacin (5 mg.kg-1), ventilation with three per cent O2 increased total resistance by 87 per cent over baseline with the increase primarily in the middle vascular segment. During normoxic ventilation PCRIT was 7.9 cm H2O and this increased significantly with hypoxia to 11.5 cm H2O). Only 2.0 per cent halothane blocked the increases in middle segment resistance and in PCRIT. We conclude that following cyclooxygenase blockade, halothane inhibits HPV by acting on middle segment vessels.

Animals↗
PubMed1990

Temperature-dependent effects of halothane and isoflurane on the isolated left atrium.

The aim of the present study was to examine whether changes in temperature alter the effects of halothane and isoflurane on isolated left atria. Concentration-response curves for inotropic effects at different temperatures (30 degrees C, 37 degrees C, 40 degrees C) on electrically stimulated left atria of the rat were obtained. The change of temperature modified the maximal negative inotropic response to halothane. The maximal decrease induced by halothane was 12 +/- 2.3 per cent at 37 degrees C and 18 +/- 2.5 per cent at 30 degrees C. When the temperature increased up to 40 degrees C the maximal decrease of atrial inotropism was 46 +/- 2.1 per cent--significantly higher than obtained at 37 degrees C. However, the maximal effect obtained by isoflurane was not significantly affected by temperature (30 degrees C = 7 +/- 1.6 per cent; 37 degrees C = 8 +/- 1.8 per cent; 40 degrees C = 2 +/- 0.8 per cent). Furthermore the potency of halothane (expressed as the concentration which produced 50 per cent inhibition - IC 50 per cent), decreased significantly at 30 degrees C (IC 50 = 1.34 +/- 0.18) and increased at 40 degrees C (IC 50 = 0.44 +/- 0.17) when compared with its potency at 37 degrees C (IC 50 = 0.96 +/- 0.08). On the other hand changes in temperature did not significantly modify the IC 50 for isoflurane obtained at 37 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1980

The effect of halothane with nitrous oxide on baroreflex control of heart rate in man.

The assess the effect of halothane with 70 per cent nitrous oxide on the human baroreflex, we observed the heart rate response to pharmacological elevation of blood pressure in subjects anaesthetized to the 1 MAC and 1.25 MAC levels. We observed, in comparison to the awake control, that at 1 MAC halothane with 70 per cent nitrous oxide and oxygen, the baroreflex was depressed and this became more significant at 1.25 MAC anaesthesia. In comparison to previous similar studies on the effect of halothane-oxygen anaesthesia, there was significantly less baroreflex depression at equianaesthetic doses with halothane with 70 per cent nitrous oxide.

Adult↗
PubMed1978

An assessment of operating room environment air contamination with nitrous oxide and halothane and some scavenging methods.

This study was designed to assess operating room contamination with nitrous oxide and halothane when nitrous oxide 3 1/min and oxygen 2 1/min containing halothane one per cent were passed into a semiclosed circle absorber system from which the patients' lungs were ventilated with an Ohio ventimeter through a cuffed tracheal tube, with the exhaled gas vented to the floor. The normal room ventilation did not consistently maintain levels below the suggested amounts, which are nitrous oxide 25 ppm and halothane 2 ppm. Careful daily check for and correction of high and low pressure leaks combined with the use of a Foregger scavenging device (7--351--005) and continuous wall vacuum accepting approximately 22 1/min enabled geometric mean values below the suggested levels to be achieved. The Protection Filter Foregger 7--365--001 was only effective in removing halothane and only if the plastic holder provided was radically modified. Attention is drawn to the numerous factors influencing the magnitude of contamination, aspects of controlling it, and the necessity to cope with the problem of dealing with scavenged gases and vapours.

Air Pollutants↗
PubMed1991

Attenuation of contraction of isolated canine coronary arteries by enflurane and halothane.

Contraction of vascular smooth muscle such as that existing in coronary arteries is regulated in part by Ca++ entry into cells via Ca++ channels. Volatile anaesthetics are known to attenuate agonist-induced coronary artery constriction. The purpose of this experiment was to determine if 1.5 MAC concentrations of halothane or enflurane attenuated contractions evoked by activation of one type of Ca++ channel--the potential operator channel. In the current experiment, potential operator channels were activated by depolarizing isolated canine coronary artery rings with high concentration of K+, causing Ca++ entry and vessel contraction. Rings without endothelium were suspended for isometric force measurement in organ chambers containing aerated Krebs-Ringer solution. Maximum response to Ca++ in rings depolarized with K+ was 120 +/- 5 per cent in untreated versus 101 +/- 3 per cent in rings treated with enflurane (P less than 0.01). The maximum response was 123 +/- 6 per cent in untreated versus 111 +/- 5 per cent during halothane administration (P less than 0.05). In contrast, nifedipine 10(-9) M depressed maximum contractions from 114 +/- 5 per cent to 37 +/- 4 per cent (P less than 0.01) and nifedipine 10(-8) M depressed contractions to 30 +/- 4 per cent (P less than 0.01). In a further series of experiments, sustained contractions were depressed by continued administration of the anaesthetics, indicating no loss of anaesthetic effect with time. The results indicate that 1.5 MAC halothane and enflurane attenuate contractions of canine coronary arteries evoked by depolarization and Ca++ entry through potential operated channels. However, neither halothane nor enflurane exhibited the marked depressant effect exerted by nifedipine.

Animals↗
PubMed1988

Local spinal cord glucose utilization in conscious and halothane-anaesthetized rats.

The authors used the 2-[14C]deoxyglucose method to study local spinal and cerebral glucose utilization simultaneously during 1.2 per cent halothane anaesthesia in adult Sprague-Dawley rats. In conscious animals (n = 5) the rate of glucose utilization in lumbar spinal gray matter was about 50 per cent lower than that of cerebral cortex. Halothane anaesthesia (n = 6) reduced spinal cord and cerebral metabolic rate. Spinal glucose utilization was reduced 12-35 per cent, but this was less than the 45-70 per cent decrease halothane produced in 8 of 16 cerebral structures examined and was independent of the hypotension produced. These results indicate that halothane is a spinal metabolic depressant but that its effects on this tissue are substantially less than those it has on many cerebral structures.

Anesthesia, Inhalation↗
PubMed1988

Drive and timing components of respiration in young children following induction of anaesthesia with halothane or ketamine.

Timing and drive components of respiration were studied in 18 young children following induction of anaesthesia with ketamine and were compared with results from ten children following induction of anaesthesia with halothane. During one minute of quiet breathing, signals from a pneumotachograph attached to the anaesthetic mask were analysed for tidal volume (Vt), respiratory frequency (f), minute volume (Ve), inspiratory and expiratory times (Ti, Te) and flow pattern. Following induction of anaesthesia with ketamine, children breathed more slowly and deeply than children receiving halothane, but there was no significant difference in Ve or in Vt/Ti, suggesting that respiratory drive was similar in the two groups of children. In the children receiving ketamine, Ti was more than twice as long, and thus the ratio Ti/Te was significantly increased, in comparison with the group receiving halothane. In addition to the prolonged Ti in the children induced with ketamine, there was a more rapid increase in volume in early inspiration than in late inspiration, which is an apneustic breathing pattern. There was a slower decrease in volume in early expiration, with occasional early expiratory breath holding lasting up to three seconds, in the ketamine-induced children. The unique breathing pattern demonstrated with ketamine, consisting of large Vt, increased Ti/Te ratio, apneustic inspiratory pattern, and expiratory braking, contributed to an increased mean lung volume above functional residual capacity, of 2.40 ml.kg-1 body weight, in comparison to 1.27 ml.kg-1 in the children receiving halothane.

Anesthesia, Inhalation↗
PubMed1999

Factitious halothane detection during trigger-free anesthesia in a malignant hyperthermia susceptible patient.

PURPOSE: To discuss the problems encountered when halothane was detected in a presumed 'clean' patient circuit during the 'trigger-free' anesthetic management of a known Malignant Hyperthermia Susceptible (MHS) patient for routine orthopedic surgery. CLINICAL FEATURES: A 29-yr-old MHS woman had a wrist arthroscopy/exploration/fusion under general anesthesia. During the course of the 'trigger-free' anesthetic the respiratory gas analyser detected end-tidal halothane in the patient circuit. The patient was disconnected from the circuit as attempts to identify the source of the readings were undertaken. After ruling out the presence of halothane by various clinical manoeuvre the patient was reconnected to the circuit without sequelae. CONCLUSION: By exclusion the problem was presumed to be a factitious reading resulting from the respiratory gas analyser incorrectly identifying patient-expired methane as halothane.

Adult↗
PubMed2001

Desflurane, compared to halothane, augments phenylephrine-induced contraction in isolated rat aorta smooth muscle.

PURPOSE: The mechanism responsible for the mediation of hypertension in response to increased desflurane levels is unclear. This study compared the effect of desflurane and halothane on phenylephrine (PE)-induced contraction in rat aorta ring and the effect of desflurane in the presence and absence of nitric oxide (NO) synthase activity. METHODS: Endothelium-free rat aorta rings were exposed serially to 10(-7) M, 10(-6) M and 10(-5) M PE alone and subsequently in the presence of 2 MAC desflurane and halothane. Secondly, endothelium-free preparations were exposed to 10(-6) M PE serially in the presence of 0, 1, 2 and 3 MAC desflurane and halothane. Thirdly, using an endothelium-intact preparation, the effect of desflurane on PE-induced contraction was examined, in the presence or absence of NG-nitro-L-arginine (L-NNA), an inhibitor of constitutive and inducible NO synthase. RESULTS: Contraction amplitudes secondary to 10(-6) and 10(-5) M PE in endothelium-free preparations were increased by 74% and 36% respectively (P <0.05) in the presence of 2 MAC desflurane compared to controls. In endothelium-free preparations, contraction amplitudes secondary to 10(-6) M PE were increased in the presence of 1 and 2 MAC desflurane by 32% and 18% respectively (P <0.05) and reduced by 16% in the presence of 3 MAC halothane (P <0.05). In endothelium-intact preparations an expected absolute increase in contraction amplitude occurred in the presence of L-NNA but the desflurane effect was detectable both in the presence and absence of L-NNA. CONCLUSION: Our results suggest that desflurane may have a local vasoconstrictive effect independent of endothelium and NO synthase activity. The mechanism remains to be determined.

Anesthetics, Inhalation↗
PubMed2006

Behavioural effects of chronic exposure to subanesthetic concentrations of halothane, sevoflurane and desflurane in rats.

BACKGROUND: A double-blind, randomized trial was conducted to determine the behavioural effects of chronic exposure to subanesthetic concentrations of halothane, sevoflurane and desflurane in rats. METHODS: Halothane, sevoflurane and desflurane group rats received 0.1%, 0.3%, and 0.6% concentrations in a flow rate of 3 L.min(-1) O(2) respectively. Control animals also received 3 L.min(-1) O(2) in another investigation room, which had the same properties as the study group rooms. Rats breathed inhaled agents or oxygen between 09:00-13:00 hr every day for 30 days. After 30 days of inhalation of subanesthetic doses of inhaled agents or oxygen, behavioural tests were applied. RESULTS: Tests of exploratory activity and curiosity (hole-board test), anxiety (elevated plus maze test) and learning and memory functions (multiple T maze test), demonstrated that chronic exposure to subanesthetic concentrations of all three anesthetics alters behavioural functions in rats. However, impairment of learning (P<0.05) and memory function (P<0.05) were greater in association with desflurane, in comparison to halothane and sevoflurane-treated rats. CONCLUSION: Chronic exposure to subanesthetic concentrations of halothane, sevoflurane and desflurane is associated with behavioural change in rats. Of the three drugs, desflurane was associated with the lowest learning and memory function test scores.

Analysis of Variance↗
PubMed2005

Halothane does not protect against vascular injury in isolated cerebral and mesenteric arteries.

PURPOSE: This study was designed to examine regional differences in the vascular injury induced by hydrogen peroxide (H2O2) and to determine its modulation by halothane in canine basilar and mesenteric arteries. METHODS: Rings of canine basilar and mesenteric arteries with intact endothelium were mounted in Krebs bicarbonate solution for isometric tension recording. The relaxation responses to substance P (10(-8) M) and sodium nitroprusside (SNP; 10(-8) to 10(-5) M) were examined before and after exposure to H2O2 (1 mM) for eight minutes in the presence or absence of halothane (2%), to evaluate the effects of oxidative injury on the endothelium-dependent and -independent relaxation. The contractile responses to KCl (30 mM) and prostaglandin (PG) F(2alpha) (3 x 10(-6) M) were also compared in rings with and without exposure to H2O2. RESULTS: After exposure to H2O2 the relaxant responses to substance P were significantly inhibited in basilar arteries (P < 0.01), but not in mesenteric arteries. Exposure to H2O2 also attenuated SNP-induced relaxation in basilar (P < 0.05), but not in mesenteric arteries. The attenuation of the contractile responses to KCl and PGF(2alpha) after H2O2 exposure was observed only in basilar arteries (P < 0.01). Simultaneous exposure to halothane did not affect the attenuation of these relaxant and contractile responses. Scanning electron microscopy revealed that H2O2 resulted in marked disruption of the endothelial layer in basilar arteries, compared to almost no morphological changes in mesenteric arteries. CONCLUSION: These results indicate that the endothelium and vascular smooth muscle of the basilar artery are more susceptible to oxidative stress than those of the mesenteric artery. Halothane, at clinically relevant concentrations, exerts no significant influence on this vascular injury.

Anesthetics, Inhalation↗
PubMed1979

Effect of halothane on the pulmonary vascular response to hypoxia in dogs.

The pulmonary vascular response to alveolar hypoxia with and without halothane exposure was measured in dogs. Hypoxia increased pulmonary artery pressure (Ppa) and pulmonary vascular resistance (PVR) so that in each case inverse linear relationships were found with arterial oxygen saturation. These responses were highly significant and reproduceable but varied greatly between individuals. Halothane administration resulted in an increased slope of PVR against oxygen saturation due to the fact that reduction in cardiac output exceeded the reduction in Ppa. An analysis of variance showed that it was possible to predict accurately the hypoxic PVR and Ppa responses under halothane anaesthesia from the control hypoxic responses. Animals with low PVR responses showed the greatest arterial oxygen desaturation with hypoxia, whereas high responders showed least oxygen desaturation. Thus it was possible to predict those individuals at risk from severe arterial oxygen desaturation under halothane anaesthesia.

Animals↗
PubMed1998

Effects of halothane, enflurane, isoflurane, and sevoflurane on slowly adapting pulmonary stretch receptor activity in anesthetized dogs.

The aim of this study was to evaluate the effects of halothane, enflurane, isoflurane, and sevoflurane on slowly adapting pulmonary stretch receptor (SAR) activity in dogs. Eight beagles were anesthetized with an intravenous injection of a mixture of urethane and alpha-chloralose as a basal anesthesia, then vagotomized, artificially ventilated, and chest opened. Single afferent activities from SARs were recorded from the peripheral nerve cut end of the left vagus. Changes in SAR activities with inhalation of halothane, enflurane, isoflurane, and sevoflurane at 1, 1.5, and 2 times the minimal alveolar anesthetic concentration (MAC) were measured, and differences in the discharges within and among four anesthetics were evaluated. As a result, two different types of SARs, low threshold SARs and high threshold SARs, were detected in this study. In all anesthetics, expiratory discharges of low threshold SARs decreased significantly in a dose-dependent manner, whereas inspiratory discharges did not change significantly at any anesthetic level. Discharges of high threshold SARs tended to decrease with increasing anesthetic level; however, no statistical significance was observed at any anesthetic level. Only one exception to these changes was observed at 1 MAC of halothane where no significant decrease in the expiratory discharge of low threshold SARs or significant increase in the discharge of high threshold SARs was induced against a control value. In conclusion, recent inhalation anesthetics, except for halothane at the light anesthetic level, tended to decrease SAR activities depending on the anesthetic level, suggesting attenuation of the Hering-Breuer inflation reflex.

Action Potentials↗
PubMed2004

The volatile anesthetics halothane and isoflurane differentially modulate proinflammatory cytokine-induced p38 mitogen-activated protein kinase activation.

PURPOSE: Volatile anesthetics affect the cardiovascular and immune systems. Toward a better understanding of the molecular mechanisms behind the modulation exerted by these agents, we focused on the effects of halothane and isoflurane on the activation of p38 mitogen-activated protein kinase (MAPK), which plays a critical role in the cellular responses to extracellular stimuli such as lipopolysaccharide (LPS) and proinflammatory cytokines, including tumor necrosis factor (TNF) and interleukin 1 (IL-1). METHODS: Human umbilical vein endothelial cells and HeLa cells, an established cell line, were examined by molecular biological methods. Cells were treated with proinflammatory compounds with or without the volatile anesthetics. p38 MAPK activation was investigated by Western blotting analysis with phosphospecific anti-p38 MAPK antibodies. RESULTS: Isoflurane activated p38 MAPK by itself, but halothane did not. Halothane or isoflurane augmented the LPS- and TNF-induced activation of p38 MAPK. In contrast, neither halothane nor isoflurane enhanced the p38 MAPK activation induced by IL-1. Neither of the anesthetics affected H(2)O(2) or MAPK kinase 3 (MKK3)-induced p38 MAPK activation. CONCLUSION: Our in vitro results indicate that the volatile anesthetics used in the clinical field and in animal experiments modify the p38 MAPK signaling cascade and suggest that the target molecules of the anesthetics are not unique and the anesthetics regulate them differentially at clinically relevant doses.

Anesthetics, Inhalation↗
PubMed1984

Myocardial depression by anesthetic agents (halothane, enflurane and nitrous oxide): quantitation based on end-systolic pressure-dimension relations.

The end-systolic pressure-diameter relation of the left ventricle was used to examine the effect of halothane, enflurane and nitrous oxide on left ventricular (LV) contractility in 10 dogs chronically instrumented with dimension transducers to measure LV diameter and micromanometers to measure LV transmural pressure. Contractility was assessed by the slope (EES) of the end-systolic pressure-diameter relation. A new index that identifies the dose of anesthetic necessary to depress the inotropic state by 20% (ID20) was calculated to be 0.63% for halothane and 1.55% for enflurane, indicating a greater apparent myocardial depressant effect of halothane than enflurane. However, when these agents were compared at equi-anesthetic concentrations by normalizing the ID20 to the minimal alveolar concentration of each drug, they had comparable degrees of myocardial depressant effects. This measurement technique was used in 7 patients undergoing coronary artery bypass grafting conducted under narcotic anesthesia showing that halothane induced a similar depression of contractility. The use of ID20 should allow reclassification of anesthetic agents according to their myocardial depressant effects.

Anesthesia↗
PubMed1978

Recurrent hepatitis following halothane exposures.

The existence of hepatotoxicity due to halothane remains subject to debate. Three cases are presented in which multiple exposures to halothane were followed in several instances by evidence of postoperative fever and/or hepatitis. In one case, hepatitis with bridging necrosis developed; the patient responded to long-term steroid therapy. In another, fulminant hepatic necrosis proved fatal. A brief review of halothane hepatitis is given. Otherwise unexplained fever and hepatitis following the use of halothane, especially if recurrent or accompanied by evidence of hypersensitivity, should contraindicate subsequent use of that drug.

Biopsy↗
PubMed1985

Effect of halothane on Ca2+-induced Ca2+ release from sarcoplasmic reticulum vesicles isolated from rat skeletal muscle.

Halothane induces the release of Ca2+ from a subpopulation of sarcoplasmic reticulum vesicles that are derived from the terminal cisternae of rat skeletal muscle. Halothane-induced Ca2+ release appears to be an enhancement of Ca2+-induced Ca2+ release. The low-density sarcoplasmic reticulum vesicles which are believed to be derived from nonjunctional sarcoplasmic reticulum lack the capability of both Ca2+-induced and halothane-induced Ca2+ release. Ca2+ release from terminal cisternae vesicles induced by halothane is inhibited by Ruthenium red and Mg2+, and require ATP (or an ATP analogue), KCl (or similar salt) and extravesicular Ca2+. Ca2+-induced Ca2+ release has similar characteristics.

Animals↗
PubMed1990

Proton flow along lipid bilayer surfaces: effect of halothane on the lateral surface conductance and membrane hydration.

Impedance dispersion in liposomes measures the lateral charge transfer of lipid membrane surfaces. Depending on the choice of frequency between 1 kHz and 100 GHz, relaxation of the counterions at the interface, orientation of the head group, and relaxation of the bound and free water are revealed. This study measured the impedance dispersion in dipalmitoylphosphatidylcholine (DPPC) liposomes at 10 kHz. The surface conductance and capacitance showed breaks at pre- and main transition temperatures. Below the pre-transition temperature, the activation energy of the ion movement was 18.1 kJ.mol-1, which corresponded to that of the spin-lattice relaxation time of water (18.0 kJ.mol-1). At temperatures between pre- and main transition it increased to 51.3 kJ.mol-1, and agreed with 46.2-58.0 kJ.mol-1 of the activation energy of the dielectric relaxation of ice. Because the present system was salt-free, the ions were H3O+ and OH-, hence, their behavior represents that of water. The above results show that below the pre-transition temperature, the conductance is regulated by the mobility of free ions, or the number of free water molecules near the interface. On the other hand when the temperature exceeded pre-transition, melting of the surface-bound water crystals became the rate-limiting step for the proton flow. Halothane did not show any effect on the ion movement when the temperature was below pre-transition. When the temperature exceeded pre-transition, 0.35 mM halothane (equilibrium concentration) decreased the activation energy of the ion movement to 29.3 kJ.mol-1. This decrease indicates that halothane enhanced the release of the surface-bound water molecules at pre-transition. The surface-disordering effect of halothane was also shown by depression of the pre-transition temperature and decrease of the association energy among head groups from 9.7 kJ.mol-1 of the control to 5.2 kJ.mol-1 at 0.35 mM.

1,2-Dipalmitoylphosphatidylcholine↗