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PubMed2002

Effect of halothane and isoflurane on binding of ADP- and TRAP-6- activated platelets to leukocytes in Whole blood.

BACKGROUND: Adhesion of activated platelets to neutrophils and monocytes has an important role in the regulation of inflammatory processes. This study investigates whether halothane and isoflurane affect binding of activated platelets to leukocytes in human whole blood. METHODS: Citrated whole blood was incubated for 60 min with either 1 or 2 minimum alveolar concentration (MAC) halothane or isoflurane. After stimulation with adenosine-5-diphosphate (ADP) or the thrombin receptor agonist protein TRAP-6, platelet-leukocyte adhesion and surface expression of CD62P on platelets were evaluated by flow cytometry. RESULTS: Halothane led to an inhibition of agonist-induced adhesion of activated platelets to neutrophils and monocytes. One MAC halothane reduced the formation of TRAP-6-induced platelet-monocyte conjugates. After exposure to 2 MAC halothane, agonist-induced platelet-monocyte and platelet-neutrophil adhesion were inhibited. Surface expression of CD62P on ADP- and TRAP-6-stimulated platelets were significantly reduced after 1 and 2 MAC halothane. After 2 MAC isoflurane, the authors observed an increase of the percentage of lymphocytes with bound platelets after activation with ADP. The percentage of neutrophils with bound platelets after activation with ADP or TRAP-6 was also increased in this group. Two MAC isoflurane led to an increase of the percentage of platelets expressing CD62P in the unstimulated and TRAP-6 stimulated samples, and of the amount of CD62P epitopes on the surface of platelets in the ADP-stimulated samples. CONCLUSION: This study indicates that halothane inhibits, whereas isoflurane enhances, adhesion of agonist-activated platelets to leukocytes. Interaction of both anesthetics with the expression of CD62P on platelets contribute to theses effects.

Adenosine Diphosphate↗
PubMed2002

Effects of halothane and enflurane anesthesia on sympathetic beta-adrenoreceptor-mediated pulmonary vasodilation in chronically instrumented dogs.

BACKGROUND: The authors previously reported that the pulmonary vasodilator response to the sympathetic beta-adrenoreceptor agonist isoproterenol is potentiated during isoflurane anesthesia compared with the conscious state. In the present in vivo study, the authors tested the hypothesis that halothane and enflurane anesthesia also enhance sympathetic beta adrenoreceptor-mediated pulmonary vasodilation. The authors also used the membrane-permeable analog of cyclic adenosine monophosphate (cAMP), dibutyryl cAMP, to help delineate the site in the signaling pathway for an anesthesia-induced effect on beta adrenoreceptor-mediated pulmonary vasodilation. METHODS: Mongrel dogs were chronically instrumented to measure the left pulmonary vascular pressure-flow (LPQ) relationship. LPQ plots were measured on separate days in the conscious, halothane-, and enflurane-anesthetized states at baseline, after preconstriction with the thromboxane analog U46619, and during the cumulative intravenous administration of isoproterenol. LPQ plots were also measured in conscious, halothane-, and isoflurane-anesthetized dogs after U46619 preconstriction and during the cumulative intravenous administration of dibutyryl cAMP. RESULTS: Compared with the conscious state, neither halothane nor enflurane had an effect on the baseline LPQ relationship. The magnitude of the pulmonary vasodilator response to isoproterenol was potentiated during halothane anesthesia but unchanged during enflurane anesthesia. The pulmonary vasodilator response to dibutyryl cAMP was not altered during either halothane or isoflurane anesthesia compared with the conscious state. CONCLUSIONS: These results indicate that inhalational anesthetic agents can exert differential effects on the pulmonary vasodilator response to sympathetic beta-adrenoreceptor activation. The potentiated vasodilator response observed during halothane and isoflurane anesthesia is the result of effects proximal to cAMP accumulation in the beta-adrenoreceptor signaling pathway.

Anesthesia, Inhalation↗
PubMed2003

Dual effects of hexanol and halothane on the regulation of calcium sensitivity in airway smooth muscle.

BACKGROUND: Contraction of airway smooth muscle is regulated by receptor-coupled mechanisms that control the force developed for a given cytosolic calcium concentration (i.e., calcium sensitivity). Halothane antagonizes acetylcholine-induced increases in calcium sensitivity by inhibiting GTP-binding (G)-protein pathways. The authors tested the hypothesis that hexanol, like halothane, inhibits agonist-induced increases in calcium sensitivity in airway smooth muscle by inhibiting G-protein pathways. METHODS: Calcium sensitivity was assessed using alpha-toxin-permeabilized canine tracheal smooth muscle. In selected experiments, regulatory myosin light chain phosphorylation was also determined by Western blotting in the presence and absence of 10 mm hexanol and/or 100 microm acetylcholine. RESULTS: Hexanol (10 mm) and halothane (0.76 mm) attenuated acetylcholine-induced calcium sensitization by decreasing regulatory myosin light chain phosphorylation during receptor stimulation. Hexanol also inhibited increases in calcium sensitivity due to direct stimulation of heterotrimeric G-proteins with tetrafluoroaluminate but not with 3 microm GTPgammaS, consistent with prior results obtained with halothane. In contrast, in the absence of receptor stimulation, both compounds produced a small increase in calcium sensitivity by a G-protein-mediated increase in regulatory myosin light chain phosphorylation that was not affected by pertussis toxin treatment. CONCLUSIONS: The authors noted dual effects of hexanol and halothane. In the presence of muscarinic receptor stimulation, hexanol, like halothane, decreases calcium sensitivity by interfering with heterotrimeric G-protein function. However, in the absence of muscarinic receptor stimulation, hexanol and halothane slightly increase calcium sensitivity by a G-protein-mediated process not sensitive to pertussis toxin. Hexanol may represent a useful experimental tool to study the effect of anesthetics on heterotrimeric G-protein function.

Aluminum Compounds↗
PubMed2003

Halothane inhibits an intermediate conductance Ca2+-activated K+ channel by acting at the extracellular side of the ionic pore.

BACKGROUND: Actions of volatile anesthetics on ligand-gated ion channels, such as gamma-aminobutyric acid type A receptors, have been studied extensively. However, actions on other types of channels, such as K+ channels, are poorly understood. The authors previously showed that a Ca2+-activated K+ channel, IK, is sensitive to halothane, whereas SK1, another Ca2+-activated K+ channel, is insensitive. To explore how halothane acts on Ca2+-activated K+ channels, chimeras between IK and SK1 were constructed, and halothane sensitivity was analyzed. METHODS: IK, SK1, and chimera channels were expressed in Xenopus laevis oocytes. Currents of expressed channels were measured in the presence of 10 microm Ca2+ by excised patch clamp analysis. Time constants of inhibition by halothane were compared between inside-out and outside-out patch configurations. RESULTS: Currents from chimera channels possessing the pore domain derived from IK were inhibited by halothane, whereas those possessing the SK1 pore domain were insensitive. Time constants of inhibition by halothane were significantly smaller in the outside-out patches than in the inside-out patches of both wild-type IK and a chimera with pore domain of IK. CONCLUSIONS: It is suggested that halothane interacts with the extracellular part of the ionic pore of IK. Whether this type of interaction is involved in the mechanism of anesthetic actions on ligand-gated ion channels warrants further investigation.

Anesthetics, Inhalation↗
PubMed2004

Myocardial effects of halothane and sevoflurane in diabetic rats.

BACKGROUND: Diabetes induces significant myocardial abnormalities, but the effects of halogenated anesthetics on this diseased myocardium remain a matter of debate. METHODS: Left ventricular papillary muscles and triton-skinned cardiac fibers were provided from control and streptozotocin-induced diabetic rats. The effects of halothane and sevoflurane were studied on inotropic and lusitropic responses, under low (isotony) and high (isometry) loads in papillary muscles and then on isometric tension-Ca2+ concentration (pCa) relations obtained in triton-skinned cardiac fibers. Data are presented as mean +/- SD. RESULTS: Sevoflurane and halothane induced a negative inotropic effect that was more important in diabetic rats (active force: 1.5% halothane, 19+/-6 vs. 24+/-6% of baseline, P < 0.05; 3.6% sevoflurane, 47+/-14 vs. 69+/-17% of baseline, P < 0.05). However, when differences in minimum alveolar concentration were considered, no significant difference was observed between groups for halothane. The effects of halothane and sevoflurane on isotonic relaxation and postrest potentiation were not significantly different between groups. In contrast, the decrease in Ca myofilament sensitivity produced by each anesthetic agent was greater in diabetic rats than in control rats (0.65% halothane, -0.15+/-0.07 vs. -0.05+/-0.04 pCa unit, P < 0.05; 1.8% sevoflurane, -0.12+/-0.06 vs. -0.06+/-0.04 pCa unit, P < 0.05). CONCLUSIONS: The negative inotropic effect of halothane and sevoflurane was greater in diabetic rats, mainly because of a significant decrease in myofilament Ca sensitivity.

Animals↗
PubMed2005

Effect of halothane on galphai-3 and its coupling to the M2 muscarinic receptor.

BACKGROUND: Halothane is an effective bronchodilator and inhibits airway smooth muscle contraction in part by inhibiting intracellular signaling pathways activated by the M2 muscarinic receptor and its cognate inhibitory heterotrimeric guanosine-5'-triphosphate (GTP)-binding protein (G protein), Gi. This study hypothesized that halothane inhibits nucleotide exchange at the alpha isoform-3 subunit of Gi (Galphai-3), but only when regulated by the M2 muscarinic receptor. METHODS: GTP hydrolysis by Galphai-3 and the Galphai-3beta1gamma2HF heterotrimer expressed in Spodoptera frugiperda cells was measured using a phosphohydrolase assay with [gammaPi]-labeled GTP. Anesthetic binding to Galphai-3 was measured by saturation transfer difference nuclear magnetic resonance spectroscopy. Galphai-3 nucleotide exchange was measured in crude membranes prepared from COS-7 cells transiently coexpressing the M2 muscarinic receptor and Galphai-3. A radioactive analog of GTP, [S]GTPgammaS, was used as a reporter for Galphai-3 nucleotide exchange. RESULTS: Although spectroscopy demonstrated halothane binding to Galphai-3, this binding had no effect on [gammaPi]-labeled GTP hydrolysis by the Galphai-3beta1gamma2HF heterotrimer expressed in Spodoptera frugiperda cells, nor basal Galphai-3 nucleotide exchange measured in crude membranes when the muscarinic receptor agonist acetylcholine was omitted from the assay. Conversely, halothane caused a concentration-dependent inhibition of Galphai-3 nucleotide exchange with acetylcholine included in the assay. CONCLUSION: These data indicate that despite halothane binding to Galphai-3, halothane has no direct inhibitory effect on the intrinsic activity of the Galphai-3beta1gamma2HF heterotrimer but inhibits M2 muscarinic receptor regulation of the heterotrimer. This novel effect is consistent with the ability of halothane to inhibit airway smooth muscle contraction and bronchoconstriction induced by acetylcholine.

Acetylcholine↗
PubMed1999

Microcirculatory response to halothane and isoflurane anesthesia.

Microcirculatory hemodynamics are often used to monitor tissue and organ survival. This study investigated the effect of halothane and isoflurane anesthesia on peripheral microcirculation using the cremaster muscle during intravital microscopy. Twenty-three Sprague-Dawley rats were studied in four groups. Two groups served as controls and did not undergo flap isolation but did receive halothane (N = 6) or isoflurane (N = 5). After induction with a single dose of intraperitoneal pentobarbital (40 mg per kilogram), rats were ventilated with either 2 minimum alveolar concentration (MAC) halothane or 2 MAC isoflurane. Esophageal temperature, electrocardiography, central venous pressure, mean arterial pressure, and blood gases were measured over 4 hours. In groups receiving surgery with either halothane (N = 6) or isoflurane (N = 6), the cremaster muscle was isolated on the neurovascular pedicle. Microcirculatory responses to both halothane and isoflurane anesthesia were evaluated by measuring red blood cell (RBC) velocity, vascular diameters in arterioles (A1, A2-1, A2-2, and A3) and the main venule (V1), functional capillary perfusion, and leukocytic endothelial interactions in postcapillary venules (rolling, adherent, and transmigrating leukocytes). Hemodynamic variables were compared among all four groups, and microcirculatory variables were compared between the two surgical groups. During isoflurane anesthesia in animals with flaps, significantly higher (p < 0.05) RBC velocities were recorded in arterioles A1 (24.4%), A2-2 (28.2%), and A3 (17.4%). Capillary perfusion was significantly higher in animals with flaps and halothane anesthesia (17.8%; p < 0.05). The number of rolling leukocytes (39.4%) was significantly higher during isoflurane anesthesia in animals with flaps (p < 0.05). Better flow hemodynamics in the peripheral microcirculation were seen during halothane anesthesia, and were confirmed by greater functional capillary perfusion and fewer activated leukocytes. In the isoflurane group, RBC velocity alone cannot serve as an indicator of microcirculatory function.

Anesthesia, General↗
PubMedDate not supplied

Effect of halothane on contractile function of ischemic myocardium.

Effects of halothane on the force of myocardial contraction and energy demand-supply balance (NADH fluorescence) were studied in two rabbit heart preparations--the interventricular septum perfused through the septal artery at various flow levels, and a Langendorff whole-heart preparation with ischemia caused by graded reduction of perfusion pressure. The septum experiments showed that halothane [1.2% = 1.5 minimum alveolar concentration of anesthetic preventing movement response to a noxious stimulus (MAC)] increased NADH fluorescence (+9%, p less than 0.02) at a normal level of perfusion (3 ml/g/min) and, at the same time, decreased it (-6%, p less than 0.02) when myocardial energy balance deteriorated from severe hypoperfusion (0.2 ml/g/min). The inhibitory effect of halothane on developed systolic tension was less pronounced at the low (ischemic) level of myocardial perfusion as compared with the high level--leads to 24% (0.2 ml/g/min) vs. leads to 38% (3 ml/g/min), p less than 0.025. However, if control and halothane values of developed tension were compared at equi-NADH levels (the same state of energy balance), the depressive effect of halothane on the force of myocardial contraction was not less pronounced in severe energy imbalance. Similar results were obtained in the Langendorff preparation experiments. The results suggest that halothane partially restores energy balance in hypoperfused myocardium; however, at the normal level of perfusion, its effect is in an opposite direction. Halothane depresses contractility in the hypoperfused myocardium to a lesser degree than at the normal level of myocardial perfusion. This effect is probably determined by the interaction of two influences: direct depressive effect of the agent on contractile mechanisms, and indirect positive inotropic effect due to improvement in energy balance.

Animals↗
PubMed1993

Effects of halothane on beta-adrenoceptors and M-cholinoceptors in human myocardium: radioligand binding and functional studies.

We investigated whether a postsynaptic sensitization by halothane for beta-adrenoceptor-mediated effects occurs in diseased human myocardium. In addition, we hoped to achieve further insights into the cellular mechanism and, in particular, the role of M-cholinoceptors and beta-adrenoceptors. The experiments were performed on isolated, electrically driven atrial and ventricular preparations and membranes isolated from human hearts obtained at cardiac surgery. Halothane concentration-dependently reduced binding of [3H]quinuclidinylbenzilate ([3H]QNB) to M-cholinoceptors but had no effect on equilibrium saturation binding of 125-iodocyanopindolol (125I]Cyp) to beta-adrenoceptors. High-and low-affinity states of agonist binding of carbachol to M-cholinoceptors were not affected, but halothane inhibited high-affinity binding of isoprenaline to beta-adrenoceptors. In contrast, halothane augmented the potency and efficacy of the positive inotropic effect of isoprenaline in atrial and ventricular myocardium. The "direct" negative inotropic effect in atrial and the "indirect" negative inotropic effect in ventricular myocardium by M-cholinoceptor stimulation with carbachol was unchanged by halothane. We conclude that in human atrial and ventricular myocardium a sensitization to catecholamines is induced by halothane, the mechanism of which is likely to be located at the postsynaptic level of the sympathetic neuroeffector junction. Facilitated coupling of beta-adrenoceptors or an uncoupling of M-cholinoceptors with reduced negative inotropic effects of agonist does not play a role. We showed that sensitization of this system apparently is due to direct actions of halothane on the G-protein-coupled adenylate cyclase complex.

Catecholamines↗
PubMed1994

Effect of halothane on in vivo and in vitro cardiotoxicity of an aminocardenolide.

Halothane opposes cardiotoxicity of neutral-sugar digitalis compounds in intact animals, presumably by depressing a sympathetic component of arrhythmogenesis. However, halothane also produces a dose-related reduction in arrhythmogenicity of ouabain in isolated canine Purkinje fibers, suggesting that the anesthetic may oppose direct mechanisms of cardiotoxicity as well. The present study examined in vivo and in vitro the effect of halothane on the arrhythmogenicity of ASI-222 (3-beta-O[4-amino-4-6-dideoxy-beta-D-galactopyranosyl] digitoxigen in HCl), a highly polar aminocardenolide with no sympathetic component to cardiotoxicity. For in vivo studies, ASI-222 was infused at a rate of 1 microgram/kg/min until appearance of third-degree atrioventricular (AV) block or sustained ventricular arrhythmias in 5 conscious (control) and 6 halothane-anesthetized (1.4% end-tidal) dogs. For in vitro studies, standard microelectrode techniques were used to measure action potentials (AP) in seven excised canine Purkinje fibers superfused with oxygenated Krebs-Henseleit buffer. AP were recorded during control superfusion, after induction of toxicity with 10(-7) M ASI-222, and during exposure to 0.5, 1.0, and 2.0% halothane. Purkinje fibers were paced at 500-ms cycle lengths (CL) for 20 beats, and the amplitude of delayed afterdepolarizations (DAD) were recorded. Pacing at 250 ms CL was used to trigger ectopy. In vivo studies showed no difference in the cardiotoxic dose of ASI-222 between control dogs and those anesthetized with 1.4% halothane. However, in 4 of 6 anesthetized dogs, acutely increasing the inspired halothane concentration suppressed arrhythmias once end-tidal concentration were >2.2%.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1995

The role of nitric oxide in cerebrocortical laser Doppler flow response to halothane in the rat.

Laser Doppler flowmetry was utilized to investigate whether nitric oxide (NO) plays a role in the cerebrocortical hyperemic effect of halothane in rats. A particular objective was to elucidate whether the increased vascular tone or the removal of basal NO secondary to NO synthase inhibition influenced the response to halothane. The animals were anesthetized with i.p. pentobarbital for surgery and 90 min later were ventilated with 1.0 minimum alveolar concentration (MAC) halothane for 1 h to achieve a steady-state baseline. The control group was infused with either 1 ml of saline or 20 mg/kg of D-NAME, and the treatment group received 20 mg/kg of L-NAME intravenously. In a subset of the treatment group, we restored baseline flow and vascular tone using i.v. sodium nitroprusside (SNP). Mean arterial pressure (MAP) was maintained constant with an infusion of phenylephrine (0.5-5 micrograms/kg/min). Then, 30 to 45 min later, inspired halothane was raised to 1.7 MAC in each group, and the increase in laser Doppler flow (LDF) was measured. On increasing halothane MAC in the control group, LDF increased by 28 +/- 4%. L-NAME increased MAP by 21 +/- 4% and reduced baseline LDF by 26 +/- 2%. In the L-NAME-only treated group, 1.7 MAC halothane increased LDF by 12 +/- 3%, significantly less than control. The decrease in cerebrovascular resistance induced by increasing inspired halothane MAC was similar in the control group and in the L-NAME treated group at 23 +/- 6% and 22% +/- 7, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthetics, Inhalation↗
PubMed2000

Inhibitory effects of halothane, isoflurane, sevoflurane, and pentobarbital on the constriction induced by hypocapnia and bicarbonate in isolated canine cerebral arteries.

The effects of halothane, isoflurane, sevoflurane (0.5, 1 and 2 MAC) and pentobarbital (10(-5) M, 10(-4) M and 3 x 10(-4) M) on hypocapnia- and bicarbonate-induced constriction of isolated dog middle cerebral arteries were investigated in vitro. The isometric tension of isolated cerebral arterial rings was measured in an organ bath containing Krebs bicarbonate solution, aerated with 5% CO2 and 95% O2. Hypocapnia, induced by replacing the bathing solution with one that had been equilibrated with 2.5% CO2 and 97.5% O2, produced a sustained vasoconstriction (268 +/- 36 mg, mean +/- SEM). Exposure of arterial rings to a bathing solution that contained double the concentration of NaHCO3 (50 mM) elicited a phasic constriction followed by a gradual decrease in tension (309 +/- 34 mg). Although halothane, isoflurane, and sevoflurane attenuated both hypocapnia- and bicarbonate-induced constrictions in a dose-dependent manner, the inhibition of these constrictions was greater in rings treated with halothane than in those treated with isoflurane or sevoflurane when compared at equipotent concentrations. These alkaline-induced constrictions were attenuated by pentobarbital only at the highest concentration of 3 x 10(-4) M. Halothane (1 and 2 MAC) attenuated the constriction induced by hypocapnia to a greater extent than that induced by 15 mM KCl, whereas pentobarbital (10(-4) M and 3 x 10(-4) M) attenuated hypocapnia-induced constriction less than KCl-induced constriction. These results indicate that alkaline-induced constriction is more vulnerable to halothane than other volatile anesthetics and pentobarbital. The mechanisms of the inhibitory effects of halothane and pentobarbital on alkaline-induced cerebral vasoconstriction seem to differ; the inhibitory effect of pentobarbital, but not of halothane may be, in part, ascribed to its inhibitory effect on the Ca++ influx.

Anesthetics, Inhalation↗
PubMed1984

Accumulation of thymol in halothane vaporizers.

Thymol may accumulate in halothane vaporizers and influence their accuracy. We determined the thymol concentration in residual liquid halothane of 28 vaporizers in regular use. Two halothane samples were brownish, probably due to a long exposure to light and irregular drainage. Irregularly drained vaporizers contained higher thymol concentrations than those drained weekly (p less than 0.05). The highest individual thymol concentration was 19 times that found in fresh halothane. Halothane vapour concentration deviated most from setting in Fluotec Mark II vaporizers, but this did not correlate with thymol concentrations in halothane liquid. The need for weekly drainage and regular service of halothane vaporizers is stressed.

Anesthesia, Inhalation↗
PubMed1976

The effect of halothane anaesthesia upon cerebral oxygen consumption in the rat.

The influence of halothane (0.6 and 2%) upon cerebral (cortical) blood flow (CBF) and cerebral metabolic rate for oxygen (CMRo2) was studied in artificially ventilated rats, using a modified technique of Kety & Schmidt (1948). The values obtained in halothane anaesthesia were compared to those recorded in nitrous oxide anaesthesia, or to those measured in unanesthetized animals given an analgesic drug (fentanyl citrate). Although it could be confirmed that halothane induces vasodilatation in the brain, there were relatively small differences in CBF between the groups. The results demonstrate that, in the rat, halothane depresses CMRo2 in a dose-dependent way. With 0.6% halothane, CMRo2 was reduced by 20-30% and, with 2% halothane, CMRo2 was reduced by about 50%. Thus, in the rat the effect of 2% halothane upon metabolic rate is comparable to that observed in barbiturate anaesthesia.

Anesthesia, Inhalation↗
PubMed1978

The combined effects of antihypertensive drugs and anaesthetics (halothane and ketamine) on the isolated heart.

The effects of three concentrations of halothane or ketamine were investigated on isolated rabbit hearts, which were perfused with hydralazine, clonidine, propranolol or methyldopa. In hearts not subjected to the influence of an anaesthetic, clonidine was the only drug stimulating myocardial function. In those perfused with halothane or ketamine alone, both anaesthetics exerted a negative chronotropic and inotropic action in a dose-related manner. Ketamine markedly increased the coronary flow. Clonidine distinctly reduced the myocardial depression caused by halothane or ketamine. Hydralazine had no marked effects with either of these anaesthetics, except that it sensitized the hearts to the arrhythmic action of a high concentration of halothane. Propranolol, when combined with halothane, aggravated myocardial depression and decreased coronary flow. With ketamine, propranolol caused no other harmful interactions, apart from inhibiting the increase in coronary flow caused by this anaesthetic. Methyldopa intensified the myocardial depression induced by halothane, but tended to diminish that caused by ketamine. The results suggest that clonidine has a stimulatory cardiac action when combined with either of these anaesthetics. Disadvantageous interactions may exist between methyldopa or propranolol and halothane.

Animals↗
PubMed1981

Baroreceptor control of systemic haemodynamic at incremental halothane levels in the dog.

The open-loop carotid sinus reflex control of systemic haemodynamics was studied in an acute dog preparation with isolated perfused carotid sinuses at three end-tidal halothane levels of 0.66 +/- 0.02% (HI); 0.88 +/- 0.02% (H2); and 1.17 +/- 0.02% (H3), in order to investigate the dose dependency of the carotid sinus reflex operating characteristics for halothane. Corresponding to the above halothane levels were reflex operating point pressures (set point pressures) of 104.9 +/- 2.9, 103.3 +/- 4.1 and 76.0 +/- 3.8 mmHg, respectively. Carotid sinus reflex gain decreased significantly with progressively increasing halothane levels (1.4. +/- 0.18; 0.84 +/- 0.12; 0.48 +/- 0.09), as did the range of reflex changes in systemic arterial pressure for equal overall changes in carotid sinus pressure (87.1 +/- 7.9; 64.1 +/- 7.4; 33.6 +/- 5.1 mmHg; P less than 0.01). For halothane levels below approximately 0.9%, this depression was not dependent upon changes in mean systemic arterial pressure. The relationship between reflex gain and halothane concentration could be described by a first-order exponential which suggested virtual ablation of the carotid sinus reflex control of mean arterial pressure at an end-tidal halothane concentration exceeding about 1.6%.

Animals↗
PubMed1983

Attenuation of the cardiovascular intubation response with N2O, halothane or enflurane.

The circulatory intubation response was studied in 75 normotensive, otolaryngological patients after a thiopentone-suxamethonium induction followed by 2 min artificial ventilation with 100% oxygen (control), 70% nitrous oxide in oxygen (N2O), halothane 2% with N2O, enflurane 3% with N2O or enflurane 5% in oxygen. The above study groups (n = 15) were chosen after preliminary experiments performed in 25 different patients with halothane 2% (n = 8) or enflurane 3% (n = 6) in oxygen, which did not prevent the increase of arterial pressure after intubation, or with halothane 3% (n = 11) which attenuated the pressor response but caused cardiac arrhythmias in 55% of patients. Enflurane 5% in oxygen attenuated the increase of systolic arterial pressure by 53%, enflurane 3% with N2O by 34% and halothane 2% with N2O by 31%. The increase in heart rate after intubation was lowest in the halothane 2% with N2O group, but there were no statistically significant differences between the groups. Cardiac arrhythmias were commonest in the enflurane 3% with N2O group (20%) and they did not occur in the halothane 2% with N2O group. Considering the total effect on arterial pressure, heart rate and rate-pressure product, we recommend the combination of halothane 2% with N2O.

Adolescent↗
PubMed1985

Halothane-relaxant anaesthesia in elderly patients.

Twenty-three elderly patients, scheduled for elective cholecystectomy, were studied during halothane-relaxant anaesthesia. Anaesthesia was induced with thiopentone and maintained with halothane in 12 patients, six of whom had also received premedication. Eleven patients were anaesthetized with halothane, without thiopentone induction and with no premedication. Measurements of central haemodynamics were performed awake and during anaesthesia at end-tidal halothane concentrations of 0.5 and 1.0%; at the lower concentration, measurements were also made after addition of nitrous oxide. Premedication and thiopentone had no influence on the subsequent halothane anaesthesia. Halothane caused reductions of cardiac index, mean arterial blood pressure and oxygen uptake. However, neither right atrial nor pulmonary capillary venous pressure increased and the arterio-venous oxygen content difference decreased. These findings differ from those made by others in younger subjects and are probably attributable to a dose-dependent reduction in systemic vascular resistance. The addition of nitrous oxide had only minor effects on central circulation. The results suggest that the age of the patients influences their reaction to halothane anaesthesia.

Aged↗