Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental asthma was induced in 6 dogs previously sensitized to ascaris antigen by ventilating them with aerosolyzed ascaris antigen for 10 minutes. Pulmonary resistance was calculated from simultaneous pressure and flow measurements at a long volume 200 ml above functional residual capacity. Prior to administration of aerosolyzed ascaris antigen, pulmonary resistance was 2.35 +/- 0.56 (mean +/- SEM) cm H2O/L/sec in dogs anesthetized with thiopental. Twenty minutes after the end of ascaris antigen administration, pulmonary resistance was 5.72 +/- 1.29 in dogs given additional thiopental, 3.18 +/- 0.62 in dogs anesthetized with halothane (0.87% inspired concentration), and 3.03 +/- 0.60 in dogs anesthetized with enflurane (2.2% inspired concentration). These differences in responses of pulmonary resistance were statistically significant at 0.05 level. Halothane and enflurane were equally effective in decreasing pulmonary resistance in an ascaris antigen dog model of asthma.
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PMID:Halothane and enflurane protect against bronchospasm in an asthma dog model. 56 87

When Chinese hamster fibroblasts divide in the presence of halothane there is an increased incidence of cells with abnormal nuclei, both in mitosis and in interphase. The authors compared the effects of halothane and nitrous oxide separately and in combination. Nitrous oxide, 75 percent, alone had no significant effect compared with controls, less than 1.4 per cent of cells showing abnormalities, while halothane alone had a dose-dependent effect on both phases of the cell cycle. Halothane, 1 per cent, caused abnormalities in 7 per cent (SEM +/- 0.32) of cells in interphase and in 12 per cent (SEM +/- 0.95) of cells in mitosis, but the combination of 0.75 per cent halothane with 75 percent nitrous oxide produced 15 per cent (SEM +/- 0.68) abnormal cells in interphase and 22 per cent (SEM +/- 0.51) abnormal mitoses. Similar highly significant differences were obtained throughout the dose-response curves to as much as 4 per cent halothane in air and 2.35 per cent halothane in 75 per cent nitrous oxide. This appears to demonstrate synergism between halothane and nitrous oxide in the production of this particular side effect. In contrast, the effects of halothane and nitrous oxide on growth rate were additive.
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PMID:Synergism between halothane and nitrous oxide in the production of nuclear abnormalities in the dividing fibroblast. 127 13

Omega-oxidation of leukotrienes is the initial step of hepatic degradation and thus inactivation of these proinflammatory mediators. Omega-oxidation is followed by beta-oxidation of leukotrienes from the omega-end. After exposure of rats to a single dose of the anesthetic agent halothane, a transient decrease in leukotriene omega-oxidation was induced both in vivo and in vitro. In untreated rats, 44.1 +/- 6.0% of N-[3H]acetylleukotriene E4 injected intravenously was recovered unchanged in bile collected for 60 min in vivo; 46.5 +/- 3.0% was recovered as omega-/beta-oxidation products, of which 24.7 +/- 4.5% were associated with beta-oxidation products only (mean +/- SEM; n = 5). In rats receiving a single dose of halothane 18 h before the experiment, recovery of unchanged N-[3H]acetylleukotriene E4 was significantly increased to 79.8 +/- 4.8%, while the fraction of omega-/beta-oxidation products decreased to 9.0 +/- 1.7% (n = 5); 90 h after exposure to halothane, N-[3H]acetylleukotriene E4 recovery decreased to 30.0 +/- 3.0% and omega-/beta-oxidation products amounted to 49.1 +/- 3.8%; the fraction of beta-oxidation products was significantly increased to 43.1 +/- 3.4% (n = 5). Ten days after exposure of rats to halothane, the recoveries of N-[3H]acetylleukotriene E4, of omega-/beta-oxidation products, and of beta-oxidation products alone, returned to almost normal values. Microsomal fractions obtained from rat hepatocytes catalyzed the NADPH- and O2-dependent leukotriene omega-oxidation in vitro. The formation of omega-hydroxy-metabolites of leukotriene B4, leukotriene E4, and N-acetylleukotriene E4 was decreased by 50% in microsomal fractions obtained from rats 18 h and 90 h after halothane treatment, and returned back to control levels in microsomal fractions obtained 10 days after halothane treatment. The Km value of leukotriene B4 omega-oxidation revealed no significant change in enzyme affinity towards leukotriene B4; in contrast, as reflected by the reduction of the Vmax value by 65%, a decrease in the amount of the active enzyme in microsomes obtained from rats 18 h after halothane treatment was observed. Halothane-metabolism-dependent trifluoroacetylation of hepatic proteins may mediate this process. Thus, the time course of the density on immunoblots of trifluoroacetylated protein adducts paralleled that of the transient decrease in leukotriene omega-oxidation. In contrast to its omega-oxidation, leukotriene B4 synthesis from 5-hydroperoxyeicosatetraenoate was not inhibited in hepatocyte homogenates obtained from rats pretreated with halothane. The data suggest that metabolism of halothane causes a transient derangement of hepatic leukotriene homeostasis in vivo.
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PMID:Halothane metabolism. Impairment of hepatic omega-oxidation of leukotrienes in vivo and in vitro. 131 37

To determine whether anesthetics alter endothelial eicosanoid release, cultured bovine pulmonary artery endothelial cells were studied during constant flow and pressure perfusion at two oxygen tensions (hypoxia, 50 +/- 2 mm Hg; normoxia, 144 +/- 5 mm Hg; mean +/- SEM) with and without 1% halothane. Endothelialized microcarriers containing approximately 5 x 10(6) cells were loaded into cartridges and perfused (3 mL/min) with Krebs' solution (pH 7.4, at 37 degrees C) equilibrated with each gas mixture. Eicosanoids (6-keto prostaglandin F1 alpha, thromboxane B2, and total peptidoleukotrienes [C4, D4, E4, F4]) were measured by radioimmunoassay and quantified per gram of cellular protein per minute. Eicosanoid release did not vary over time. The 6-keto prostaglandin F1 alpha release increased during hypoxia (normoxia 291 +/- 27 vs hypoxia 395 +/- 35 ng.min-1 x g protein-1; P < 0.01). Halothane (H) increased release of each eicosanoid during both normoxia and hypoxia: 6-keto prostaglandin F1 alpha-normoxia 291 +/- 27 versus normoxia + H 356 +/- 32 ng.min-1 x g protein-1, hypoxia 395 +/- 35 versus hypoxia + H 464 +/- 40 ng.min-1 x g protein-1, P < 0.05; thromboxane B2-normoxia 19 +/- 2 versus normoxia + H26 +/- 2 ng.min-1 x g protein-1, hypoxia 20 +/- 2 versus hypoxia + H 38 +/- 5 ng.min-1 x g protein-1, P < 0.001; leukotriene-normoxia 363 +/- 35 versus normoxia + H 489 +/- 52 ng.min-1 x g protein-1, hypoxia 329 +/- 29 versus hypoxia + H 455 +/- 39 ng.min-1 x g protein-1, P = 0.001.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Halothane enhances pulmonary artery endothelial eicosanoid release. 144 80

The effects of halothane, isoflurane, and enflurane on proximal (false tendon) and distal (apical) canine Purkinje fibers were measured in vitro to assess their comparative effects on fibers exhibiting characteristically long (proximal) and short (distal) action potential duration. High- and low-dose anesthetic effects were evaluated in three groups of six left ventricular preparations and were compared with the changes occurring at identical times in six control preparations using analysis of variance with repeated measures. Under control conditions in all groups, the action potential duration, measured at 90% repolarization (APD90, mean +/- SEM), of proximal fibers was longer than that of distal fibers (320 +/- 16 vs 252 +/- 11 ms, P less than or equal to 0.01). Halothane (0.3 and 0.7 mM), isoflurane (0.4 and 0.8 mM), and enflurane (0.6 and 1.0 mM) produced a dose-dependent decrease (P less than or equal to 0.01) of proximal fiber APD90 with less (P less than or equal to 0.01) change of distal fiber APD90 and reduced (P less than or equal to 0.05) regional differences of APD90 at the higher dose. The decreases of proximal fiber APD90 were greater (P less than or equal to 0.01) for 1.0 mM (1.7 MAC) enflurane (-66 +/- 7 ms) and 0.8 mM (3.0 MAC) isoflurane (-69 +/- 9 ms) than for 0.7 mM (2.9 MAC) halothane (-33 +/- 8 ms). We conclude that the regional actions of anesthetics on Purkinje fiber repolarization may influence conduction during the relative refractory period and the occurrence of arrhythmias associated with disparity of regional refractory characteristics in the ventricular conduction system.
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PMID:Actions of halothane, isoflurane, and enflurane on the regional action potential characteristics of canine Purkinje fibers. 195 42

To determine whether halothane has protective effects on the ischemic heart, the influence of various concentrations (0.5%-1.5%) of halothane on metabolic and functional recovery during reperfusion after 60-min hypothermic (20 degrees C) and 40-min normothermic cardioplegic arrest was determined in the isolated rat heart. Halothane was administered either before and after arrest or intermittently during arrest. Hearts not receiving halothane demonstrated a reduction in adenosine triphosphate (ATP) content from a control value of 20.35 +/- 1.66 mumol/g dry wt (mean +/- SEM) (before arrest) to 9.34 +/- 1.12 mumol/g dry wt at the end of arrest (P less than 0.001). The myocardial ATP content, when measured 20 min after arrest and during reperfusion, remained decreased (9.57 +/- 0.62 mumol/g dry wt). Under these experimental conditions, aortic flow was reduced from 43.62 +/- 2.40 mL/min before arrest to 1.80 +/- 1.80 mL/min 20 min after arrest and during reperfusion (P less than 0.001). The administration of adrenaline after 20 min of reperfusion resulted in partial recovery to 22.01 +/- 8.36 mL/min. Administration of halothane (0.5%) before the cardioplegic period was associated with a reduction of ATP at the end of the normothermic arrest (4.02 +/- 0.38 mumol/g dry wt; P less than 0.01), but the ATP increased significantly (13.45 +/- 0.32 mumol/g dry wt) when measured after the arrest and after 20 min of reperfusion and stimulation with adrenaline.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Halothane does have protective properties in the isolated ischemic rat heart. 195 71

Halothane (1.3 MAC) and ethanol (0.4%) depress albumin synthesis in isolated perfused rat livers (IPRLs). Addition of amino acids prevents depression by ethanol. We have examined the effects of amino acids on albumin synthesis by IPRLs exposed to halothane. Seventeen livers were perfused with a mixture of rat erythrocytes and rabbit plasma. Five were exposed to oxygen/carbon dioxide alone and 12 to oxygen/carbon dioxide with 1.5% halothane. A mixture of 10 essential amino acids was added to the perfusate of six of the halothane-exposed livers to a concentration approximately 10 times the normal rat plasma level. Perfusate concentrations of newly synthesized albumin were measured by radial immunodiffusion, and the rate of synthesis for the 4.25-h study period was calculated. The mean +/- SEM albumin synthetic rate (mg/h per 300-g rat) in the control group (12.13 +/- 1.36) was significantly greater than in the group receiving halothane alone (6.98 +/- 0.92). Amino acid treatment failed to prevent halothane depression of albumin synthesis (8.68 +/- 0.84). Thus, although amino acids block ethanol depression of albumin synthesis, we could show no such effect in rat livers exposed to halothane.
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PMID:Amino acids fail to prevent halothane depression of albumin synthesis: studies in the isolated perfused rat liver. 198 65

The antidysrhythmic drug amiodarone may be given during general anesthesia. We examined the single and combined direct cardiac effects of amiodarone and halothane in the isolated guinea pig heart. Guinea pig hearts were isolated and perfused retrogradely through the aorta with oxygenated Krebs-Ringer solution at 37 degrees C at constant pressure (55 mm Hg). Variables measured in 61 hearts included spontaneous heart rate (HR), atrioventricular conduction time (AVCT), isovolumetric left ventricular pressure (LVP), and coronary flow (CF). Amiodarone was administered as a single bolus into the retrogradely perfused aortic root and halothane was vaporized into the perfusing solution. Mean control values of pooled data before treatment were as follows: HR, 228 +/- 4 (SEM) beats/min; AVCT (during atrial pacing at 240 beats/min), 82 +/- 2 ms; LVP, 97 +/- 4 mm Hg; and CF, 6.1 +/- 0.2 mL.min-1.g-1. Amiodarone, 100 micrograms and 200 micrograms, decreased HR by 8% +/- 2% and 8% +/- 2%, increased AVCT by 5 +/- 2 and 15 +/- 3 ms, decreased LVP by 22% +/- 3% and 27% +/- 3%, and increased CF by 20% +/- 1% and 40% +/- 2%, respectively; all these changes were sustained for 60 min and, except for HR, were dose dependent. Halothane, 0.5% and 1%, transiently and dose-dependently decreased HR by 6% +/- 2% and 12% +/- 2% increased AVCT by 4 +/- 2 and 8 +/- 2 ms, decreased LVP by 15% +/- 3% and 31% +/- 3%, and increased CF by 2% +/- 1% and 6% +/- 2%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Additive depressant effects of amiodarone given with halothane in isolated hearts. 200 39

Seventy-two adult surgical patients were studied to compare neuromuscular and cardiovascular effects of mivacurium chloride during nitrous oxide-fentanyl-thiopentone (BAL group) or nitrous oxide-halothane (HAL group) anaesthesia. Eighteen patients in the BAL group received an initial bolus of mivacurium, either the ED25 (n = 9) or the ED50 (n = 9) (0.03 and 0.05 mg kg-1). These doses were based on the assumption that the slope of the dose-response curve during nitrous oxide-opioid anaesthesia would be approximately the same as the slope of the neuromuscular response from the first human studies with mivacurium. Twenty-seven additional patients were allocated to subgroups of nine patients to receive mivacurium 0.04, 0.08 or 0.15 mg kg-1. Twenty-seven patients in the HAL group were allocated also to subgroups of nine patients to receive mivacurium 0.03, 0.04 or 0.15 mg kg-1. During stable anaesthesia, mean endtidal halothane concentrations were maintained at 0.49 +/- 0.01%. The estimated ED50, ED75 and ED95 for BAL and HAL groups were 0.039, 0.05 and 0.073 mg kg-1 and 0.040, 0.053 and 0.081 mg kg-1, respectively. Halothane did not potentiate maximum block or time to maximum block. Halothane did affect spontaneous recovery. With the 0.15-mg kg-1 dose, time to 95% recovery was prolonged significantly in the HAL group (30.0 (SEM 1.4) min) compared with the BAL group (24.1 (1.5) min). Recovery index from 25% to 75% recovery was also prolonged significantly in the HAL group (7.0 (0.4) min) compared with the BAL group (5.4 (0.4) min). There were no significant haemodynamic changes in groups given mivacurium doses up to and including 2 x ED95 by bolus i.v. administration.
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PMID:Neuromuscular and cardiovascular effects of mivacurium chloride (BW B1090U) during nitrous oxide-fentanyl-thiopentone and nitrous oxide-halothane anaesthesia. 213 90

Baroreflex sensitivity (BS) was used to quantitatively assess the effects of halothane and isoflurane on the heart rate/arterial pressure relationship during steady-state (10 minutes) and dynamic pressure changes in adult horses. Arterial pressure was decreased in response to nitroglycerin or sodium nitroprusside and increased in response to phenylephrine HCl. Mean (+/- SEM) BS in awake horses was 28.9 +/- 2.6 and 13.2 +/- 2.0 ms/mm of Hg during steady-state decreases and increases in systolic arterial pressure (SAP), respectively. Halothane and isoflurane either significantly (P less than 0.05) decreased or eliminated BS during steady-state decreases in SAP, with no significant differences detected between anesthetic agents. During steady-state decreases in SAP, significant (P less than 0.05) correlation between R-R interval and arterial pressure was not observed for 6 of 10 and 4 of 11 halothane and isoflurane anesthesia periods, respectively. Halothane significantly (P less than 0.05) decreased BS during steady-state increases in SAP to 7.9 +/- 0.6 and 6.5 +/- 1.1 ms/mm of Hg during low and high minimal alveolar concentration (MAC) multiples, respectively. Isoflurane decreased BS during steady-state increases in SAP to 9.6 +/- 1.5 and 6.6 +/- 1.1 ms/mm of Hg during low and high MAC anesthesia, respectively, with high MAC of isoflurane decreasing BS significantly (P less than 0.05), compared with awake and low MAC values. Plasma catecholamine (epinephrine and norepinephrine) concentrations increased significantly (P less than 0.05), compared with baseline values during steady-state vasodilator infusions in halothane- and isoflurane-anesthetized horses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of halothane and isoflurane on baroreflex sensitivity in horses. 261 Apr 41


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