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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using the open ventriculocisternal perfusion method, the rate of cerebrospinal fluid (CSF) production was examined in dogs anesthetized with either halothane (0.8%) or fentanyl (3.0 micrograms/kg/min for 20 min, then 0.2 micrograms/kg/min, intravenously), and nitrous oxide (60-70%) in oxygen. Halothane decreased the mean rate of CSF production from 0.047 +/- 0.006 ml/min (mean +/- SEM) in controls to 0.033 +/- 0.005 ml/min. This effect persisted throughout 3.0-3.5 h of anesthesia. When the expired concentration of halothane was decreased from 0.8% to less than 0.1%, the mean rate of CSF production returned to control values within 45-50 min. Fentanyl produced no change in the mean rate of CSF production compared to controls. These data suggest that increased CSF volume does not contribute to increased intracranial pressure during prolonged halothane anesthesia. In patients at risk for increased intracranial pressure due to increased CSF volume, either halothane or fentanyl may be preferable to anesthetics that may increase CSF production, e.g., enflurane.
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PMID:Effects of halothane and fentanyl on the rate of CSF production in dogs. 684 81

The effect of halothane on the availability of different sources of activator calcium for myocardial contraction was evaluated in relationship to the negative inotropic effect on the anesthetic. This was studied in rabbit papillary muscle under various stimulation conditions that are known to vary the importance of one or another of two sources of Ca2+ for production of contraction. The rested-state contraction is known to depend primarily on the transsarcolemmal influx of Ca2+ for its activation whereas the potentiated-state contraction is dependent largely on Ca2+ released from intracellular stores. In the presence of 0.6% halothane (gas phase) the rested-state and potentiated-state contractions were depressed (mean +/- SEM) 38% +/- 5% (n = 15) and 32% +/- 3% (n = 7), respectively (no statistically significant difference). Halothane accelerated the decay of the potentiated state, indicating that it stimulates the loss of Ca2+ from internal stores. Halothane also acted to slow the time course of force increase following restimulation of rested muscles, indicating that it inhibits the filling of internal stores. These observations suggest that the negative inotropic effect of halothane is caused by a combination of quantitatively similar effects of the anesthetic on the transsarcolemmal and intracellular sources of activator Ca2+.
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PMID:Effect of halothane on rested-state and potentiated-state contractions in rabbit papillary muscle: relationship to negative inotropic action. 719 62

Acute myocardial infarction was induced by ligation of the anterior descending branch of the left main coronary artery in greyhound dogs anaesthetized with pentobarbitone. Blood flow in the area of ischaemia was measured by xenon clearance and compared with flow in the circumflex artery measured with electromagnetic flow meters. Halothane 1% produced an approximate 40% reduction in flow to both ischaemic and normal areas in association with a 20% reduction in collateral perfusion pressure and a 40% reduction in mean arterial pressure. Comparison of the percentage change in the ratio of oxygen availability/consumption in response to halothane revealed a significant difference between the ischaemic and the normal areas. The former increased to 113 +/- 9.3% (mean +/- SEM) whilst the latter decreased to 91 +/- 5.02%. This suggests that, in the non-failing heart, halothane improves oxygenation in areas of acute myocardial ischaemia.
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PMID:Halothane improves the balance of oxygen supply to demand in acute experimental myocardial ischaemia. 742 28

We have shown previously that inhalation anaesthetics inhibit dopamine transport in rat synaptosomes. In order to determine if this inhibition is associated with occupancy of the cocaine site, we examined binding of [3H] (2 beta-carbomethoxy-3 beta-(4-fluorophenyl)-tropane) (3H-CFT) in the presence of halothane or isoflurane 0.01-5 mmol litre-1 in rat brain synaptosomes. Both anaesthetics inhibited 3H-CFT binding (mean Ki 0.61 (SEM 0.12) and 0.75 (0.21) mmol litre-1, respectively), by increasing Kd (13.8 (0.6) and 29.8 (12.8) nmol litre-1, respectively) compared with control (8.02 (0.5) nmol litre-1) (P < 0.01). Halothane did not change Bmax, but isoflurane increased it significantly. Cocaine protected CFT sites from N-ethylmaleimide alkylation, but neither anaesthetic did. Photoaffinity labelling with halothane significantly inhibited 3H-CFT binding compared with UV-exposed controls. We conclude that clinically relevant concentrations of both anaesthetics inhibit high-affinity CFT binding, and the data suggest overlapping sites for halothane and CFT.
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PMID:Inhalation anaesthetic competition at high-affinity cocaine binding sites in rat brain synaptosomes. 788 Jun 73

The effects of sevoflurane and halothane on reperfusion-induced arrhythmia in the isolated rat heart were examined. Reperfusion-induced ventricular fibrillation (VF) occurred in all rat hearts, and the duration of VF was 151 +/- 11 (mean +/- SEM) seconds in the control group (no anesthetics administered). Sevoflurane changed neither incidence nor duration of VF at 1, 2, and 3 minimum alveolar concentrations (MAC) of anesthetic. Halothane altered neither the incidence nor duration of VF compared with the control group at 1 MAC; however, at 2 and 3 MAC, halothane significantly reduced the incidence and duration of VF (P < 0.05 at 1, 2, and 3 MAC halothane: respective incidences were 100%, 18%, and 55% and respective durations, 82 +/- 27 seconds, 20 +/- 6 seconds, and 13 +/- 9 seconds). In the isolated rat heart, we found that halothane has antiarrhythmic effects against reperfusion-induced arrhythmia at 2 and 3 MAC. Sevoflurane, however, did not have any antiarrhythmic effects against reperfusion-induced arrhythmia at 1, 2, or 3 MAC.
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PMID:Effects of sevoflurane and halothane on reperfusion-induced arrhythmia in the isolated rat heart. 811 6

We selected nine normal subjects (8M, 1F; aged 25-43 yr) with brisk hypoxic ventilatory responses, and studied their ventilatory response to sustained isocapnic hypoxia (SaO2 82 (SEM 0.1) % for 25 min) in the presence and absence of 0.1% inspired halothane. Halothane had no significant effect on baseline ventilation or gas exchange. In the absence of halothane, ventilation increased initially from mean 7.57 (0.35) litre min-1 to 14.54 (0.91) litre min-1, and decreased subsequently to 10.74 (0.32) litre min-1 during hypoxia (both P < 0.05). In the presence of 0.1% inspired halothane, ventilation increased initially from 7.19 (0.47) litre min-1 to 12.08 (0.99) litre min-1 (P < 0.05), then decreased to 10.12 (0.28) litre min-1 during sustained hypoxia (ns compared with baseline normoxic ventilation). Halothane reduced significantly the initial increase in ventilation (P < 0.05), but did not enhance the subsequent decrease. These results confirm that a sub-anaesthetic concentration of halothane depresses the initial hypoxic ventilatory response; the response during prolonged periods of hypoxia is, however, less than the initial response and is reduced in the presence or absence of a sub-anaesthetic concentration of halothane.
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PMID:Effect of a sub-anaesthetic concentration of halothane on the ventilatory response to sustained hypoxia in healthy humans. 825 Dec 71

The effects of halothane, isoflurane, and enflurane on proximal (false tendon) and distal (apical) Purkinje fibers were measured in vitro in infarcted canine hearts to assess their effects on action potentials of fibers located within the nonischemic and ischemic regions, respectively. High- and low-dose anesthetic effects were evaluated in three groups of eight preparations and compared to changes occurring at identical times in eight infarcted control preparations. Under control conditions in all groups, the action potential duration at 90% repolarization (APD90, mean +/- SEM) of ischemic distal fibers (396 +/- 9 ms) was longer (P < or = 0.01) than that of nonischemic proximal fibers (344 +/- 5 ms) and the ischemic fibers exhibited (P < or = 0.05) reduced maximum diastolic potential, amplitude, and Vmax relative to nonischemic fibers. Halothane (0.25 and 0.6 mM), isoflurane (0.4 and 0.8 mM), and enflurane (0.8 and 1.6 mM) produced dose-dependent decreases of nonischemic fiber APD90 with less decrease (P < or = 0.01) of ischemic fiber APD90 and thereby accentuated (P < or = 0.05) regional differences of APD90 at high dose. The decreases of nonischemic fiber APD90 were greater (P < or = 0.01) for 0.8 mM (2.9 minimum alveolar anesthetic concentration [MAC]) isoflurane (-95 +/- 5 ms) and 1.6 mM (2.5 MAC) enflurane (-79 +/- 12 ms) than for 0.6 mM (2.2 MAC) halothane (-41 +/- 3 ms). Isoflurane increased the pathologic difference (ischemic > nonischemic) between the repolarization times (APD90) of Purkinje fibers in the infarcted heart more (P < or = 0.05) than halothane.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Actions of volatile anesthetics on ischemic and nonischemic Purkinje fibers in the canine heart: regional action potential characteristics. 846 8

The effects of halothane and isoflurane on ventricular intracellular action potentials recorded in situ in pentobarbital anesthetized rats were studied. Halothane (0.5, 1 and 2 vol.%) and isoflurane (0.75, 1.5 and 3 vol.%) did not have identical effects on rat epicardial action potentials recorded by floating microelectrodes. However, over the concentration range tested, both anesthetics reduced blood pressure and heart rate to a similar extent. Isoflurane did not effect the maximum rate of rise of the action potential amplitude. However, 3 vol.% isoflurane reduced the resting membrane potential from -72+/-2 to -65+/-3 mV (mean+/-SEM, p<0.05) while the highest concentration of halothane had no effect. Halothane (2 vol.%) reduced action potential amplitude from 74+/-4 to 65+/-3 mV (p<0.05) and reduced the maximum rise rate of action potential from 175+/-21 to 133+/-8 V/s (p<0.05). Both isoflurane and halothane prolonged action potential duration at 10, 25 and 50% repolarization while only halothane significantly shortened action potential duration at 75% repolarization, Thus the effects of halothane and isoflurane on ventricular transmembrane action potentials were similar, but not identical. The relevance of such observations to the antiarrhythmic actions of halothane, but not isoflurane in this species is not clear.
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PMID:Effects of halothane and isoflurane on rat ventricular action potentials recorded in situ. 861 95

Several studies have reported a protective effect of halothane on myocardial injury in an ischaemia-reperfusion situation. It is unclear if the protection is a result of the haemodynamic effects of halothane or if halothane has a specific action on ischaemia or reperfusion pathomechanisms. To examine this question, we have used an isolated rat heart model where heart rate (300 beat min-1), ventricular volume and coronary flow are constant. Left ventricular developed pressure (LVDP) and release of creatine kinase (CK) were measured as variables of myocardial performance and cellular injury, respectively. Five control hearts were subjected to 35 min of low-flow (2 ml min-1) anoxic and substrate-free perfusion and were then perfused for 1 h with the oxygenated buffer. In the treatment groups, halothane 0.4 mmol litre-1 was added during the first 30 min of anoxic perfusion (n = 5) or during the first 30 min of reoxygenation (n = 5). In five additional hearts, the effect of halothane 0.4 mmol litre-1 was tested under normoxic conditions. Mean basal CK release was 0.29 (SEM 0.13) iu g-1 min-1 and LVDP was 105.5 (4.0) mm Hg. Under normoxic conditions, halothane reduced LVDP to 52.0 (2.6) mm Hg. In control hearts, the major cell injury occurred at the onset of reoxygenation (CK release increased to 149.1 (9.1) iu g-1 min-1) and functional recovery after 1 h of reoxygenation was poor (control LVDP, 14.2(2.)% of baseline). Halothane during anoxia attenuated myocardial injury only moderately (CK release 50.2(5.7) iu g-1 min-1) and LVDP recovered to 30.8(3.0)% (each P < 0.05 vs control). When halothane was administered at reoxygenation, CK release was reduced to 10.1 (0.9) iu g-1 min-1 and LVDP recovered to 69.4(4.9)% (each P < .05 vs control). We conclude that halothane not only attenuated ischaemic injury but had a specific protective action against reoxygenation injury.
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PMID:Effect of halothane on myocardial reoxygenation injury in the isolated rat heart. 867 63

Cardiac dysrhythmias during inhaled anesthesia are well documented and may, in part, involve depression of the fast inward Na+ current (INa) during the action potential upstroke. In this study, we examined the effects of halothane, isoflurane, and sevoflurane at clinically relevant concentrations on INa in single ventricular myocytes isolated enzymatically from adult guinea pig hearts. INa was recorded using standard whole-cell configuration of the patch clamp technique. Halothane at 0.6 mM and 1.2 mM produced significant (P < 0.05) depressions of peak INa of 12.3% +/- 1.8% and 24.4% +/- 4.1% (mean +/- SEM, n = 12), respectively. Isoflurane (0.5 mM, n = 12; 1.0 mM, n = 15) and sevoflurane (0.6 mM, n = 14; 1.2 mM, n = 12) were less potent than halothane, decreasing peak INa by 4.8% +/- 1.1% and 11.4% +/- 1.4% (isoflurane) and 3.0% +/- 0.7% and 10.7% +/- 3.9% (sevoflurane). The depressant effects on INa were reversible in all cases. For all anesthetics tested, the degree of block increased at more depolarizing potentials. Anesthetics induced significant shifts in the steady-state inactivation and activation of the channel toward more hyperpolarizing potentials. The present findings indicate that volatile anesthetics at clinical concentrations decrease the cardiac INa in a dose- and voltage-dependent manner. At approximately equianesthetic concentrations, the decrease of INa caused by halothane was twice that observed with isoflurane or sevoflurane.
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PMID:Voltage-dependent effects of volatile anesthetics on cardiac sodium current. 902 16


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