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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mechanical hyperventilation may produce hypocapnic apnoea below the carbon dioxide off-switch threshold whereas an increase in arterial PCO2 after post-hyperventilation apnoea causes reappearance of respiratory effort above the carbon dioxide on-switch threshold. To study the effects of surgical stimulation on these two thresholds, we have measured end-tidal PCO2 (PE'CO2) at the two thresholds, before and during surgical stimulation, in 14 patients undergoing mastectomy, anaesthetized with sevoflurane (1.2 MAC). Based on the reproducibility of the results, data from 11 patients were analysed and data from the three other patients were discarded. Before surgical stimulation, mean resting PE'CO2' off-switch threshold and on-switch threshold were 5.7 (SEM 0.2), 5.2 (0.2) and 6.1 (0.2) kPa, respectively. The off-switch threshold was significantly less than resting PE'CO2 (P < 0.01) but the on-switch threshold was significantly greater than resting PE'CO2 (P < 0.01). During surgical stimulation, resting PE'CO2' off-switch threshold and on-switch threshold were 4.8 (0.2), 4.1 (0.2) and 4.7 (0.2) kPa, respectively. Although the off-switch threshold was significantly less than resting PE'CO2 (P < 0.01), there were no significant differences between resting PE'CO2 and on-switch threshold. These results indicate that surgical stimulation does not affect equally the carbon dioxide on- and off-switch thresholds.
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PMID:Effects of surgical stimulation on the apnoeic thresholds for carbon dioxide during anaesthesia with sevoflurane. 782 82

We investigated the influence of parasympathetic tone on the arrhythmogenic dose of dobutamine in horses premedicated with xylazine, anesthetized with guaifenesin and thiamylal, and maintained on halothane in oxygen. Six horses were used in 12 randomized trials. In each trial, after end-tidal halothane concentration was stabilized at 1.1% (1.25 times minimum alveolar concentration [MAC]) in oxygen, either saline solution (0.02 ml/kg of body weight) or atropine (0.04 mg/kg) was administered IV. Five minutes later, dobutamine infusion was started at dosage of 2.5 micrograms/kg/min, IV. The dobutamine infusion was continued for 10 minutes, or until 4 or more premature ventricular complexes occurred within 15 seconds, or sustained narrow-complex tachyarrhythmia clearly not sinus in nature occurred. If the criteria for termination were not met, dobutamine infusion was increased by 2.5 micrograms/kg/min, after the hemodynamic variables had returned to baseline. The horses were allowed to recover, and were rested for at least 1 week before the second trial. The arrhythmogenic dose of dobutamine was calculated by multiplying the infusion rate by the elapsed time into infusion when arrhythmia occurred. There was significant difference between the arrhythmogenic dose of dobutamine (ADD) in saline-treated horses (mean +/- SEM, ADD = 105.6 +/- 16.3 micrograms/kg) and atropinized horses (ADD = 36.2 +/- 8.7 micrograms/kg). There were no differences in the prearrhythmia or immediate postarrhythmia ventricular heart rate (HR) or systolic (SAP), diastolic (DAP), or mean (MAP) arterial pressures between treated and control groups. The change in hemodynamic variables from prearrhythmia to immediate postarrhythmia formation was not different between the 2 groups. (ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of atropine on the arrhythmogenic dose of dobutamine in xylazine-thiamylal-halothane-anesthetized horses. 811 45

To investigate the effects of enflurane on the control of breathing we have studied the ventilatory responses to isocapnic hypoxia in 12 adults with and without sedation with enflurane. Design 1 consisted of three steps into hypoxia (PE' O2 = 6.7 kPa), each lasting 3 min, separated by periods of euoxia lasting 5 min (PE' O2 = 13.3 kPa). Design 1 was repeated four times in each subject on the same day in random order: with carrier gas (control) and with 0.04 MAC, 0.07 MAC and 0.13 MAC of end-tidal enflurane concentrations. Design 2 consisted of 20-min exposures to hypoxia with and without 0.07 MAC of enflurane. Each exposure was preceded and followed by 5 min of euoxia. End-tidal PCO2 was held constant at 0.13-0.27 kPa greater than the resting level throughout both designs. Mean (SEM) ventilatory responses to hypoxia for design 1 were: 8.2 (1.3) litre min-1 (control), 6.6 (1.4) litre min-1 (0.04 MAC), 5.7 (1.1) litre min-1 (0.07 MAC) and 3.7 (0.5) litre min-1 (0.13 MAC) (P < 0.001). For design 2, enflurane produced a 15% reduction in resting ventilation (P < 0.01), a 40% decrease in the acute ventilatory response to hypoxia (P < 0.01) and a 32% reduction in ventilatory decline (ns) which occurred during sustained hypoxia.
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PMID:Effect of low-dose enflurane on the ventilatory response to hypoxia in humans. 819 97

Volatile anaesthetics may modulate cerebrovascular resistance, but their direct actions on human cerebral arteries are unknown. In the present study, we have evaluated the effects of halothane and isoflurane at different MAC (0.4, 1.0 and 2.0) on contractions induced by depolarization (potassium) or receptor stimulation (prostaglandin F2 alpha) in isolated ring segments of human pial arteries. Neither halothane nor isoflurane had significant effects on potency (unaffected EC50 value) or the maximum response (Emax) in potassium-contracted arteries, even though there was a general tendency to attenuation of Emax. Similarly, the potency of prostaglandin F2 alpha was unchanged (unaffected EC50 value). However, the Emax value for prostaglandin F2 alpha at normocapnia (mean PCO2 4.3 (SEM 0.1) kPa, pH 7.41 (0.01)) and addition of halothane (0.4, 1.0 and 2.0 MAC) was significantly attenuated to 96 (2)%, 91 (3)% and 84 (4)% at the respective MAC concentrations. Isoflurane at 2 MAC and normocapnia also reduced Emax to 94 (3)%. During hypocapnia (PCO2 2.7 (0.1) kPa, pH 7.64 (0.01)), the vasodilator effect of halothane was reduced, whereas isoflurane at 0.4 and 1.0 MAC enhanced the contraction induced by prostaglandin F2 alpha.
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PMID:Influence of halothane and isoflurane on the contractile responses to potassium and prostaglandin F2 alpha in isolated human pial arteries. 819 13

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

To compare the effects of sub-anaesthetic concentrations of propofol and halothane on the respiratory control system, we have studied the acute ventilatory response to isocapnic hypoxia (AHVR) in 12 adults with and without three different concentrations of propofol and halothane. Target doses for propofol were 0, 0.05, 0.1 and 0.2 of the effective plasma concentration (EC50 = 8.1 micrograms ml-1). Target doses for halothane were 0, 0.05, 0.1 and 0.2 minimum alveolar concentration (MAC = 0.77%). The doses achieved experimentally were 0.01, 0.06, 0.13 and 0.26 of the EC50 for propofol and 0, 0.05, 0.11 and 0.20 MAC for halothane. During the experiment subjects breathed via a mouthpiece from an end-tidal forcing system. End-tidal PO2 (PE'O2) was held at 13.3 kPa for 5 min, and then at 6.7 kPa for 5 min. End-tidal PCO2 (PE'CO2) was held constant at 0.13-0.27 kPa greater than the subject's natural level throughout. The mean values for AHVR with propofol were: 12.8 (SEM 2.4) litre min-1 (0.01 EC50), 10.0 (1.9) litre min-1 (0.06 EC50), 9.8 (2.3) litre min-1 (0.13 EC50) and 4.9 (1.2) litre min-1 (0.26 EC50). The values for AHVR with halothane were: 11.9 (2.4) litre min-1 (0 MAC), 7.8 (1.6) litre min-1 (0.05 MAC), 5.9 (1.2) litre min-1 (0.11 MAC) and 3.2 (1.6) litre min-1 (0.2 MAC). The decline in AHVR with increasing dose for both drugs was statistically significant (ANOVA, P < 0.001); there was no significant difference between the two drugs with respect to this decline. Normoxic ventilation with propofol declined from 13.2 (1.6) litre min-1 (0.01 EC50) to 8.3 (0.9 litre min-1 (0.26 EC50), and with halothane declined from 13.5 (2.0) litre min-1 (0 MAC) to 11.8 (1.6) litre min-1 (0.2 MAC). This was significant for both drugs (ANOVA, P < 0.001).
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PMID:Comparison of the effects of sub-hypnotic concentrations of propofol and halothane on the acute ventilatory response to hypoxia. 867 19

Earlier studies have suggested that halothane may relax smooth muscle in part by opening adenosine triphosphate-sensitive potassium (KATP) channels. We tested this hypothesis in vitro by examining the interaction of halothane with glibenclamide, a KATP channel blocker, and YM934, a KATP channel opener, in strips of canine tracheal smooth muscles mounted in an organ bath system. To examine the specificity of any effects of halothane on the KATP channel, we assessed the interaction of halothane with tetraethylammonium (TEA), an antagonist of the large-conductance, calcium-activated potassium channel. Experiments were conducted with drugs added before exposure to increasing concentrations of acetylcholine (ACh), and with drugs added after stable increases in force produced by ACh were achieved (ACh precontraction). Exposure to halothane 0.62 mmol litre-1 (equivalent to approximately 2 MAC) increased significantly the ED50 for ACh-induced contractions (by 0.24 (SEM 0.07) mumol litre-1). TEA 1 mmol litre-1 but not glibenclamide 10 mumol litre-1 significantly augmented this increase in ED50 (by an additional 0.17 (0.06) mumol litre-1). In strips precontracted with ACh, TEA, but not glibenclamide, potentiated concentration-dependent relaxation induced by halothane. Incubation with YM934 0.32 mumol litre-1 increased significantly the ED50 for ACh-induced contractions (from 0.12 (0.02) to 0.55 (0.11) mumol litre-1), an increase not affected by exposure to halothane 0.72 mmol litre-1. When added to strips precontracted with approximately ACh 0.3 mumol litre-1, YM934 produced concentration-dependent relaxation; halothane had little effect on this relaxation. These results do not support the hypothesis that halothane relaxes canine tracheal smooth muscle in part by opening KATP channels.
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PMID:Halothane and potassium channels in airway smooth muscle. 867 61

We have studied the effects of magnesium on atrioventricular (AV) conduction times and surface electrocardiogram during both sinus rhythm and atrial pacing in seven dogs anaesthetized with 1 MAC of sevoflurane. A bolus dose of magnesium sulphate (MgSO4) 30, 60 and 90 mg kg-1 significantly increased plasma magnesium concentrations from 1.3 (SEM 0.1) to 15.3 (1.3) mg dl-1. MgSO4 significantly prolonged A-H (AV nodal conduction time during sinus rhythm), St-H (intra-atrial and AV nodal conduction time during atrial pacing) and H-S (total ventricular conduction time) intervals at doses > or = 30 mg kg-1 ; H-V interval (His-Purkinje conduction time) at doses > or = 60 mg kg-1; RR and PR intervals and QRS duration at doses > or = 30 mg kg-1 in a dose-related manner during both sinus rhythm and atrial pacing. QTc interval remained unchanged during sinus rhythm. The doses of MgSO4 used did not have deleterious effects on AV conduction times and surface electrocardiogram during 1 MAC of sevoflurane anaesthesia. This finding suggests that MgSO4 in high doses was safe and may be indicated for cardiac arrhythmia and hypertension during sevoflurane anaesthesia. However, further study is required to apply these findings to clinical anaesthesia.
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PMID:Effects of magnesium sulphate on atrioventricular conduction times and surface electrocardiogram in dogs anaesthetized with sevoflurane. 905 8

Nitrous oxide and isoflurane have different effects on absolute cerebral blood flow (CBF) and regional distribution of CBF in humans. In this study we examined the effects of isoflurane in combination with nitrous oxide on CBF. We studied 10 patients (two groups of five patients, ASA I) anaesthetized with 50% nitrous oxide and either 0.5 or 1.0 MAC of isoflurane during normocapnia (PaCO2 5.7 kPa) using two-dimensional CBF measurement (CBFxenon) (i.v. 133xenon washout technique) and a three-dimensional method for measurement of regional CBF (rCBF) distribution with SPECT (single photon emission computer-aided tomography with 99mTc- HMPAO). The results were compared with 1.0 MAC of isoflurane from a previous study performed in exactly the same way as the present investigation. During normocapnia, anaesthesia with 50% nitrous oxide and 0.5 MAC of isoflurane resulted in a mean CBFxenon of 45 (SEM 5) ISI units. Increasing the isoflurane concentration to 1.0 MAC had no significant effect on mean CBFxenon (53 (5) ISI units). Both flow values were significantly (P = 0.01) higher than the CBFxenon value obtained when 1 MAC of isoflurane was administered alone (33 (3) ISI units). There were no significant differences in rCBF distribution regardless of whether or not isoflurane was given alone or together with nitrous oxide at 0.5 or 1 MAC. In all situations there were higher relative flows in subcortical regions (thalamus and basal ganglia, 10%) and in the pons (7-10% above average). rCBF in the cerebellum was approximately 10% greater than average. In summary, we have found that mean CBF was greater with combined nitrous oxide and isoflurane anaesthesia than previously found with isoflurane alone; however, relative flow distribution was similar.
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PMID:Regional cerebral blood flow (SPECT) during anaesthesia with isoflurane and nitrous oxide in humans. 913 62

In common with halogenated anaesthetics, nicorandil, a new KATP channel opener, has been shown to have cardioprotective and vasodilator effects. Recent studies have also suggested that the vasodilator and protective effects of halogenated anaesthetics are mediated partly via KATP channel opening. This study examined the effects of concurrent administration of nicorandil and isoflurane on haemodynamic state and ventricular function before, during and after 15 min of ischaemia. We studied left ventricular function in 40 anaesthetized rabbits using ultrasonomicrometry. Measurements were obtained before, during and after 15 min of regional ischaemia. Regional ventricular function was assessed in terms of systolic shortening (SS%) and preload recruitable work area (PRWA, the area beneath the regional stroke work vs end-diastolic length relationship) during reperfusion. Four groups were studied: group F (n = 10) received a bolus dose of fentanyl 100 micrograms kg-1 and then 400 micrograms kg-1 h-1 throughout; group 1 (n = 10) received 2.05% end-tidal concentration of isoflurane (1 MAC); group FN (n = 10) received fentanyl, a bolus does of nicorandil 100 micrograms kg-1 and then 25 micrograms kg-1 min-1, 15 min before occlusion; and group IN (n = 10) received isoflurane and nicorandil. Isoflurane decreased left ventricular systolic pressure and ventricular contractility (+dP/dtmax, slope of preload recruitable stroke work, and SS%). Nicorandil increased -dP/dtmax in group FN. Post-ischaemic regional left ventricular contractility in group I did not differ from that in group F, however, groups receiving nicorandil recovered to a greater extent. Group IN showed better recovery compared with all other groups when ventricular contractility was assessed by PRWA normalized to pre-occlusion values (mean 99.3 (SEM 10.5)% vs 73.4 (7.5)%, 50.2 (5.8)% and 52.4 (3.7)% at 120 min reperfusion in groups FN, I and F, respectively). Tissue ATP and lactate contents did not differ between groups. We conclude that concurrent administration of nicorandil and isoflurane enhanced post-ischaemic recovery compared with isoflurane anaesthesia or nicorandil and fentanyl administration.
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PMID:Beneficial effect of concomitant administration of isoflurane and nicorandil. 930 92


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