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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Membrane hyperpolarization (increase in resting potential) together with a conductance increase has been suggested as a common mechanism of anesthetic action. The current study compared the effects of halothane, enflurane, and isoflurane on resting membrane potential and conductance of hippocampal CA1 neurons in vitro. At 1 MAC, halothane produced significant (P less than 0.01) hyperpolarization (-2.8 +/- 1.3 mV, mean +/- SD) accompanied by a conductance increase (6.2 +/- 2.7%). Enflurane also produced a significant (P less than 0.001) hyperpolarization (-3.15 +/- 1.2 mV); however, this was accompanied by a conductance decrease (-4.5 +/- 1.5%). Isoflurane produced variable effects. Anesthetic-induced hyperpolarization was maximal in neurons with more negative initial resting potentials and was reduced by depolarization. Across agents, these relatively small changes in resting potential were not correlated with decreases in excitability as measured by synaptically evoked population spike depression. The results are not consistent with a common action of the three agents on a single ionic channel.
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PMID:Anesthetic effects on resting membrane potential are voltage-dependent and agent-specific. 198 63

Seven dogs were chronically instrumented for measurements of mean aortic blood pressure and cardiac output and for simultaneous measurements of hepatic, portal, and renal blood flows. Each animal was studied on two separate occasions, awake and during 1.2, 1.4, 1.75, and 2.0 MAC isoflurane and enflurane. Both anesthetics induced tachycardia; to a greater degree than isoflurane, enflurane lowered mean aortic blood pressure in a dose-dependent manner (-37, -45, -48, and -62% vs. -19, -25, -41, and -44%, respectively) and cardiac output (-20, -26, -41, and -48% vs. -3, -5, -11, and -15%, respectively). With isoflurane, cardiac output decreased only at 1.75 and 2.0 MAC, and portal blood flow did not change significantly, whereas hepatic arterial blood flow increased at 1.75 and 2 MAC (by 28 and 33%, respectively). With enflurane, no significant changes were recorded in hepatic arterial blood flow, whereas portal blood flow decreased in a dose-dependent manner. Except at 2 MAC, hepatic circulation did not differ between anesthetics. Likewise, neither anesthetic significantly changed renal blood flow, except for enflurane at 2.0 MAC, which was associated with a 35% reduction. Both anesthetics led to similar systemic, hepatic, and renal vasodilations. Our data suggest that high concentrations of enflurane are associated with decreases in portal, total hepatic, and renal blood flows, most likely as a result of an anesthetic-induced cardiac depression.
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PMID:Effects of enflurane and isoflurane on hepatic and renal circulations in chronically instrumented dogs. 199 Sep 4

The systemic and coronary hemodynamic effects of desflurane were compared to those of isoflurane, halothane, and enflurane in chronically instrumented dogs. Since autonomic nervous system function may significantly influence the hemodynamic actions of anesthetics in vivo, a series of experiments also was performed in the presence of pharmacologic blockade of the autonomic nervous system. Eight groups comprising a total of 80 experiments were performed on 10 dogs instrumented for measurement of aortic and left ventricular pressure, the peak rate of increase of left ventricular pressure (dP/dt), subendocardial segment length, coronary blood flow velocity, and cardiac output. Systemic and coronary hemodynamics were recorded in the conscious state and after 30 min equilibration at 1.25 and 1.75 MAC desflurane, isoflurane, halothane, and enflurane. Desflurane (+79 +/- 12% change from control) produced greater increases in heart rate than did halothane (+44 +/- 12% change from control) or enflurane (+44 +/- 9% change from control) at 1.75 MAC. Desflurane preserved mean arterial pressure to a greater degree than did equianesthetic concentrations of isoflurane. This result was attributed to a smaller effect on peripheral vascular resistance as compared to isoflurane and greater preservation of myocardial contractility as evaluated by peak positive left ventricular dP/dt and the rate of increase of ventricular pressure at 50 mmHg (dP/dt50) compared to other volatile anesthetics. Increases in diastolic coronary blood flow velocity (+19 +/- 6 and +35 +/- 12% change from control at 1.75 MAC, respectively) and concomitant decreases in diastolic coronary vascular resistance (-41 +/- 12 and -58 +/- 6% change from control at 1.75 MAC, respectively) were produced by desflurane and isoflurane. In the presence of autonomic nervous system blockade, the actions of desflurane and isoflurane were nearly identical with the exception of coronary vasodilation. After autonomic nervous system blockade, isoflurane increased coronary blood flow velocity, but desflurane did not. Furthermore, both desflurane and isoflurane continued to produce less depression of myocardial contractility than did halothane and enflurane. In summary, at equianesthetic concentrations, desflurane and isoflurane produced similar hemodynamic effects; however, in the absence of drugs that inhibit autonomic reflexes, desflurane had less negative inotropic activity and produced less decrease in arterial pressure. The coronary vasodilator actions of desflurane and isoflurane within the limitations of this model were not similar. When the increase in heart rate and rate-pressure product produced by desflurane were prevented in dogs with autonomic nervous system blockade, desflurane produced no change in coronary blood flow velocity.
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PMID:Comparison of the systemic and coronary hemodynamic actions of desflurane, isoflurane, halothane, and enflurane in the chronically instrumented dog. 200 Oct 33

Desflurane is a potent inhaled anesthetic associated with a dose-dependent depression of cortical electrical activity. Recently, it has been suggested that the burst suppression pattern seen in dogs given moderately high doses (2.0 MAC) of desflurane may spontaneously subside. This observation suggests the development of acute tolerance to at least some of the anesthetic effects of this drug. No other volatile anesthetic has been found to produce acute tolerance. We attempted to replicate these findings in domestic swine. Five juvenile swine (25-30 kg) were anesthetized with desflurane in oxygen and during normocapnia were exposed to two doses of desflurane sufficient to induce burst suppression (1.5 and 1.7 MAC) for 35 min at each dose, with a period of EEG recovery (0.6 MAC) before, between (in 3 of 5 animals), and after the high doses. Frontoparietal EEG was continuously recorded and the burst suppression ratio continuously calculated. Suppression was more complete at 1.7 MAC than at 1.5 MAC (98.24 +/- 1.75 vs. 90.80 +/- 3.05%, respectively, mean +/- standard deviation). The degree of burst suppression activity did not change over time at either 1.5 (P greater than 0.33) or 1.7 MAC desflurane (P greater than 0.41). There was no EEG evidence of tolerance to desflurane anesthesia in swine.
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PMID:No EEG evidence of acute tolerance to desflurane in swine. 202 Dec 6

Global and regional myocardial functions were studied in seven open-chest dogs with constant low plasma concentrations of verapamil as increasing concentrations of isoflurane (0.75, 1, 1.5 MAC) were administered in the presence of normal myocardial perfusion and after application of critical constriction of the left anterior descending coronary artery. In the presence of verapamil, increases in isoflurane concentrations caused dose-dependent myocardial depression both before and after critical coronary constriction. The systemic and coronary vasodilatation associated with high concentrations of isoflurane did not occur in the presence of verapamil. The association of verapamil with isoflurane caused regional myocardial dysfunction that worsened at high isoflurane concentrations. This regional dysfunction could not be antagonized in two dogs. The effects of isoflurane on regional function were not modified by application of a critical coronary constriction.
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PMID:Dose-related effects of isoflurane associated with low plasma concentrations of verapamil on global and regional function in normal and compromised canine myocardium. 206 83

Preliminary disposition studies of the investigational, long-acting muscle relaxant doxacurium chloride (Nuromax) have demonstrated dual elimination by renal and hepatobiliary pathways, as well as slow hydrolysis by plasma cholinesterase. The present study compares the kinetics and dynamics of doxacurium in eight ASA physical status I or II elderly patients (67-72 yr of age) and eight ASA I or II young patients (22-49 yr of age). After institutionally approved written informed consent, kinetic and dynamic measurements were made after a 25-micrograms/kg bolus injection of doxacurium during 1.25 MAC nitrous oxide/oxygen/isoflurane anesthesia. Maximum twitch depression was similar in older patients (96.4% +/- 1.3%) to that in the young patients (96.6% +/- 1.8%). The time to achieve this level of block was significantly longer in the elderly than in the young (11.2 +/- 1.1 min versus 7.7 +/- 1.0 min, respectively). Recovery times to twitch heights of 5% and 25% of control tended to be prolonged and were more variable in the elderly (82.6 +/- 17.2 and 97.1 +/- 20.1 min, respectively) than in the young (54.8 +/- 9 and 67.5 +/- 8.2 min, respectively). Elimination half-life (96 +/- 20 min) and clearance (2.47 +/- 0.69 mL.kg-1.min-1) in the elderly patients were not statistically different from values found in the younger group. Volume of distribution at steady state in the elderly (220 +/- 80.2 mL/kg) was significantly larger than in the young (150 +/- 40.0 mL/kg).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pharmacokinetics and pharmacodynamics of doxacurium in young and elderly patients during isoflurane anesthesia. 214 83

One hundred seventeen adult surgical patients were studied to compare neuromuscular and cardiovascular effects of mivacurium chloride during nitrous oxide-narcotic (BAL, n = 45) nitrous oxide-halothane (HAL, n = 27) and nitrous oxide-isoflurane (ISF, n = 45) anesthesia. Anesthesia was maintained with nitrous oxide (60%-70%) and oxygen (30%-40%) with end-tidal concentrations of halothane or isoflurane to yield a total MAC of approximately 1.25, or with supplemental fentanyl and thiopental as clinically indicated. Twitch response of the adductor pollicis muscle was elicited by supramaximal square wave pulses of 0.2 msec duration at a frequency of 0.15 Hz (Grass S44 stimulator) to the ulnar nerve and quantitated by a Grass FT10 transducer. Nine patients in each of the HAL and ISF groups received one of four doses of mivacurium (0.03, 0.05, 0.10 or 0.15 mg/kg). Ninety patients in the balanced anesthesia group received one of seven doses of mivacurium (0.03, 0.04, 0.05, 0.08, 0.15, 0.20, 0.25 mg/kg). The ED50, ED75 and ED95 of mivacurium in each group were estimated from linear regression plots of log dose versus probit of maximum percentage depression of twitch height. The ED50, ED75 and ED95 for halothane and isoflurane are 0.040, 0.053 and 0.081 and 0.037, 0.043 and 0.053, respectively. The ED50, ED75, and ED95 for the balanced group are 0.039, 0.050, and 0.073 mg/kg respectively. There was no significant difference between the slopes of the HAL and BAL inhalation anesthetic dose-response curves. The slope of the ISF group was significantly than the slope of the BAL group. Intercepts of the HAL and BAL curves were not different. The isoflurane curve's intercept was significantly less than the other groups' intercepts, lying above the halothane curve, but below the BAL curve. For the 0.05 mg/kg dose, maximum block was greater in the ISF group (89.1 +/- 2.7%, n = 9) than in the HAL (70.3 +/- 7.6%, n = 9) or BAL (67.7 +/- 6.4%, n = 9) groups. At higher doses of mivacurium, isoflurane produces a greater potentiation of neuromuscular block than halothane or balanced anesthesia. There were no significant cardiovascular changes seen in any group following mivacurium doses up to 0.15 mg/kg (approximately 2xED95).
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PMID:Neuromuscular and cardiovascular effects of mivacurium chloride (BW B109OU) during nitrous oxide-narcotic, nitrous oxide-halothane and nitrous oxide-isoflurane anesthesia in surgical patients. 214 82

We studied EEG and brainstem auditory evoked potentials (BAEP) during routine surgery at various concentrations of isoflurane (12 patients) or halothane (11 patients) or during prolonged (mean 2.5 h, range 1.9-3.5 h) administration of 1% isoflurane (five patients). Recording and analysis was performed with the cerebral function analysing monitor (CFAM). At equivalent MAC, the two agents exhibited distinctive neurophysiological profiles. Increasing concentrations of isoflurane produced a clear sequence of EEG changes (decreasing fast and increasing slow components) then burst suppression activity suggesting cortical depression. With halothane, changes in EEG amplitude were less pronounced and those in frequency content less systematic, with no periods of suppression. Simultaneous BAEP showed greater latency increase with halothane than with isoflurane. Prolonged administration of 1% isoflurane was associated with a stable EEG (no periods of suppression) and BAEP.
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PMID:Quantitative EEG and brainstem auditory evoked potentials: comparison of isoflurane with halothane using the cerebral function analysing monitor. 222 58

Short periods of coronary artery occlusion are known to produce prolonged periods of ventricular dysfunction. The effects of halothane or isoflurane on contractility and metabolism in postischemic "stunned" myocardium were studied in an open-chest canine model in which the left anterior descending artery (LAD) was occluded for 15 min and then reperfused. Regional function in the LAD and circumflex artery (CIRC) areas were measured with sonomicrometry, and metabolic data were determined from simultaneous arterial and venous measurements of oxygen and lactate. Halothane and isoflurane produced equivalent decreases in systolic shortening in both normal (CIRC) and stunned (LAD) areas of the heart. Furthermore, the amount of depression was similar with either halothane or isoflurane. Halothane 0.75 MAC significantly decreased systolic shortening in both the LAD region (from 38.8 +/- 25.9% to 11.0 +/- 21.8%) and in the CIRC region (from 116.7 +/- 24.7% to 87.5 +/- 23.3%). At equivalent MAC concentrations of isoflurane, the values were 42.5 +/- 45.7 to -7.0 +/- 49.9% in the LAD region and 91.5 +/- 11.9% to 66.9 +/- 23.9% in the CIRC area. At 1.5-MAC halothane, systolic shortening in the LAD region decreased from 47.9 +/- 47.2% to -0.6 +/- 20.3% and in the CIRC area from 114.6 +/- 16.8% to 76.0 +/- 18.7%. Isoflurane at 1.5 MAC produced significant decreases, from 23.4 +/- 54.5% to -15.6 +/- 27.1% in the LAD region and from 94.4 +/- 33.2% to 61.3 +/- 28.2 in the CIRC area.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of halothane and isoflurane on postischemic "stunned" myocardium in the dog. 224 1

Recovery of motor and mental functions were investigated in two groups with 20 young patients each. One group received total intravenous anaesthesia (TIVA) with propofol and alfentanil for urological surgery and the other group received nitrous oxide-oxygen anaesthesia in combination with 1.3 MAC of enflurane for lumbar nucleotomy. The following parameters were investigated before and up to 100 minutes after extubation: simple and discriminating motor activities, vigilance and short and long term memory. --Simple and in discriminating motor actions show a significantly faster recovery was seen in the TIVA group during the first 20 minutes after extubation compared to the enflurane-treated patients. Speech-related functions were particularly inhibited in the inhalational anaesthesia group. After 30 to 40 minutes the propofol-alfentanil group was able to meet all requirements while patients with inhalational anaesthesia needed 80 minutes to reach the same level. Recovery of short and long-term memory was also significantly shorter in the TIVA group. This clearly indicates a faster return of mental and motor functions following total intravenous anaesthesia with propofol and alfentanil. However the large dosages of alfentanil may be a problem with regard to post-anaesthetic respiratory depression. Further studies with larger numbers of patients will be necessary to evaluate the potential side effects of continuous propofol/alfentanil infusion. Presently, safety demands require, at least a sixty-minute post anaesthesia monitoring for patients receiving this new anaesthesia method.
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PMID:[The recovery period following total intravenous anesthesia using propofol and alfentanil versus inhalation anesthesia using nitrous oxide and enflurane at 1.3 MAC]. 225 70


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