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Query: UMLS:C0026916 (MAC)
 5,226 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hemodynamic dose-response curves and MAC, apneic and lethal concentrations for halothane were determined in two groups of dogs at a normal hematocrit (Hct) (39 +/- 6), and during acute anemia (n = 4) and subacute anemia (n = 4), with a combined Hct of 18 +/- 6. The ratio of subendocardial/subepicardial blood flow was determined by the injection of radioactive microspheres. MAC, apneic, and lethal concentrations of halothane were not significantly different in anemic animals. There were also no differences in the halothane dose-response curves plotted for cardiac output, blood pressure, heart rate, left ventricular end-diastolic pressure, or arterial base excess. In 32 microsphere injections with Hct as low as 13, no dog had redistribution of myocardial blood flow suggestive of subendocardial ischemia. We conclude that halothane is a safe anesthetic during severe anemia.
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PMID:The hemodynamic effects of halothane in anemic dogs. 57 56

There is general concern that major blood loss during deliberate hypotension could produce severe organ ischemia, but documentation of the magnitude of this response remains obscure. To examine this response, we studied 43 male Sprague-Dawley rats that were divided into seven groups: the control animals received 1 MAC (1.4%) isoflurane only; the hypotensive animals received a 1.4% isoflurane baseline anesthetic and were then rendered hypotensive by either increasing the isoflurane concentration (dISO), or by adding sodium nitroprusside (SNP), or 2-chloroadenosine (2AD) to the baseline anesthetic, decreasing the MAP to 51 mmHg; hemorrhaged animals had hypotension produced in the same manner as for the hypotensive animals, but additionally were bled 20% of estimated blood volume during deliberate hypotension produced with either deep isoflurane (dISOH), sodium nitroprusside (SNPH), or 2-chloroadenosine (2ADH). After a 25-min period of hypotension, or hypotension plus hemorrhage, cardiac output and blood flow to brain, heart, gastrointestinal tract, kidney, and liver were measured with 141Ce-labelled 15-microns microspheres. Hypotension was associated with decreased blood flow to the kidneys in all groups and to the liver in the 2AD group and an increased blood flow to the heart in the SNP and 2AD groups. Hemorrhage decreased blood flow during deliberate hypotension to the brain and the gastrointestinal tract in the dISOH and 2ADH groups and to the liver in the dISOH group. Our results suggest that hemorrhage during deliberate hypotension with dISO or isoflurane plus 2AD may be associated with compromised organ blood flow, whereas blood flow to vital organs is maintained after 20% hemorrhage during isoflurane and superimposed SNP-induced hypotension.
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PMID:The influence of hemorrhage on organ perfusion during deliberate hypotension in rats. 834 11

The effects of varying concentrations and types of volatile anesthetics on neurochemical sequelae of brain ischemia were evaluated in the rat. Rats were assigned to treatment defined by a 3 x 3 design (anesthetic type and dose) with 5 rats/cell. Each group received halothane, enflurane, or isoflurane 0.5, 1.0, or 2.0 MAC (minimal alveolar concentration). This was followed by preischemic plasma glucose sampling, 5 min hypotension (30 mmHg) and 5 min decapitation cerebral ischemia. Preischemia plasma glucose increased with increasing anesthetic concentration and was highest in the isoflurane groups, varying from a low (+/- SD) of 7.19 +/- 1.79 mumol/ml in the 0.5 MAC halothane group to a high of 12.68 +/- 3.65 mumol/ml in the 2.0 MAC isoflurane group. End-ischemic brain lactate correlated with preischemic plasma glucose (r = 0.5, alpha = 0.5). We conclude that increasing concentration of volatile anesthesia with iv phenylephrine blood pressure support produces higher levels of plasma glucose and brain lactate with cerebral ischemia.
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PMID:Comparison of the effects of volatile anesthetics in varying concentrations on brain energy metabolism with brain ischemia in rats. 151 13

The present study was undertaken to examine the cerebral protective properties attributed to isoflurane and at the same time to compare its protective effects with those of mild hypothermia (temperature reduction by 3 degrees C). Twenty-one fasted Wistar-Kyoto rats were assigned to one of three groups (n = 7); 1.3 MAC (end-tidal) isoflurane-normothermia (pericranial temperature 38.0 degrees C), 1.3 MAC halothane-normothermia, and 1.3 MAC halothane-hypothermia (pericranial temperature 35.0 degrees C during ischemia). In each animal the trachea was intubated and the lungs were mechanically ventilated. Each animal was subjected to temporary incomplete forebrain ischemia induced by 10 min of bilateral carotid artery occlusion with simultaneous hypotension (mean arterial pressure 35 mmHg) induced by trimetaphan and blood withdrawal. After a 3-day survival period, perfusion-fixation was performed, and two blinded observers assessed histopathologic injury according to a four-point scale (0 = no damage; 1 = less than 10% of neurons damaged; 2 = 10-50% damaged; and 3 = greater than 50% damaged). The assessment was performed at two points in the rostrocaudal axis chosen to permit evaluation of regions with varying levels of ischemic damage. In the rostral sections, in the isoflurane- and halothane-normothermia groups, moderate to severe injury was observed in striatum, cerebral cortex, hippocampus (CA1 and CA3 areas), and reticular nucleus of the thalamus (e.g., the median scores for the CA1 area were 3 in both the halothane-hypothermia and the isoflurane-normothermia groups), and there were no differences between the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A comparison of the cerebral protective effects of isoflurane and mild hypothermia in a model of incomplete forebrain ischemia in the rat. 173 91

To determine the extent to which different electrocardiographic systems account for differences in reported incidence of perioperative myocardial ischemia, the authors simultaneously recorded in 109 patients undergoing coronary artery bypass grafting (CABG) the V5 or modified CM5 lead on five ECG systems by means of a specially constructed common V5 lead. The systems included a Spacelabs Alpha 14 Model Series 3200 ECG Cardule at bandwidths of 0.05-125 Hz and 0.5-30 Hz (a typical operating room monitor), a Marquette Electronics MAC II ECG at 0.05-40 Hz and 0.05-100 Hz (a standard ECG), and a Del Mar Holter recorder at 0.1-100 Hz. Relative ST-segment position and incidence of new ischemia compared to the preoperative ECG were determined in 109 sets of preinduction traces and 877 sets of intraoperative traces. ST-segment position on the three recording systems conforming with the American Heart Association (AHA) low-frequency response recommendations (0.05 Hz) were similar. Compared to the standard ECG, ST-segment position on the Spacelabs at 0.5-30 Hz was consistently more negative. Displacement on the Holter was consistently less negative and less positive. By the 0.1-mV displacement criterion for diagnosis of myocardial ischemia on any one ECG system, 16.5% of patients on arrival and 32.1% of patients intraoperatively suffered new myocardial ischemia. Based on the operating room monitor, arrival and intraoperative ischemia were present in 15.6 and 27.5% of patients, respectively. Ischemia at the same periods was less frequent by the standard ECG system (5.5 and 12.8%, respectively) and least frequent by the Holter recorder (4.6 and 8.3%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Incidence of perioperative myocardial ischemia detected by different electrocardiographic systems. 204 84

Using a rat model of incomplete cerebral ischemia the effects of isoflurane (iso) and methohexital (metho) were compared with those of 70% nitrous oxide controls (N2O). Two levels of incomplete cerebral ischemia were produced by right carotid occlusion plus hypotension for 30 min: moderate = 30 mmHg, FIO2 = 0.30; severe = 25 mmHg, FIO2 = 0.20. The iso doses (1 and 2 MAC) and metho doses (0.01 and 0.1 mg.kg-1.min-1) were tested at each ischemic level. These iso and metho doses were selected because without ischemia they produced similar decreases in cerebral oxygen consumption (CMRO2) compared with that produced in N2O controls. In the absence of ischemia, the electroencephalogram (EEG) was suppressed by 0.01 mg.kg-1.min-1 metho and 1 MAC iso and showed burst-suppression with 0.1 mg.kg-1.min-1 metho and 2 MAC iso. The EEG was further depressed by ischemia under all anesthetic conditions. Neurologic outcome was evaluated for 3 days following incomplete cerebral ischemia by using a graded deficit score (0 = normal, 5 = death associated with stroke). Following moderate ischemia all four anesthetic treatments improved outcome compared with N2O controls, but after severe ischemia only 2 MAC iso significantly improved outcome. Neurohistopathology was evaluated on a scale of 0 to 40, 24 h after ischemia. The neurohistopathology score was significantly improved by all four anesthetic treatments compared with N2O following moderate ischemia and was better with 2 MAC iso compared with 0.1 mg.kg-1.min-1 metho after both moderate and severe ischemia. These results show that both iso and metho improve outcome from cerebral ischemia compared with that associated with N2O, but only 2 MAC iso resulted in an improved outcome following severe ischemia. This difference in outcome between the two anesthetics may be related to greater neuronal depression with iso, which may occur with little difference in cerebral metabolic depression.
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PMID:Comparison of methohexital and isoflurane on neurologic outcome and histopathology following incomplete ischemia in rats. 229 37

In rats with incomplete cerebral ischemia the effects of 70% N2O alone, isoflurane alone (0.5 and 1 MAC), and the combination of N2O + isoflurane on neurologic outcome, neurohistopathology, and EEG were compared. Moderate and severe ischemia were produced by right carotid artery occlusion combined with hemorrhagic hypotension (moderate ischemia, MAP = 30 mmHg, FIO2 = 0.30; severe ischemia, MAP = 25 mmHg, FIO2 = 0.20). Neurologic outcome was evaluated using a graded deficit score from 0 to 5 (0 = normal, 5 = death associated with stroke), and neurohistopathology was evaluated using a 40-point scale from 0 = normal to 40 = total hemisphere infarct at the level of the caudate nucleus in coronal section. Compared with N2O alone, isoflurane (0.5 and 1 MAC) improved neurologic outcome following moderate ischemia (P less than 0.05). Isoflurane also decreased histopathologic damage following moderate ischemia (N2O control = 33 +/- 1 vs. 0.5 MAC isoflurane = 11 +/- 4 and 1 MAC isoflurane = 12 +/- 3, P less than 0.05), whereas only 0.5 MAC isoflurane decreased histopathologic damage following severe ischemia (N2O control = 38 +/- 1 vs. 0.5 MAC isoflurane = 25 +/- 5; P less than 0.05) Adding N2O to 0.5 MAC isoflurane attenuated the neurologic protective effect of isoflurane alone and increased histopathologic damage following both moderate and severe ischemia (moderate = 23 +/- 5, severe = 37 +/- 2; both P greater than 0.05 compared with N2O controls). The effect of adding 70% N2O to isoflurane on cerebral blood flow (CBF) and cerebral oxygen consumption(CMRO2) was also evaluated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The interaction of nitrous oxide and isoflurane with incomplete cerebral ischemia in the rat. 271 9

The effect of age on outcome after induced cerebral ischemia was tested in rats. Cerebral ischemia was produced by unilateral carotid ligation and hemorrhagic hypotension to 30 mm Hg (moderate ischemia) or 25 mm Hg (severe ischemia) in young (6 month) and old (26-28 month) rats anesthetized with 1 MAC halothane. Young rats had significantly better neurologic outcomes than old rats after similar ischemic challenges. This advantage disappears, however, when the inspired oxygen tension is altered to produce similar PaO2 in both age groups during ischemia. Measures of regional CBF with radioactive microspheres showed a 70% decrease in cortical blood flow in the ischemic cerebral hemisphere in both young and old rats. Plasma glucose concentrations increased from 150 to 250 mg/100 mL during ischemia in both age groups. Histologically, the brains showed similar signs of focal ischemic damage in striatum, hippocampus, and cortex in young and old rats. These results indicate that when blood pressure and respiratory factors are controlled experimentally during ischemia, young and aged rats have similar neurologic outcomes after cerebral ischemia.
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PMID:Neurologic outcome in aged rats after incomplete cerebral ischemia. 338 41

Myocardial tolerance to total ischemia was compared in animals anesthetized with halothane or isoflurane by measuring the time required for development of cardiac rigor in the absence of coronary circulation or wall stress. Sixteen dogs, eight in each group, were anesthetized with equally potent inspired concentrations of either halothane (2 MAC) or isoflurane (2 MAC), intubated, and ventilated. Thirty minutes later, the heart was rapidly excised. A left ventricular slab was prepared and maintained at 37 degrees C. A portion of each slab was placed in a compressibility gauge that detects rigor onset by an abrupt increase in resistance to tissue deformation. Subendocardial tissue pressure was continuously measured in a second slab using needle-tipped Millar pressure transducers. A third slab was used for intermittent tissue sampling and HPLC assay of high-energy nucleotide levels. There were no differences in pre-ischemic heart rate, mean arterial pressure, glucose, lactate, PO2, PCO2, pH, plasma epinephrine, or norepinephrine levels between the two groups. The onset of rigor as measured by the compressibility gauge was delayed in the halothane group (68 +/- 7.2 vs. 60 +/- 5.0 min; P less than .05). Tissue ATP and ADP levels declined throughout the period of ischemia, with a trend towards preservation in the halothane group. The data show that myocardial tolerance to total normothermic ischemia is improved in animals anesthetized with halothane compared to isoflurane, independent of the effects on hemodynamics or collateral coronary circulation.
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PMID:Myocardial tolerance to total ischemia in the dog anesthetized with halothane or isoflurane. 338 63

Using rats in which incomplete cerebral ischemia was induced, the authors evaluated the effects of halothane (H) and isoflurane (I) on neurologic outcome compared to nitrous oxide (N2O) controls. Incomplete cerebral ischemia was produced by right carotid artery occlusion combined with hemorrhagic hypotension. Neurologic outcome was evaluated using a graded deficit score from 0 to 5 (0 = normal, 5 = death associated with stroke). Two levels of cerebral ischemia were tested. At moderate ischemia with hypotension of 30 mmHg, an FIO2 of 0.3, and ischemic periods of 30 or 45 min, N2O produced a deficit of 4.7-5.0 and a mortality rate of 90-100%. In contrast, halothane (1 MAC) and isoflurane (1 MAC) resulted in similar deficit scores (H = 1.1-1.8, I = 1.4-1.6) and mortality rates (H = 17-30%, I = 17-20%). Cerebral blood flow (CBF) measured with radioactive microspheres showed a 60-65% decrease in the ischemic hemisphere at this level of hypotension. With severe ischemia with hypotension = 25 mmHg, FIO2 = 0.2, and a 30-min period of ischemia, deficit scores increased to 3.0 and 3.9 with 1 MAC halothane and 1 MAC isoflurane, respectively. Mortality rates also increased to 40% with halothane and 70% with isoflurane. Increasing the concentration of halothane or isoflurane to 2 MAC did not significantly improve outcome. Brain histology demonstrated extensive neuronal damage in striatal, hippocampal, and neocortical regions of N2O control treated rats, and less damage with little difference between H- and I-treated rats at each level of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neurologic outcome in rats following incomplete cerebral ischemia during halothane, isoflurane, or N2O. 340 68


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