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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nitrous oxide (N2O) has been implicated as a cause of myocardial ischemia. We investigated whether substitution of N2O for a portion of the anesthesia supplied by isoflurane increased myocardial ischemia in patients at risk for such ischemia. Seventy patients having carotid endarterectomies (63 patients) or other carotid surgery (seven patients) were prospectively, randomly assigned to an anesthetic regimen that included or excluded N2O. All other aspects of anesthetic management were similar, except for greater concentrations of oxygen and isoflurane in patients not given N2O. Perioperative monitoring for myocardial ischemia and infarction included 12- or 5-lead electrocardiography, transesophageal echocardiography, and creatine kinase isoenzyme levels. By transesophageal echocardiographic or electrocardiographic criteria, 44% of patients given oxygen but only 21% of those given N2O had myocardial ischemia intraoperatively (P = 0.065). Similarly, myocardial infarction, identified by changes in creatine kinase isoenzymes, occurred in only one patient given N2O but in three given oxygen (not significantly different). Thus we found no trend indicating a greater incidence of myocardial ischemia or infarction associated with the use of N2O.
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PMID:No finding of increased myocardial ischemia during or after carotid endarterectomy under anesthesia with nitrous oxide. 224 Jun 29

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

We describe delayed neuronal damage in ipsilateral remote areas outside the ischemic area of rat brain after transient focal ischemia. The distribution of the neuronal damage was determined by using the 45Ca autoradiographic technique and the histological method, and we investigated the mechanism involved by measuring local cerebral glucose metabolism. Wistar rats were used throughout the experiments. Under 2% halothane anesthesia with a mixture of 70% N2O and 30% O2, the right middle cerebral artery (MCA) was embolized by insertion from the internal carotid artery of a nylon surgical thread with a cylindrical coating of silicone on the distal portion. Animals were divided into 4 groups based on duration of ischemia. After 15, 30, 60 and 90 min of MCA occlusion, recirculation was achieved by removal of the embolus. Immediately after recirculation and then after 24 hr, 3 days, 1 week and 2 weeks of recirculation, 300 microCi 45CaCl2 in aqueous solution (0.3 ml) was administered intravenously; 6 hr later, animals were decapitated to obtain autoradiograms. Histological examination was carried out according to the same protocol. In the 15-min MCA occlusion group, neither 45Ca accumulation nor histological change was observed. In the 30-min MCA occlusion group, 45Ca accumulation extended from the lateral margin to the lateral segment of the caudate-putamen and the cerebral cortex supplied by the occluded MCA depending on the duration of recirculation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Exo-focal neuronal death in the rat brain]. 235 15

The effect of intravenous (IV) nitroglycerin (NTG) on perioperative myocardial ischemia as detected by single pass radionuclide angiocardiography was studied in 20 patients scheduled for elective coronary artery bypass grafting (CABG). Ten patients, selected at random, received IV NTG 1 microgram.kg-1.min-1 (NTG group) and 10 others, IV saline (control group). Anesthetic induction consisted of midazolam 0.2 mg.kg-1, vecuronium 0.1 mg.kg-1, and 50% N2O in O2. ECG leads I, II, and V5 were monitored for ST segment changes. Single pass radionuclide angiocardiography (RNA) was performed at 5 times: prior to induction, prior to tracheal intubation, and at 1, 3.5, and 6 min following intubation. The presence of new regional wall motion abnormalities (RWMA) was determined from each RNA study as compared with the preinduction measurement. Apart from one patient in the control group who developed a new "v" wave after intubation, there was no evidence of ischemia by pulmonary capillary wedge pressure. No ECG evidence of ischemia was detected in any patient. Despite this, new regional wall motion abnormalities were observed in 3 patients in the control group and 1 patient in the NTG group. Blood pressure and heart rate responses of patients with new RWMA were not significantly different from other patients. The low incidence of ischemia in this population precludes a definitive statement regarding the efficacy of IV NTG, but the lower incidence of RWMA in the NTG group suggests a protective effect.
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PMID:The effect of nitroglycerin on response to tracheal intubation. Assessment by radionuclide angiography. 250 40

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

Differential effects of isoflurane (ISOF) and N2O on cerebral blood flow, metabolism and electrocorticogram (ECoG) were examined in rats subjected to 15 min-incomplete cerebral ischemia. In the first study, regional cerebral blood flow (rCBF) and ECoG were measured during and after ischemia. In the second study, local cerebral blood flow (LCBF) and glucose utilization (LCGU) were determined at 60 min after reperfusion. In the N2O group, rCBF in both the cerebral cortex and hippocampus decreased significantly to less than 10% of the pre-ischemic value during ischemia, and it increased to 170% at 10 min after reperfusion. The ECoG became flat during ischemia and reappeared at 21 min after reperfusion. In the ISOF group, rCBF decreased significantly to 25% during ischemia and returned to the preischemic value after reperfusion. The ECoG became flat during ischemia and reappeared at 14 min. In the N2O group, LCBFs decreased significantly to 40-50% of the pre-ischemic values in the forebrain. LCGUs decreased significantly to 30-50% in all structures of the forebrain. In the ISOF group, LCBFs decreased significantly to 60-80% in the forebrain, but were not different in other structures. LCGUs did not differ from pre-ischemic values in all structures except for in the thalamus and habenula. These results may indicate cerebral protective effects of ISOF on incomplete cerebral ischemia in rats.
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PMID:[Differential effects of isoflurane and nitrous oxide on cerebral blood flow, metabolism and electrocorticogram after incomplete cerebral ischemia in the rat]. 279 63

Despite evidence from animal experiments to the contrary, nitrous oxide (N2O) reportedly does not induce myocardial ischemia when used as an adjunct to fentanyl anesthesia in patients with coronary artery disease who have well-preserved left ventricular (LV) function. However, the incidence of ischemia with N2O administration in similar patients with poor LV function may be different. The effects of N2O on segmental LV function, as determined by two-dimensional transesophageal echocardiography, changes in the ST-segment of the electrocardiogram were compared with the effects of an equal concentration of nitrogen (N2) (crossover design) in 70 patients who required elective coronary artery bypass grafting. Of these patients, 24% had left ventricular ejection fraction (LVEF) less than or equal to 40%. Myocardial ischemia was diagnosed in 14 patients during the study: four while awake, seven during induction of anesthesia and tracheal intubation, and four during the remainder of the study (one during N2O and three during 100% oxygen; one patient had two distinct periods of ischemia). No value for LVEF could be found that would distinguish between patients who did or did not have ischemia during the study. Patients treated with beta-adrenergic blocking drugs preoperatively were less likely to develop ischemia (P less than 0.05). Preoperative calcium channel blockers made no such differences. Onset of ischemia was not closely associated with hemodynamic changes. Thus, N2O does not induce clinically detectable myocardial ischemia in patients who have coronary artery disease, and poor LV function in situations in which the effects of deepening anesthetic depth and mild depression of global myocardial function are deemed desirable or harmless.
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PMID:Nitrous oxide does not induce myocardial ischemia in patients with ischemic heart disease and poor ventricular function. 280 10

We looked at FiO2, choice of anesthetic, nutritional status, and body temperature in a gerbil model of forebrain ischemia to determine their effect on data interpretation, ischemic outcome, and extent of pharmacologic protection. We subjected 484 gerbils to 5 minutes of forebrain ischemia under different experimental conditions. The gerbils were anesthetized with 3% halothane and inspired 21% O2, 37% O2 and 60% N2O, or 97% O2. Six groups of gerbils pretreated with 200 mg/kg phenytoin or 2 ml/kg polyethylene glycol (vehicle) underwent ischemia in the fasted or fed state. Three groups of gerbils receiving no pretreatment underwent ischemia with rectal temperatures of 32-33 degrees C, 34-35 degrees C, or 37 degrees C. We counted intact neurons in the CA1 hippocampal sector in brains fixed on Day 7 after ischemia. t tests of square-root-transformed cell counts were used to assess the effect of hypothermia, and analysis of variance of the transformed data was used to test for the effects of phenytoin, FiO2, and nutritional status. Phenytoin pretreatment provided significant protection from CA1 neuron loss in all groups tested (p less than 0.001), but the degree of protection varied from 20% to 44%. In spite of significantly higher serum glucose concentrations in fed than in fasted gerbils (173 and 118 mg/dl, respectively), we found no significant effect of nutritional status upon neuron loss in phenytoin- or vehicle-pretreated gerbils. An FiO2 of 21% significantly decreased the number of viable neurons in both vehicle- and phenytoin-pretreated groups (p less than 0.03), despite the lack of an effect of hypoxemia on arterial blood gases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Conditions for pharmacologic evaluation in the gerbil model of forebrain ischemia. 281 90

We studied the cardiovascular effects of esmolol, a newly synthesized beta-adrenocepter antagonist, in anesthetized humans. Forty patients (four groups of 10 each) with ischemic heart disease and normal ventricular function were anesthetized with diazepam, pancuronium, and N2O in O2. Esmolol was given by continuous infusion in cumulative doses of 1100 micrograms/kg (group 1), 2000 micrograms/kg (group 2), and 2700 micrograms/kg (group 3); a control group received no esmolol. Infusion of esmolol was begun 3 min prior to and ended 4 min after tracheal intubation. All three doses of esmolol significantly (P less than 0.001) attenuated the heart rate responses to intubation. Rate-pressure products were significantly (P less than 0.001) lower in esmolol-treated patients than in controls after intubation, but ST-segment changes compatible with ischemia occurred in one patient in each group. Increases in heart rate were associated with significant increases in plasma norepinephrine levels (r = 0.45, P = 0.02) in the control group, but not in esmolol-treated patients, a demonstration that esmolol antagonizes the beta-adrenergic effects of norepinephrine. The effect of esmolol on heart rate was absent 5 min after cessation of infusion, and plasma levels of esmolol were undetectable in 26 of 30 treated patients 15 min after the termination of esmolol infusion. Esmolol has a rapid onset and short duration of effect. It can be used safely during anesthesia in patients with normal ventricular function to attenuate cardiac response to sympathetic stimulation.
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PMID:Cardiovascular effects of esmolol in anesthetized humans. 285 69

The relation between duration of ischemia, use of adjunctive ganglionic blockade and long-term recovery was studied in a rat model giving reversible subtotal forebrain ischemia. Ischemia was induced by bilateral carotid artery clamping and controlled hemorrhage to a mean arterial pressure of 50 mm Hg in animals artificially ventilated under 70% N2O. After variable lengths of time, the clamps were removed and the drawn blood was reinfused. In some animals, the ganglion blocker Arfonad was given (group A+) on induction of ischemia to facilitate hypotension. There was a strict dose-response relationship between duration of ischemia and mortality. Mortality was higher among animals not given Arfonad (group A-; 37% after 10 min of ischemia and 100% after 13 min) than in group A+ (about 20% after 12-13 min of ischemia, 50% after 15 min and 80% after 19 min). In group A+ more than half of the animals died later than 24 h after ischemia. All of them were hyperexcitable and 12% died during witnessed epileptic fits. Group A- animals regularly died within the first 24 h, with no indication of central nervous system involvement. Less blood had to be drawn to attain hypotension (mean arterial pressure 50 mm Hg) in group A+ (1.5 +/- 0.3 ml/100 g b.w.) than in group A- (2.5 +/- 0.2 ml/100 g b.w.). Group A+ also had less "washout" acidosis 5 min after reinfusion of the shed blood than group A- (15 min of ischemia: pH 7.24 +/- 0.07 v 6.96 +/- 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Forebrain ischemia in the rat. Relation between duration of ischemia, use of adjunctive ganglionic blockade and long-term recovery. 287 36


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