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

Some coronary vasodilators, paradoxically, may endanger patients with coronary artery disease by causing "coronary steal." To determine the capacity of isoflurane and halothane to cause coronary steal, the authors studied their effects on coronary vascular resistance (CVR), diastolic coronary artery pressure, and collateral myocardial blood flow. Using ameroid constrictors, chronic occlusions of the left anterior descending (LAD) coronary artery were created in ten dogs. Six to eight weeks after implantation, the dogs were anesthetized with fentanyl and pentobarbital, and a stenosis was created on the circumflex (Cx) coronary artery. Isoflurane and halothane were each administered in doses of 0.5 and 1.5 MAC. Diastolic aortic pressure was held constant. Using small catheters in the circumflex and LAD coronary arteries, the authors measured diastolic coronary artery pressures. Collateral myocardial blood flow was measured by the microsphere method. In this model, halothane and isoflurane minimally affect CVR. The maximum change in CVR, which was found during 1.5 MAC isoflurane, was -8% (not significant). Diastolic coronary pressures distal to the Cx stenosis (54.5 +/- 11.5 mmHg) and distal to the LAD occlusion (44.5 +/- 5.2 mmHg) did not change significantly with either isoflurane or halothane. Transmural collateral blood flow distal to the LAD occlusion (0.51 +/- 0.11 cc.g-1.min-1) was unaltered by either drug. There was no evidence of coronary steal. Epicardial ECG S-T segments showed no evidence of ischemia. The finding of minimal direct effects of halothane and isoflurane on CVR, diastolic coronary pressure, and collateral myocardial blood flow suggest that, under the conditions of this study, neither agent, when used as an adjuvant to high-dose narcotic anesthesia, is likely to cause myocardial ischemia by a coronary "steal" mechanism.
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PMID:Effects of isoflurane and halothane on coronary vascular resistance and collateral myocardial blood flow: their capacity to induce coronary steal. 367 66

Effects of halothane on the force of myocardial contraction and energy demand-supply balance (NADH fluorescence) were studied in two rabbit heart preparations--the interventricular septum perfused through the septal artery at various flow levels, and a Langendorff whole-heart preparation with ischemia caused by graded reduction of perfusion pressure. The septum experiments showed that halothane [1.2% = 1.5 minimum alveolar concentration of anesthetic preventing movement response to a noxious stimulus (MAC)] increased NADH fluorescence (+9%, p less than 0.02) at a normal level of perfusion (3 ml/g/min) and, at the same time, decreased it (-6%, p less than 0.02) when myocardial energy balance deteriorated from severe hypoperfusion (0.2 ml/g/min). The inhibitory effect of halothane on developed systolic tension was less pronounced at the low (ischemic) level of myocardial perfusion as compared with the high level--leads to 24% (0.2 ml/g/min) vs. leads to 38% (3 ml/g/min), p less than 0.025. However, if control and halothane values of developed tension were compared at equi-NADH levels (the same state of energy balance), the depressive effect of halothane on the force of myocardial contraction was not less pronounced in severe energy imbalance. Similar results were obtained in the Langendorff preparation experiments. The results suggest that halothane partially restores energy balance in hypoperfused myocardium; however, at the normal level of perfusion, its effect is in an opposite direction. Halothane depresses contractility in the hypoperfused myocardium to a lesser degree than at the normal level of myocardial perfusion. This effect is probably determined by the interaction of two influences: direct depressive effect of the agent on contractile mechanisms, and indirect positive inotropic effect due to improvement in energy balance.
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PMID:Effect of halothane on contractile function of ischemic myocardium. 619 Nov 43

We studied the effect of sevoflurane on ischaemic myocardium in terms of myocardial energy and carbohydrate metabolism. Mongrel dogs were anaesthetized initially with sodium pentobarbitone, and then inhaled sevoflurane at 0% (0 MAC), 2.4% (1.0 MAC) or 4.7% (2.0 MAC) of inspired concentration for 60 min. Ischaemia was then induced for 3 min by ligating the left anterior descending coronary artery. The tissue levels of energy and carbohydrate metabolites were determined before and after sevoflurane inhalation, and after 3 min of ischaemia. Sevoflurane significantly decreased systolic and diastolic blood pressures, heart rate, and rate-pressure product in a dose dependent manner. When the animals did not inhale sevoflurane (0 MAC), ischaemia significantly decreased adenosine triphosphate and creatine phosphate levels, and produced alterations of carbohydrate metabolism. These metabolic changes induced by ischaemia were lessened by inhalation of sevoflurane. To exclude the influence of haemodynamic changes, blood pressure and heart rate were maintained during 1.0 MAC sevoflurane inhalation. Significant attenuation of ischaemia-induced metabolic changes caused by sevoflurane was still observed in some metabolites. These results indicate that the ischaemic influences on the myocardium may be reduced by sevoflurane, and this protective effect can be explained not only by its haemodynamic effect.
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PMID:Effects of sevoflurane on ischaemic myocardium in dogs. 767 77

Etomidate and thiopental reduce ischemic neuronal injury but the mechanism by which they do so is not clear. Ischemia-induced release of the excitatory neurotransmitters glutamate and glycine is thought to play a major role in the pathophysiology of ischemic injury. To determine how etomidate and thiopental modulate excitatory transmitter release, their effect on the release of glycine and glutamate during ischemia was evaluated by microdialysis in the hippocampus and cortex of rats. Three groups of Wistar-Kyoto rats (n = 5/group) were studied. In the etomidate and thiopental groups, electroencephalogram (EEG) burst-suppression was achieved and maintained by a continuous infusion of either etomidate (0.6 mg.kg-1.min-1) or thiopental (3 mg.kg-1.min-1) 40 min prior to ischemia. Halothane anesthetized (1 minimum alveolar anesthetic concentration [MAC]) rats served as controls. Ischemia was induced in all three groups by bilateral carotid artery occlusion with simultaneous hypotension to 35 mm Hg for 10 min. Pericranial temperature was controlled at 38 degrees C. Dialysate was collected before, during, and after ischemia. The levels of glutamate and glycine in the dialysate were measured by high-performance liquid chromatography. Within the hippocampus, both glutamate and glycine levels increased significantly in the thiopental and control groups. By contrast, in the etomidate group, glutamate and glycine levels did not increase during ischemia, and peak levels were significantly less than those in the thiopental group. Peak glutamate levels in the thiopental group were significantly larger than in the control group, whereas the peak glycine levels were not different among the groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Etomidate reduces ischemia-induced glutamate release in the hippocampus in rats subjected to incomplete forebrain ischemia. 772 35

One of the most prominent phenomena that occurs during the early phase of cerebral ischemia has been shown to be the immunohistochemical collapse of cytoskeletal proteins. Among these, microtubule-associated protein 2 (MAP 2) has been shown to be vulnerable to ischemic injuries. In order to select a suitable volatile anaesthetic from the standpoint of cytoskeletal protein breakdown during cerebral ischemia, we compared the effect of isoflurane, halothane and sevoflurane on MAP 2 degradation during 20 min of forebrain ischemia in the rat. Under 1 MAC of three volatile anesthetics, forebrain ischemia was induced by the occlusion of the bilateral common carotid artery combined with a lowering of mean arterial pressure to 50 mmHg. Immediately after cerebral ischemia, four regions of the brain, the frontoparietal cortex, brainstem, hippocampus and cerebellum, were removed separately and homogenized. Subsequently, MAP 2 from each region was quantitatively measured using an enzyme-linked immunosorbent assay. MAP 2 in the frontoparietal cortex and hippocampus was significantly protected from degradation with isoflurane anaesthesia more than with halothane and sevoflurane anaesthesia.
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PMID:[Effects of volatile anesthetics on microtubule-associated protein 2 degradation during forebrain ischemia in the rat]. 783 96

Types of anaesthesia in different experimental models of ischemia vary, with consequent difficulties in analysis of results obtained by the authors. The aim of this work was to evaluate EEG and SEPs parameters in a group of rabbits submitted to anaesthesia with halothane. We used White New Zealand rabbits prepared for EEG recording according to the Monnier and Gangloff's stereotaxic method. SEPs were obtained by medial nerve stimulation according to a method standardized in our laboratory. Each animal was anaesthetized with halothane plus nitrous oxide and oxygen or halothane plus oxygen for surgical MAC, which was maintained for a time corresponding to the duration of surgical intervention. We evaluated all parameters in basal conditions and after the administration of anaesthesia until EEG and SEPs returned to basal values. Evoked potentials remained altered for a longer period of time and returned to basal levels only two hours after anaestethic suspension.
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PMID:Neurophysiological parameters during halothane anaesthesia in experimental models of cerebral ischemia. 812 97

Cerebral protection means prevention of cerebral neuronal damage. Severe brain damage extinguishes the very "human" functions such as speech, consciousness, intellectual capacity, and emotional integrity. Many pathologic conditions may inflict injuries to the brain, therefore the protection and salvage of cerebral neuronal function must be the top priorities in the care of critically ill patients. Brain tissue has unusually high energy requirements, its stores of energy metabolites are small and, as a result, the brain is totally dependent on a continuous supply of substrates and oxygen, via the circulation. In complete global ischemia (cardiac arrest) reperfusion is characterized by an immediate reactive hyperemia followed within 20-30 min by a delayed hypoperfusion state. It has been postulated that the latter contributes to the ultimate neurologic outcome. In focal ischemia (stroke) the primary focus of necrosis is encircled by an area (ischemic penumbra) that is underperfused and contains neurotoxic substances such as free radicals, prostaglandins, calcium, and excitatory neurotransmitters. The variety of therapeutic effort that have addressed the question of protecting the brain reflects their limited success. 1) Barbiturates. After an initial enthusiastic endorsement by many clinicians and years of vigorous controversy, it can now be unequivocally stated that there is no place for barbiturate therapy following resuscitation from cardiac arrest. One presumed explanation for this negative statement is that cerebral metabolic suppression by barbiturates (and other anesthetics) is impossible in the absence of an active EEG. Conversely, in the event of incomplete ischemia EEG activity in usually present (albeit altered) and metabolic suppression and hence possibly protection can be induced with barbiturates. Indeed, most of the animal studies led to a number of recommendations for barbiturate therapy in man for incomplete ischemia. 2) Isoflurane. From a cerebral metabolic standpoint, exposure to isoflurane at concentration of 2 MAC is credited with providing the same potential for protection as high dose barbiturate (isoelectric EEG). A possible major difference between barbiturates and isoflurane is the modest cerebral vasodilation induced by the latter while barbiturates are associated with decreased CBF. This suggests that in focal ischemia isoflurane may elicit an intracerebral steal. 3) Calcium entry blockers. Some calcium entry blockers with the distinctive feature of acting preferably on cerebral as opposed to systemic vascular smooth muscles may exert beneficial effects during or after brain ischemia. Two such drugs which have shown promise are nimodipine and lidoflazine. In animal and human studies nimodipine has been reported to improve the neurologic outcome of both the cerebral vasospasm and the postischemic hypoperfusion state.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Cerebral protection]. 827 62

Isoflurane causes vasodilation in the coronary circulation. The present study evaluated whether this action is preserved after a brief coronary occlusion followed by reperfusion. Fourteen open-chest dogs anesthetized with fentanyl and midazolam were studied. The left anterior descending coronary artery was perfused via an extracorporeal system with normal arterial blood or with arterial blood equilibrated with 1.4% (1 minimum alveolar anesthetic concentration [MAC]) isoflurane. Coronary perfusion pressure was maintained at 90 mm Hg. Coronary blood flow (CBF) was measured with a Doppler flow transducer. Steady-state changes in CBF during isoflurane, and during intracoronary infusions of acetylcholine (Ach; 20 micrograms/min), an endothelium-dependent vasodilator, and sodium nitroprusside (SNP; 80 micrograms/min), an endothelium-independent vasodilator, were compared in normal myocardium and in myocardium subjected to 15 min of ischemia (due to cessation of perfusion) followed by 30 min of reperfusion. Ischemia-reperfusion had no significant effect on the increases in CBF by isoflurane (421% +/- 88% vs 388% +/- 84%) or SNP (115% +/- 18% vs 135% +/- 19%), whereas it attenuated these increases in CBF by Ach (232% +/- 38% vs 143% +/- 21%). In conclusion, a brief period of myocardial ischemia followed by reperfusion did not affect the coronary vasodilating effects of isoflurane and SNP, although it blunted these effects of Ach. The present findings provide further evidence suggesting that the ability of isoflurane to relax coronary vascular smooth muscle is independent of the nitric oxide-cyclic guanosine monophosphate pathway.
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PMID:Isoflurane-induced coronary vasodilation is preserved in reperfused myocardium. 871 15

The present studies were undertaken to investigate the effects of gender and estrogen treatment on focal cerebral ischemia in male and female rats. Focal ischemia was created by inserting a 3-0 surgical suture through the left cervical internal carotid artery to obstruct the blood flow into the middle cerebral artery (MCA). The MCA was reperfused by removing the suture in 40 min. All rats were sacrificed for measurement of infarct area after 24 h. In the first study, mortalities from MAC occlusion were 12.5% (2/16) each for intact male rats and intact female rats, and 23.5% (4/17) for ovariectomized (OVX) female rats. The coronal infarct area (mean+/-S. E.M.) was 9.5+/-1.0% for intact female rats, 16.6+/-1.6% for intact male rats (p=0.0001 vs. intact female rats), and 16.0+/-1.4% for OVX female rats (p=0.0002 vs. intact female rats). In a second experiment, OVX-female rats were administrated either 17beta-estradiol (E2) or its vehicle, hydroxypropyl-beta-cyclodextrin (HPCD), at 40 min after the onset of MCA occlusion. Mortalities were 40% (4/10) for vehicle treated OVX rats and 0% for E2 treated OVX rats. The coronal infarct area (mean+/-S.E.M.) was 19.3+/-1.8% for vehicle treated rats vs. 8.0+/-1. 2% for E2 treated rats (p<0.01). Serum estrogen levels for vehicle treated OVX rats were 14.5+/-1.2% pg/ml vs. 142.7+/-23.6 pg/ml for E2 treated OVX rats (p<0.01). These results strongly suggest that the level of circulating estrogens play an important role in protecting brain tissues against ischemia induced by MCA occlusion.
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PMID:Effects of gender and estradiol treatment on focal brain ischemia. 951 71

Continuous measurement of somatosensory evoked potentials (SEP) by means of characteristic changes in the signal pattern makes it possible to identify cerebral or spinal cord ischemia during critical phases of the operative procedure. A correct interpretation of the measurements is only possible, however, if the influence of drugs acting on the central nervous system is known. The authors were able to show that inhaled anesthetics have an impact on latencies and response amplitudes. This study examined the influence of various concentrations of desflurane on the conduction of SEP of the Median nerve. In addition, the authors determined how the supplementation of nitrous oxide (N2O) influences the stimulus response of the medianus nerve's SEP. Desflurane has been shown to produce dose-dependent increases in SEP latency (data in part for latency N2O: 0.5 minimum alveolar concentration [MAC] = 20.8 +/- 0.9; 1.5 MAC = 22.2 +/- 1.5; 1.5 MAC/N2O= 23.8 +/- 1.5) and decreases in amplitude, whereas cervically recorded subcortical SEP components are minimally influenced by desflurane. When nitrous oxide is added, there were marked reductions in amplitude (p<0.01) of the cortical stimulus response (1.5 MAC = 2.4 +/- 0.9; 1.5 MAC/N2O = 1.1 +/- 1). It can therefore be recommended that supplementation with N2O should be avoided in the presence of low initial amplitudes. Based on the study's results, the use of desflurane (up to 1.0 MAC) seems to be compatible with intraoperative monitoring of median somatosensory evoked potentials.
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PMID:Modulation of somatosensory evoked potentials under various concentrations of desflurane with and without nitrous oxide. 979 5


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