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Query: UMLS:C0278134 (anesthesia)
 110,339 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of pentobarbital on survival times of mice exposed to oxygen, 5 per cent, were studied over a large dosage range in normal mice and in mice made tolerant to the effect of barbiturates. Tolerance was induced by pretreatment with phenobarbital, 210 mg/kg, for three days, which increased the median anesthetic dose (AD50) for pentobarbital from 34 to 53 mg/kg. In nontolerant mice there was a dose-related increase in mean survival times for doses between 35 and 60 mg/kg, with a maximum increase to 303 per cent above control. At doses of more than 60 mg/kg survival times progressively decreased toward control. For tolerant mice survival time as a function of pentobarbital dosage was shifted to the right, i.e., protection necessitated higher doses. This shift was not explained by lower brain concentrations of pentobarbital in tolerant animals, but rather parallelled the increased tolerance to the anesthetic effect of the barbiturate. The authors conclude that in this model the protective effect of barbiturate is a function of the anesthetic effect rather than the barbiturate concentration in brain per se. Hypothermia (29 C) resulted in an increase in mean survival time comparable to that in barbiturate-treated animals. This supports the hypothesis that protection is ultimately a function of decreased cerebral metabolism, whether produced by anesthesia or by hypothermia. This model measures only the effect on spontaneous respiration during hypoxia. It is possible that other mechanisms are involved if barbiturates protect in other situations, such as during or after periods of complete ischemia.
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PMID:Barbiturate protection in tolerant and nontolerant hypoxic mice: comparison with hypothermic protection. 45 57

Differential nerve block from peridural anesthesia was used to determine a) if the pressor response to muscle ischemia in man is caused by stimulation of small sensory nerve fibers and b) if these fibers contribute to cardiovascular-respiratory responses during dynamic exercise. Four men exercised at 50-100 W for 5 min. Muscle ischemia and a sustained pressor response were produced by total circulatory occlusion of both legs beginning 30 s before the end of exercise and continuing for 3 min postexercise. During regression of full motor and sensory block, motor strength recovered while sensory block continued; the pressor response was blocked as long as sensory anesthesia persisted (two subjects). During blockade of the pressor response, cardiovascular-respiratory responses to exercise gradually returned from augmented to normal (preblock) levels. Sensory blockade was incomplete in two subjects and the pressor response was not fully blocked. We conclude that stimulation of small sensory fibers during ischemia elicits the pressor response, but that these fibers appear not to contribute to cardiovascular-respiratory responses during mild dynamic exercise with adequate blood flow.
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PMID:Blockade of the pressor response to muscle ischemia by sensory nerve block in man. 49 28

The purpose of this study was to determine the incidence of ST-segment depression during anesthesia and operation. Graded exercise testing has demonstrated a high correlation between ST-segment depression and myocardial ischemia. Therefore, 11 patients without and 29 patients with known coronary-artery disease were monitored during surgical procedures with a commercially available exercise electrocardiographic monitor (Viagraph). Comparisons were made between this device, which monitored lead V5, and the standard operating room monitor, which monitored lead 11. Eleven of 29 patients in the disease group demonstrated significant ST depression. Nine of the 11 ischemic episodes were not recognized on the standard operating room monitor. Retrospective review of anesthetic records of those 11 patients with ST-segment depression revealed rate--pressure product values greater than 11,000 for ten of them. Postoperatively, three of the 11 patients with significant ST-segment depression had changing electrocardiograms compatible with ischemia. None of the control group demonstrated significant ST-segment depression. The incidence of ischemia was 38 per cent during anesthesia and operation in the coronary-artery-disease group. Lead V5 analysis is superior to lead 11 analysis in detecting ST-segment depression. The period in which intubation is performed is one of the highest-risk intervals during anesthesia and operation, particularly when it is associated with an increased rate--pressure product.
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PMID:Myocardial ischemia during non-cardiac surgical procedures in patients with coronary-artery disease. 49 52

Hemodynamic monitoring and care of the patient at high risk for anesthesia require a careful and systematic approach. During preoperative evaluation the patient at increased risk must be identified and correctable problems must be solved. The patient's current medications must be reviewed because they may influence the choice of anesthetic approach and may alter the physiologic response to the stresses commonly associated with anesthesia. In addition to conventional clinical and electrocardiographic monitoring, perioperative hemodynamic monitoring may be desirable for patients at special risk, who are likely to have significant associated medical problems or to undergo complicated surgical procedures. No ideal induction agent exists, and hypotension secondary to peripheral vasodilation or myocardial depression, or both, is a potential problem. Patients with an inordinately high risk may benefit from mechanical circulatory assistance prior to induction of anesthesia. Attention to oxygenation, blood volume replacement and the prevention of hypertensive episodes are particularly important during anesthesia so that optimal cardiac performance is ensured and ischemia avoided. The stresses during emergence from anesthesia contribute to lability of the cardiovascular status and hypoxemia. The period of risk does not conclude with immediate recovery from anesthesia but extends through the postoperative phase. Careful monitoring and attention to the control of pain, prevention of hypotension and hypertension, adequate oxygenation, early mobilization and resumption of the administration of cardiac medications are important factors in a successful outcome.
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PMID:Hemodynamic monitoring and care of the patient of high risk for anesthesia. 49 83

Cefamandole levels were measured in peripheral blood, and in skeletal muscle and subcutaneous fat samples taken from 20 patients during amputation of the leg for severe ischemia. Tissue samples were taken from both proximal and distal levels in the amputated limb. Cefamandole was administered as either a 2 g intravenous bolus given with induction of anaesthesia, or a combination of 1 g intramuscularly with the premedication plus 1 g intravenously with anaesthetic induction. Levels of cefamandole in serum and proximal muscle and fat samples were well above the minimum inhibitory concentrations required for most Gram-positive and Gram-negative organisms. Cefamandole levels in more distal samples were somewhat lower but still achieved therapeutic levels in most cases. Higher tissue levels of cefamandole were achieved when 2 g were given intravenously as a bolus.
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PMID:Evaluation of tissue levels of cefamandole in severely ischaemic lower limbs using two regimens of dosage. 52 48

Ischemic brain damage can be partially ameliorated by barbiturate therapy applied postinsult. Catabolism-induced brain hyperosmolality during ischemia may contribute to the development of brain edema after restoration of circulation. To determine changes in brain osmolality during ischemia and the effect of barbiturate anesthetics in altering its course, we measured whole and regional (cerebral cortex, diencephalon-midbrain, and cerebellum) brain osmolality for up to 2 hours after decapitation ischemia in unanesthetized and pentobarbital anesthetized rats. Normal (nonischemic) brain osmolality in pentobarbital anesthetized rats was 319 +/- 2 mOsm/1 (mean +/- SEM) and higher than in unanesthetized rats (307 +/- 6 mOsm/1). The rate of increase in whole brain osmolality was 60% slower in pentobarbital anesthetized rats in the first 60 minutes of ischemia and regional brain osmolality increased by a maximum of 32 mOsm/1 compared to 45 mOsm/1 in unanesthetized rats. The potential for edema based on percent change in brain osmolality as well as the rapidity of the change was greater in unanesthetized rats. The significance of the increase in brain osmolality with barbiturate anesthesia and its attenuation of the rate and magnitude of increase during ischemia is discussed.
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PMID:Rat brain osmolality during barbiturate anesthesia and global brain ischemia. 64 23

Experience with 105 lower limb arterial injuries in 103 patients in a general hospital is described. The pathology is discussed: it is noted that spasm per se could not be incriminated as a cause of ischemia. Management of the injuries and associated fractures is outlined. A plea is made for use of external fixation in compound injuries. An aggressive approach to the degloved limb, open three-compartment fasiotomy for severe vascular injury with signs of ischemia, and delayed primary closure for wounds with septic complications are recommended. Associated soft-tissue injury requires arterial reconstruction even in the presence of muscle rigor and anesthesia.
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PMID:Arterial trauma involving the lower limb. 66 Jun 85

The mitochondrial fraction obtained from brains of animals submitted to ischemia shows a decrease of phospholipid level, especially plasmalogens in the fraction of ethanolamine phospholipids and choline phospholipids. There appears simultaneously an increase of free radical oxidation processes of unsaturated fatty acids from these phospholipids. The peroxidation processes of mitochondrial lipids are stimulated by calcium ions and, to a smaller extent, by magnesium ions. Barbiturate anesthesia inhibits the peroxidation of fatty acids and increases the antioxidant abilities of the nervous tissue. Nembutal added in vitro remains without effect on the above processes. The effect of acetylcholine and the antioxidant ability of nervous tissue under barbiturate anesthesia with respect to ischemia are discussed.
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PMID:Effect of ischemic anoxia and barbiturate anesthesia on free radical oxidation of mitochondrial phospholipids. 70 72

Despite a general impression to the contrary, a recent survey showed that the current mortality rate for acute arterial ischemia approximates 25%. Much of this apparently relates to toxins and procoagulants released from the dying limb, a tendency which may be enhanced further by attempts at revascularization. Based on these observations, we have utilized selective management of acute arterial ischemia in an attempt to minimize deaths and to salvage the maximum number of limbs. If the patient presents within 6 to 8 hours of the onset of acute arterial occlusion and if paralysis or anesthesia is present, then ultimate limb loss is likely. The therapeutic choices are high-dose heparin therapy, operative removal of the clot, or amputation of the limb--the ultimate choice being dependent upon the particular status of the patient. But if sensation and motor function are present, viability of the limb is not threatened, and good results can be obtained by utilizing anticoagulation and delayed elective revascularization, if the latter is indicated. But revascularization attempts after 10 to 12 hours of severe ischemia often are unsuccessful, and ischemia is followed by either recurrent thrombosis and ultimate limb loss, or by death from the systemic effects of reperfusion of ischemic tissue. This type of limb is managed best by using high-dose heparin therapy if viable, or by amputation if it is not. Employing the above criteria, 54 patients with acute arterial ischemia averaging 59 years of age, were treated. Seventeen had immediate thrombectomy, yielding two deaths and four subsequent amputations. Twenty-nine received anticoagulation treatment, resulting in one death and five amputations, and six had immediate amputation, yielding one death. Three had no specific treatment, with one poor result. There were four deaths in the entire series--a mortality rate of 7.5%--and two thirds of the limbs were salvaged. We have concluded that selective management, as prescribed above, was responsible for a significant decrease in mortality rate with no corresponding increase in limb loss, and that high-dose heparin therapy ultimately may prove the initial treatment of choice in all cases of acute arterial ischemia.
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PMID:Management of acute lower extremity arterial ischemia due to embolism and thrombosis. 71 1

The present study, which concerns the rate of changes in the cerebral cortex concentrations of phosphocreatine (PCr), ATP, ADP, AMP, lactate and pyruvate during complete ischemia, had the objective of finding out whether or not phenobarbital retards depletion of tissue energy reserves during ischemia. Ischemia was induced for periods of 10 s to 10 min in animals maintained on 70% N2O or given 150 mg.kg-1 of phenobarbital. The results showed that the barbiturate anaesthesia delayed utilization of ATP during the first 2 min. However, after 5 min of ischemia PCr and ATP concentrations, as well as the calculated adenylate energy charge, were identical in animals anaesthetized with nitrous oxide and phenobarbital. Thus, phenobarbital induces a very moderate delay in the depletion of cerebral energy reserves that occurs during complete ischemia. The results obtained after 5-20 s of ischemia allowed calculation of energy (approximately P) utilization according to Lowry et al. (1964). The closed system method gave values for approximately P utilization which were not far from those obtained by CMRo2 measurements. However, with normal values for metabolic rate (70% N2O) valid estimates are obtained only with very short ischemic periods (5-10 s) and, with such short periods, the oxygen content of the tissue may introduce an error.
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PMID:Influence of phenobarbital on changes in the metabolites of the energy reserve of the cerebral cortex following complete ischemia. 71 81


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