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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some of the patients who suffer from cerebral ischemia may at the same time have coronary insufficiency. For such cases, not only extracranial-intracranial (EC-IC) bypass but also cardiac revascularization is considered to be necessary. One-stage surgery of both carotid endarterectomy and coronary artery bypass grafting (CABG) has not infrequently been published. However, the combination of EC-IC bypass and CABG is rarely reported in the literature. The indication of EC-IC bypass and/or CABG for such patients above stated has been searched for. In fact, CABG runs the risk of aggravating cerebral ischemia and/or intracranial hemorrhage by inevitable hypotension, hypothermia and heparinization of a large amount, while EC-IC bypass may safely be carried out so long as cardiac conditions are carefully controlled during the operation. It is consequently presumed that the preliminary EC-IC bypass followed by CABG seems to be the method of choice for simultaneous carotid and coronary ischemia. Two cases underwent the staged revascularization, first for the brain and next for the heart, with a successful result are reported in the present paper.
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PMID:[Revascularization for simultaneous carotid and coronary ischemia]. 350 Oct 72

Vinpocetine has been compared with 3 structurally related drugs for activity in protecting mice from hypoxia-induced lethality upon i.p. administration. In order of potency, vinpocetine (ED50 = 16.6 mg/kg), 1-eburnamonine (ED50 = 21.0 mg/kg), vinconate (ED50 approximately 25 mg/kg), and vincamine (ED50 = 47.0 mg/kg) increased the number of mice surviving an 80 sec exposure to 100% nitrogen gas. Furthermore, the antihypoxic effects of these drugs were not due to an induced hypothermia. All of the drugs, with the exception of vinconate, exhibited a monotonic dose-response curve and caused 100% survival at some dose. The antihypoxic effects with vinpocetine and related drugs in this model correlate with protective effects observed in animal models of cerebral ischemia and with therapeutic effects in patients with compromised cerebral blood flow. The possible mechanisms of action of these drugs are discussed.
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PMID:Protective effects of vinpocetine and structurally related drugs on the lethal consequences of hypoxia in mice. 359 69

In the 6 year period 1976 through 1981, 13 patients had surgical correction of aneurysms of the aortic arch with the use of deep systemic hypothermia (15 degrees to 24 degrees C) and partial (lower body only) or complete circulatory arrest. Three pathological groups were recognized: Group I (seven patients), with involvement of the aortic arch only; Group II (two patients), with extension of disease from the arch into its major vessels; and Group III (four patients), with predominant involvement of the major vessels. In the first eight patients (1976 to 1979), the carotid arteries were perfused directly with circulatory arrest of the rest of the body. Three of the eight patients (37.5%) died, two of cerebral complications and one of respiratory failure. Another patient had a nonfatal neurologic complication. In the last five patients (1980 to 1981), the carotid arteries were not perfused and variable periods of cerebral ischemia under hypothermic protection (18 degrees C) were permitted. All patients survived, and only one showed transient, minor neurologic changes. Our current recommended technique includes deep systemic hypothermia (15 degrees to 18 degrees C) using femoro-femoral bypass, complete circulatory arrest, and temporary occlusion of the carotid arteries. Additional protection of the myocardium is achieved by cold potassium (20 mEq/L) cardioplegia. Repair of the aneurysm is performed from within the aortic arch in a bloodless field. The hitherto high mortality and morbidity following resection of aneurysms of the aortic arch can be greatly reduced using this simplified technique.
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PMID:Hypothermia and circulatory arrest for surgical resection of aortic arch aneurysms. 662 Oct 86

We have successfully corrected interrupted aortic arch with ventricular septal defect by employing deep hypothermia and circulatory arrest, a median sternotomy incision, and a pulmonary arteriotomy. This simplified technique has the advantage of an abbreviated period of cerebral ischemia, with a relatively simple partitioning of the pulmonary artery.
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PMID:Pulmonary artery partition: new method for correction of interrupted aortic arch. 687 68

The effect of temperature (37 degrees C, 28 degrees C, and 18 degrees C), 160 mg/kg lidocaine, and 40 mg/kg thiopental on the efflux of cellular potassium in the cerebral cortex during complete global ischemia was examined. Cerebral ischemia was induced in dogs on cardiopulmonary bypass circulation by stopping the pump. Potassium concentration was measured on the brain surface by a valino-mycine-membrane electrode, which in its response corresponded well to an inserted microelectrode. Hypothermia reduced the ischemic potassium efflux rate to about 50 per cent at 28 degrees C, and about 25 per cent at 18 degrees C. At all temperature levels lidocaine caused an additional reduction in the potassium efflux rate of about 50 per cent, probably by reducing membrane ion permeability in accordance with its local anesthetic action. Thiopental had no effect on the potassium efflux during ischemia. This study opens the possibility that lidocaine, like hypothermia, may provide protection of the ischemic brain.
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PMID:Increase in extracellular potassium in the brain during circulatory arrest: effects of hypothermia, lidocaine, and thiopental. 727 Sep 50

The course of ischemic increase of extracellular potassium concentration ([K+]e) was studied in rat cerebral cortex with potassium selective microelectrodes and correlated to the preischemic functional and metabolic state. Complete cerebral ischemia was induced in artificially ventilated rats by cardiac arrest. Seven different functional states including conditions with cerebral hypermetabolism (seizures, amphetamine intoxication, hyperthermia) and hypometabolism (barbiturate anesthesia, hypothermia) were chosen in order to cover a wide range of cerebral metabolic rates (CMRO2 : 28.7--2.4 ml O2/(100 g)/min). The ischemic increase of [K+]e was delayed in conditions with low CMRO2 and accelerated in conditions with high CMRO2; the time interval to the terminal steep rise in extracellular potassium concentration varied within the extremes of 35 +/- 5 and 365 +/- 12 sec (means +/- S.E.M.), the control state (N2O-analgesia) being 116 +/- 5 sec. In groups with high CMRO2 electrocortical activity ceased within 15 sec and in groups with low CMRO2 within 22 sec. The rates of the ischemic [K+]e increase, measured as rate of change in the potassium electrode potential (mV/sec), remained high in conditions with high preischemic CMRO2 and low in conditions with low CMRO2, indicating a remaining influence of the preischemic metabolism on membrane ion permeability. These results support previous metabolic data indicating that the rate of consumption of high energy phosphates during ischemia mirrors the preischemic cerebral metabolic rate. Phenobarbital anesthesia did not change the initial rate of [K+]e increase but reduced the rate of [K+]e increase later during ischemia, suggesting a special effect of barbiturates on partly depolarized membranes.
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PMID:The increase in extracellular potassium concentration in the ischemic brain in relation to the preischemic functional activity and cerebral metabolic rate. 740 19

A case of cardiac arrest during moderate hypothermia and profound hypotension following rupture of a cerebral aneurysm is described. The patient survived with few neurological sequelae directly attributable to the period of cerebral ischaemia. The protective effect of hypothermia in the prevention of neurological damage is illustrated as are the difficulties of resuscitation.
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PMID:Cardiac arrest during moderate hypothermia for cerebrovascular surgery. 743 98

Anesthetic care for patients with traumatic brain injury involves an integration of cerebral resuscitation, resuscitation of other vital organs, the provision of "anesthesia," and the prevention of harmful physiologic responses to surgery. Adverse responses to surgery such as hypertension, tachycardia, coughing, and straining can increase intracranial pressure (ICP). Airway manipulations can aggravate spinal cord injury as well as increase ICP. Anesthetic agents can exacerbate hemodynamic instability, increase cerebral blood volume and ICP, and produce respiratory depression. Cerebral resuscitation during surgery resembles that in the preoperative and postoperative periods. ICP measurement and jugular venous saturation monitoring may help define end-points for cerebral resuscitation. Various anesthetic techniques and agents have distinct advantages and disadvantages. The choice of agents and techniques is determined by the nature and severity of the patient's injuries and by pre-existing medical problems. The investigation of drugs that might protect against cerebral ischemia has included anesthetic agents but none appear to be uniformly effective. Intraoperative hypothermia is also being investigated as a cerebral protectant.
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PMID:Anesthesia and head trauma. 749 63

The cerebroprotective effects of mild hypothermia have been extensively studied in various animal models of ischemia, but the mechanism by which mild hypothermia diminishes ischemic injury is not well understood. Nitric oxide (NO) has been implicated as a mediator of glutamate excitotoxicity in primary neuronal cultures, and its synthesis is acutely increased during focal ischemia in vivo. To evaluate possible mechanisms of hypothermic neuroprotection, we measured markers of NO synthesis--nitrite and cyclic guanosine monophosphate (cGMP) levels and NO synthase activity--during right middle cerebral artery occlusion (MCAO) in the rat under normothermic (36.5 degrees C) and mild hypothermic (33 degrees C) conditions. There was a significant increase in nitrite concentration in the right hemisphere versus the left under normothermic conditions at 10 and 20 minutes after MCAO (P < 0.01), with a return to baseline levels by 60 minutes. The increase in cortical nitrite levels in the right hemisphere versus the left was not observed with mild hypothermia. There was a threefold increase in cGMP synthesis in the normothermic right cortex 10 minutes after MCAO (P < 0.05). This rise in cGMP did not occur in hypothermic animals, and the right to left cortical disparity in cGMP production was abolished. Finally, the significant increase in NO synthase activity seen in the normothermic ischemic cortex was absent in hypothermic rats (P < 0.05). These results suggest that mild hypothermia (33 degrees C) modulates the burst of nitric oxide synthesis during cerebral ischemia and may account, at least partially, for its cerebroprotective effects.
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PMID:Effect of mild hypothermia on nitric oxide synthesis during focal cerebral ischemia. 752 62

Hypothermia results in a progressive depression of cerebral electrical activity and metabolism. In the setting of cerebral ischemia, large reductions in temperature are associated with a better preservation of high-energy phosphates, a reduced accumulation of toxic metabolites, and an improvement in post-ischemic outcome. With temperature reductions of < or = 6 degrees C, the brain is also partially protected from ischemic neurologic injury; however, this protection does not correlate with measurable alterations in high-energy phosphate depletion or lactate accumulation. Thus, cerebral protection by hypothermia may be due to a variety of factors, including alterations in basal metabolism, ion homeostasis, agonist-specific receptor activity, and cellular structure. Further, the relative influence of these factors may change with progressive reductions in temperature.
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PMID:Cerebral metabolic rate and hypothermia: their relationship with ischemic neurologic injury. 754 75


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