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

To define the part played by mild-to-moderate hypothermia in neuroprotection, it is necessary to take into account the thermoregulatory responses that occur in the normal human as the change in central temperature exceeds 0.2 degrees C. The mechanisms induced by cold are cutaneous vasoconstriction and shivering. They must be suppressed before starting controlled hypothermia. In these conditions, controlled moderate hypothermia between 32 and 35 degrees C does not seem to have deleterious side-effects, especially on coagulation. Caution is needed with the analysis of the numerous papers reporting experiments concerning the effects of moderate hypothermia in animals with induced cerebral ischaemia because of significant differences in the study designs. These differences concern mainly the time of onset of hypothermia, viz before or after ischaemia, the fact that the ischaemia is either global or focal, that it is caused by vascular occlusion posttraumatic or initiated by hypo or hyperglycemia. Some differences are also existing in the criteria used to appreciate the neuronal damage, as well as in the level of temperature and the site where it is measured. The mechanism of neuroprotection from moderate hypothermia seems to be not only a decrease in cerebral metabolism, but also involves a specific action on some intra-cellular events such as the blocking of the release of glutamate and of lipid peroxydation in brain tissue. An indirect proof of the neuroprotective effect of moderate hypothermia is the increase in the neuronal damage induced by moderate hyperthermia. It is conceivable that moderate hypothermia could exert a better neuroprotective effect than the drugs having this reputation, such as barbiturates, isoflurane and propofol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mild hypothermia and cerebral protection]. 767 76

We have previously shown that somatostatin (SS) immunoreactive (-i) neurons, located in the rat dentate hilus, are vulnerable to cerebral ischemia (Johansen et al., 1987). Within 40 h after ischemia, the cells show clear signs of cell death. At the same time, we observed that dying cells, located in the projection field of the mossy fibers (dentate hilus and CA3 mossy fiber layer), accumulate free zinc. We now demonstrate that the hilar cells, accumulating zinc after ischemia, are SS-i cells. Since it is known that hypothermia can ameliorate ischemic brain damage, we furthermore studied whether hypothermia (29 degrees C) protects the vulnerable SS-i neurons in hilus from zinc accumulation and ischemic cell death. We found that hypothermia both prevented ischemia-induced neuronal zinc accumulation and cell death. We speculate that hilar SS-i cells are highly vulnerable to ischemia, and develop rapid ischemic cell death, because they accumulate zinc shortly after ischemia.
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PMID:Hypothermia protects somatostatinergic neurons in rat dentate hilus from zinc accumulation and cell death after cerebral ischemia. 768 76

Two patients underwent carotid artery ligation for the purpose of surgical hemostasis either under hypothermia or under normothermia. One was 56-year-old man with rupture of brachiocephalic artery following esophagectomy. The bilateral common carotid arteries were ligated for bypass-grafting between the right internal carotid artery and the left common carotid artery for 35 min under surface-induced hypothermia at a rectal temperature of 30.7 degrees C. No postoperative neurological deficit developed. The other was 40-year-old woman with a malignant parotid tumor involving left internal carotid artery. The left carotid artery was ligated for 20 min at a rectal temperature of 37.3 degrees C. Cerebral ischemia developed postoperatively. Mild to moderate hypothermia should be reevaluated as one of useful measures to protect the brain from cerebral ischemia.
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PMID:[Reevaluation of hypothermia as protective measures against cerebral ischemia]. 774 96

The neuroprotective properties of hypothermia are well recognized. For many years, the ability of hypothermia to decrease the neurologic morbidity associated with episodes of ischemia has been ascribed to the reduction in metabolic rate that accompanies decreases in temperature. More recently, evidence has accumulated that hypothermia may exert some of its neuroprotective effects by reducing the ischemia-induced release of excitatory amino acids. This attenuated release occurs even with the mild degrees of hypothermia that can easily be produced in operating rooms and intensive care units. Preliminary data suggest that mild hypothermia may be of benefit in surgical patients at risk for intraoperative cerebral ischemia and patients who have suffered traumatic brain injury. Because of the minimal risk associated with lowering body temperature to 34 degrees C, additional outcome studies are in progress to ascertain the potential benefits of this mode of therapy.
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PMID:Inhibition of glutamate release: a possible mechanism of hypothermic neuroprotection. 777 69

This is the first report of cerebral blood flow measurement with transcranial Doppler (TCD) during aortic arch reconstruction using continuous retrograde cerebral perfusion (CRCP) with deep hypothermia. Cerebral blood flow velocity was measured in 6 patients. CRCP was performed via the superior vena cava (SVC) at 30 cmH2O of internal juglar vein pressure and at 18 degrees C or lower of minimum bladder temperature. During the operation, the flow velocity of the middle cerebral artery (MCA) was continuously measured with TCD fixed on the temple. The cerebral blood flow during CRCP was different in each of the 6 patient. The retrograde MCA flow could be measured during CRCP in 3 patients, and the flow velocity was 11-60% of the MCA flow velocity before cardiopulmonary bypass. In the other 3 patients, retrograde MCA flow could not be detected during CRCP, but antegrade MCA flow could be found after antegrade perfusion was resumed. The antegrade flow velocity right after CRCP became more than the MCA flow before CRCP, which was regarded as a reaction due to cerebral ischemia. All the patients awoke within several (2-9) hours after operations and had no permanent neurological complications. But 2 patients developed drowsiness for several days after the operations; their CRCP times were 127 and 131 minutes. It is concluded that CRCP is a simple technique for brain protection, but the cerebral blood flow during CRCP is a simple technique for brain protection, but the cerebral blood flow during CRCP is different in each patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Transcranial Doppler measurement of middle cerebral artery blood flow during continuous retrograde cerebral perfusion]. 779 99

Following cerebral ischemia, certain populations of neurons degenerate. Excessive accumulation of excitatory amino acids in the synaptic cleft, activation of excitatory amino acid receptors, and influx of calcium into neurons play a key role in the development of ischemia-induced neuronal death. We hypothesized that neuroprotection may be achieved by enhancing inhibitory (i.e., gamma-aminobutyric acid, GABA) neurotransmission to offset excitation. Diazepam, a drug that increases GABA-induced chloride channel opening, was administered (10 mg/kg, i.p.) to rats 1 and 2 hr following 15 min of transient global ischemia, when hippocampal GABA levels, increased during ischemia, returned to basal. Rats were maintained normothermic during ischemia and became hypothermic following the injections of diazepam. Four days later, rats were sacrificed and the brains were examined for neuronal degeneration and the presence of GABAA receptors labeled by 35S-t-butylbicyclophosphorothionate (35S-TBPS). There was substantial neuroprotection of striatal neurons and pyramidal neurons in the CA1 area of the hippocampus. In addition, diazepam prevented the loss of 35S-TBPS binding sites in the striatum and in the dendritic fields of the CA1 hippocampus following ischemia. Since hypothermia, itself, is neuroprotective, we determined if hypothermia was required for the ability of diazepam to produce neuroprotection. Diazepam was microinjected into the CA1 hippocampus 1 and 2 hr following ischemia, and rats remained normothermic. Four days later, diazepam still produced substantial protection of hippocampal neurons. Thus, postischemic hypothermia may have contributed to the neuroprotection by diazepam when it was administered systemically, but the neuroprotective effect of diazepam did not require hypothermia. We conclude that delayed enhancement of GABAergic neurotransmission directly at the site of vulnerability following an ischemic event protects the vulnerable neurons from death.
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PMID:Diazepam, given postischemia, protects selectively vulnerable neurons in the rat hippocampus and striatum. 782 61

Transcranial cerebral oximetry based on the principle of near-infrared spectroscopy has been successfully used in a variety of neurosurgical conditions, primarily those associated with disturbed cerebral circulation. The non-invasive technique of cerebral oximetry provides valuable information about brain oxygenation in patients with cerebral ischemia (due to occlusion or stenosis of the internal carotid artery). It is also used in intraoperative monitoring of carotid endarterectomy and surgical procedures performed under deep hypothermia and circulatory arrest, during neuroendovascular procedures, and in critical care settings (in patients with arterial vasospasm and during the terminal period). This article describes our preliminary clinical experience with the use of this new technique and summarizes the current literature on clinical and experimental use of transcranial cerebral oximetry.
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PMID:Clinical experience with transcranial cerebral oximetry. 782 8

This review describes recently recognized pathophysiologic mechanisms responsible for brain damage during ischemia and reperfusion and new therapeutic concepts developed on a rational basis. Mediators of secondary damage include excitotoxins such as glutamate, acidosis, free radicals, and the disturbance of the microcirculation seen in the early phase of recirculation. Glutamate is an excitatory neurotransmitter, which may turn neurotoxic when the energy supply is limited. Tissue acidosis down to pH 6.0 develops regularly in cerebral ischemia and disturbs a variety of neuronal functions, causing glial swelling and neuronal death. Free radicals attack brain lipids, the cell membrane and myelin in particular, and are produced during reperfusion. Disturbance of the microcirculation aggravates ischemic damage. Suggested therapeutic approaches include glutamate antagonists, normalization of tissue acidosis, and use of new diuretics to reduce glial swelling, protection of the brain by free radical scavengers such as 21-aminosteroids, tocopherol, allopurinol or superoxide dismutase, and hypothermia. Ways of ensuring fast reperfusion, including hypervolemic hemodilution and blood pressure stabilization, are suggested for resuscitation or early stroke. All data available indicate that the combination of several successful therapeutic principles will significantly improve outcome.
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PMID:[Neuroprotection. Models and basic principles]. 784 Apr 11

In animal models of cerebral ischemia hypothermia has been shown to have a beneficial effect. Reduction of infarct size, fewer potentially neurotoxic metabolites, and a better neurological outcome were observed compared to sham-operated animals. In clinical practice hypothermia has been widely used in cardiovascular surgery and occasionally in neurosurgery. The first trials with hypothermia in patients with severe head injury have also shown beneficial results. However, studies on therapeutic hypothermia in the clinical management of acute stroke are not yet available.
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PMID:[Therapeutic hypothermia after cerebral ischemia. Theoretical principles and possible clinical applications]. 785 3

The present study was carried out to compare the neuroprotective effect of the novel noncompetitive NMDA antagonist, FR115427, with that of(+)MK-801 in rat focal cerebral ischemia. Focal cerebral ischemia was produced by permanent occlusion of the left middle cerebral artery (MCA). Drugs were administered intraperitoneally immediately after ischemia and once a day for 6 successive days. FR115427 (10 mg/kg, i.p.) significantly improved neurologic deficit at 1 day after ischemia and reduced total infarct volume (54%) at 7 days after ischemia. Although FR115427 (10 mg/kg, s.c.) produced neuronal vacuolization similar to (+)MK-801, FR115427 did not produce adverse effects such as a loss of body weight, mortality, and hypothermia, in contrast to (+)MK-801. These results suggest that FR115427 may be useful in the treatment of stroke.
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PMID:The neuroprotective effect of the novel noncompetitive NMDA antagonist, FR115427 in focal cerebral ischemia in rats. 786 Jun 68


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