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

The relative roles of lateral hypothalamic cell bodies and fibers of passage were assessed in the development of lesion-induced hyperthermia and bombesin-induced hypothermia. Electrolytic lesions or discrete fiber transections were combined with intracisternal bombesin injection to show that each of these two thermoregulatory effects involves fibers crossing the borders of the lateral hypothalamus; however, the two effects primarily involve fibers crossing different borders. Thus, the hyperthermia and the abolition of bombesin-induced hypothermia which follow lateral hypothalamic damage appear to result from disruption of separate thermoregulatory pathways.
Brain Res 1991 Sep 27
PMID:Destruction of different fiber tracts underlies development of lateral hypothalamic lesion-induced hyperthermia and loss of bombesin-induced hypothermia. 176 Jul 39

Chlordane is a cyclopentadiene-derived insecticide that exerts its toxic action on the nervous system. In experimental animals the characteristic signs of acute toxicity are hypothermia, hyperexcitability, tremors and convulsions. In human, signs of acute chlordane toxicity are tremors and convulsions. There have been many different signs of acute toxicity attributed to chlordane, however, there is no substantiation within the primary literature for them. The literature indicates a convulsive chlordane serum level of 3 ppm and fatal serum level exceeding 5 ppm in human. Chlordane toxic action is rapid, appearing within two hours of an acute dose with improvement and recovery after 24 hours. Chlordane intoxication does not result in delayed neurotoxic effects. There is discussion of the mechanism of action of chlordane's toxicity in the central nervous system.
Biomed Environ Sci 1991 Sep
PMID:Signs and mechanisms of chlordane intoxication. 176 23

We have examined the effects on sleep and brain temperature of bilateral microinjections of adenosine and adenosine analogs to the preoptic area (PO) of rats. Administration of adenosine (12.5 nmoles), a nonselective adenosine A1/A2 receptor agonist NECA (N-ethyl-carboxamido-adenosine, 1.0 nmole), and the selective adenosine A1 receptor agonist CPA (cyclopentyladenosine, 0.25, 0.5 nmoles) increased total sleep primarily through an enhancement in deep slow-wave sleep (SWS2), while adenosine also increased REM sleep. Administration of 12.5 nmoles adenosine and 0.25 nmoles CPA did not affect brain temperature, while 1.0 nmole NECA and 0.5 nmoles CPA caused a transient and prolonged hypothermia, respectively. Administration of the selective adenosine A2 receptor agonist CV-1808 (2-phenylaminoadenosine, 5, 10 nmoles) had no effect on sleep or brain temperature. The present results demonstrate a site for the central hypnotic action of adenosine, and a functional role for adenosine A1 receptors in the hypothalamus.
Pharmacol Biochem Behav 1991 Sep
PMID:Role of adenosine in sleep and temperature regulation in the preoptic area of rats. 178 Mar 43

Small doses of morphine induce a hyperthermic response that does not change with repeated injections, whereas higher doses induce a hypothermia that changes to hyperthermia with repeated treatment. Experiment 1 confirmed these results in ovariectomized rats, using 6 repeated injections of morphine at 5 or 30 mg/kg. Using the same treatment regimen. Experiment 2 showed that the low dose of morphine induced a transient suppression of LH levels followed by a hypersecretion, and that repeated injections did not affect this response. The high dose (30 mg/kg) of morphine initially induced a sustained suppression of LH. Following the sixth injection of the high dose, subjects showed an intact or exaggerated suppression of LH, but an accelerated recovery to control levels. Experiment 3 extended the phase of repeated treatment of the high dose to 12 days and replicated the results of Experiment 2.
Physiol Behav 1991 Sep
PMID:Comparison of morphine tolerance in body temperature and luteinizing hormone secretion. 180 Oct 2

The effects of hypothermia and hyperthermia on the cerebral microcirculation were studied using isolated perfused intracerebral (parenchymal) arterioles obtained from rats. In a temperature-dependent manner, hypothermia (20.0 degrees to 35.0 degrees C) dilated the spontaneous tone developed by the arterioles and also diminished their contractile response to potassium and prostaglandin F2 alpha. In contrast, hyperthermia (40.0 degrees to 45.0 degrees C) induced a biphasic response consisting of initial vasoconstriction and secondary vasodilation. Exposure of the vessels to 45.0 degrees C for 30 minutes irreversibly abolished the spontaneous tone and responsiveness of the arterioles when the temperature of the preparation was returned to 37.5 degrees C. In calcium-free solutions, however, the arteriolar diameter was not affected within a temperature range of 20.0 degrees to 45 degrees C. Furthermore, arterioles that had been in a calcium-free solution during exposure to 45 degrees C temperature recovered their viability at 37.5 degrees C. These results suggest that changes in ambient temperature alter calcium-induced contraction in arteriolar smooth muscle, and that the irreversible effects of hyperthermia on the arterioles are dependent upon extracellular calcium. These studies indicate that alterations in brain temperature may affect the pathogenesis of cerebral ischemia by mechanisms that are in part independent of parenchymal metabolism.
J Neurosurg 1991 Sep
PMID:Effects of hypothermia and hyperthermia on the reactivity of rat intracerebral arterioles in vitro. 186 45

The effects of deep hypothermia on ischemic neuronal injury were examined using a permanent middle cerebral artery occlusion model in the rat. Animals were maintained at temporalis temperatures of either 24 degrees C or 36 degrees C and killed 6 hours after arterial occlusion. Normothermic rats displayed an average infarct volume of 25.1% +/- 1.6% of the right hemisphere, whereas hypothermic rats had an average infarct volume of 4.1% +/- 1.3% (p less than 0.001). The right/left hemispheric ratio was 1.05 +/- 0.02 in the normothermic group and 1.00 +/- 0.02 in the hypothermic group (p less than 0.05). These results suggest that hypothermia to 24 degrees C may reduce cerebral infarction and edema formation following middle cerebral artery occlusion in the rat.
Surg Neurol 1991 Sep
PMID:Hypothermic protection following middle cerebral artery occlusion in the rat. 187 67

We report on a patient with accidental deep hypothermia (23.3 degrees C) and cardiorespiratory arrest resulting from severe craniocerebral injury. Systemic anticoagulation was contraindicated, and the decision was reached to rewarm the patient with cardiopulmonary bypass without systemic heparinization using heparin-coated perfusion equipment. The patient was successfully rewarmed, was weaned from cardiopulmonary bypass, and recovered.
Ann Thorac Surg 1991 Sep
PMID:Perfusion without systemic heparinization for rewarming in accidental hypothermia. 189 50

The effect of transient postischemic hypothermia (30 degrees C) on recovery of cerebral blood flow (CBF), oxygen consumption (CMRO2) and somatosensory-evoked potentials (SEPs) was determined in anesthetized dogs. Ischemia was produced for 20 min by intracranial pressure (ICP) elevation while core temperature was lowered by cooling externalized blood. Epidural temperature was controlled at 37.6 +/- 0.2 degrees C during ischemia, lowered to 30.0 +/- 0.1 degrees C during the first hour of reperfusion, and then rewarmed to 38.0 +/- 0.1 degrees C in experimental dogs (n = 8) and maintained at 38.0 +/- 0.1 degrees C in control dogs (n = 8). ICP was lower throughout reperfusion in experimental as compared with control animals. By 240 min of reperfusion, CBF was approximately 70% of control in both groups. CMRO2 was 60% of preischemic values in control animals and 74% in experimental animals (P = 0.077). A persistent uncoupling of CBF and CMRO2 was observed throughout reperfusion only in the control group. Recovery of SEP amplitude was significantly improved in the experimental group (26 vs. 11% of preischemic values). These data suggest that transient hypothermia reduces ICP and facilitates recovery of electrophysiological function after cerebral ischemia.
Am J Physiol 1991 Sep
PMID:Hypothermic cerebral reperfusion and recovery from ischemia. 190 4

Cardiac surgery with hypothermic cardiopulmonary bypass (CPB) is among the most commonly performed operations in Canada today. The potential effects of hypothermia and CPB on the disposition of certain opioids are reviewed. Reasons for prolongation of the elimination half-time of the opioids used during cardiac surgery are explored. The roles that age, hypothermia, protein binding and drug sequestration may play in changing opioid pharmacokinetic behaviour are examined and suggestions for future research are made.
Can J Anaesth 1991 Sep
PMID:The pharmacokinetic behaviour of opioids administered during cardiac surgery. 191 58

We developed a new technique, extracorporeal venovenous rewarming (EVR), to rewarm hypothermic patients in the intensive care unit or operating room. We compared this method with the active external (standard) techniques of warming blankets; heated ventilator circuits, intravenous fluids, and gastric and peritoneal lavage; and cardiopulmonary bypass. The EVR technique warmed patients' blood or additional blood products and crystalloids to 40 degrees C at 150-400 mL/min and allowed survival from a core temperature of 31.1 degrees C after massive injury. The EVR technique rewarming patients more rapidly than standard techniques and may be most appropriate in patients with multisystem trauma when rapid correction of hypothermia-related hypovolemia, coagulopathy, and arrhythmia is necessary. Cardiopulmonary bypass is required in severely hypothermic patients with cardiac arrest. Standard techniques can be used when these immediately life-threatening conditions are not present.
J Trauma 1991 Sep
PMID:Comparison of three methods of rewarming from hypothermia: advantages of extracorporeal blood warming. 192 May 55


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