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

A basic understanding of fetal nutrition and metabolism is essential in the clinical management of the obstetric patient. The fetus depends upon a constant infusion of glucose for energy production and growth. Maternal glucose is the prime source of this nutrient. Alterations in maternal carbohydrate homeostasis will lead to changes in fetal metabolism. In diabetes mellitus, hyperglycemia may produce hyperinsulinemia and macrosomia. The growth-retarded fetus may have a decreased supply of maternal glucose and reduced amounts of hepatic glycogen and adipose tissue. The fetus must depend upon these stores for survival during periods of intrauterine hypoxia. In the newborn period, hypothermia and hypoxia may rapidly deplete energy reserves. With this information, the clinician may more knowledgeably manage dietary demands in the antepartum patient, fetal distress during labor, and the immediate newborn period.
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PMID:Fetal carbohydrate metabolism: its clinical importance. 31 3

The effect of glucose on the release of insulin from the pancreas of 19.5- to 21.5-day-old rat fetuses has been studied in utero. Fetal hyperglycemia was induced by a square-wave glucose infusion into pregnant rats over a period of 150 min. The infusion of glucose raised the fetal blood glucose concentration to that of the mother and induced a rapid increase of plasma insulin levels on day 19.5 of gestation. There was a progressive rise of the insulin response as the gestation proceeded, with an increase of the two phases of the hormonal secretion. Maternal hypothermia induced by pentobarbital anesthesia decreased markedly the insulin response to hyperglycemia in the mothers and their fetuses. In fetuses decapitated on day 18.5 and studied on day 21.5, the increase of plasma insulin concentration after a 1-hour hyperglycemia was similar to that in the littermate control fetuses.
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PMID:Dynamics of glucose-induced plasma insulin increase in the rat fetus at different stages of gestation. Effects of maternal hypothermia and fetal decapitation. 38 63

Plasma lipids, blood glucose, plasma insulin (IRI) and serum dopamine-beta-hydroxylase (DBH) were measured in 30 subjects undergoing surface-induced deep hypothermia with circulatory arrest for open-heart surgery. Non-esterified fatty acid (NEFA) in the plasma rapidly increased at the lowest temperature (23 degrees C) reached and other lipids in the plasma decreased during the cooling period. An increase of NEFA and a decrease of triglyceride have been attributed to the action of lipoprotein lipase activity stimulated by heparin. It is also likely that the decrease of other lipids and beta-lipoprotein in the plasma results from the transient hypofunction of the liver due to hypothermia. Blood glucose increased during the cooling period, while plasma insulin showed no significant change. Serum DBH reflecting catecholamine also showed no significant change during the cooling or rewarming periods. Therefore, hyperglycemia in hypothermic open-heart surgery may result from the decrease of peripheral utilization of glucose and from the inhibition of insulin secretion due to the transient pancreatic hypofunction.
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PMID:Studies on lipid and carbohydrate metabolism during surface-induced deep hypothermia with circulatory arrest for open-heart surgery. 60 91

Carbohydrate and lipid metabolism was studied in 8 patients who underwent open-heart surgery with the aid of extracorporeal circulation. Hyperglycemia was observed during perfusion. Despite the high glucose levels during perfusion, insulin responses were depressed. A rise of insulin levels was observed one hour after perfusion, and at the same time the glucose levels dropped. Suppression of insulin secretion during perfusion may be the result of increased catecholamine secretion, induced hypothermia, or heparin administration. High levels of non-esterified fatty acids (NEFA) and low levels of triglycerides were observed immediately before, during, and after perfusion while heparin was being utilized. This phenomenon was considered to be strongly affected by the use of heparin. The levels of growth hormone were depressed during perfusion but significantly elevated one hour after the end of perfusion. These phenomena may be caused by the fluctuations in glucose and NEFA levels.
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PMID:Carbohydrate and lipid metabolism in open-heart surgery. 83 44

Urethral obstruction induced in adult male cats caused clinical signs identical with those observed in naturally occurring disease. Central nervous system depression, anorexia, dehydration, vomiting, muscle weakness, and hypothermia occurred. Weight loss (due to water loss and catabolism), metabolic acidosis, mild hyponatremia, hyperkalemia, hypermagnesemia, hypocalcemia, hyperphosphatemia, hyperglycemia, azotemia, and hyperproteinemia were also observed. Serum amylase, alkaline phosphatase, and alanine aminotransferase activities were normal. Ten of 13 cats (group 1), with 72 hours' induced obstruction but not treated with parenteral fluids, died either before the obstruction was relieved or within 8 days afterward. Eight cats (group 2) with induced obstruction for 49 to 98 hours developed severe clinical and biochemical alterations. Treatment with a multiple-electrolyte solution, in addition to relief of urethral obstruction, resulted in favorable clinical and biochemical responses. These cats survived and were clinically healthy at 9 to 10 days after relief of obstruction. It was concluded that use of a multiple-electrolyte solution to correct acidosis, restore circulatory volume, and enhance renal excretion of potassium was effective supportive therapy after urethral obstruction was removed.
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PMID:Characterization and treatment of water, electrolyte, and acid-base imbalances of induced urethral obstruction in the cat. 87 80

2-Deoxy-D-glucose (2-DG), insulin, or norepinephrine (NE), when injected into the cerebral ventricles of conscious mice, produce decreased rates of O2 consumption and hypothermia. These changes are accompanied by hyperglycemia with 2-DG, hypoglycemia with insulin, and normoglycemia with NE. Desipramine blocks the reduction in body temperature and O2 consumption produced by each of these agents, but does not modify significantly their effects on plasma glucose. The latter suggests that the thermal and oxidative responses to central glucopenia can be dissociated from concurrent alterations in circulating glucose. Propranolol enhances the hypothermic response produced by administered 2-DG, insulin, or NE. Phentolamine, however, antagonizes the hypothermia only with NE, indicating the 2-DG and insulin are probably not acting through the release of endogenous NE.
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PMID:Drug modification of hypothermia induced by CNS glucopenia in the mouse. 98 1

We systematically paired auditory, olfactory, and social stimuli with each injection of morphine in rats. We found that, when morphine was kept constant at a low dose, the external stimuli acquired the property of a conditional stimulus (CS) to cause hyperthermia which was antagonized by naloxone. In rats in which morphine doses were regularly increased to cause morphine dependence, the CS presented during withdrawal, caused reduction in withdrawal signs (wet shakes, hypothermia, aggression) and produced hyperglycemia as well as elevation of striatal homovanillic acid. CS-induced alleviation of withdrawal hypothermia was blocked by mecamylamine, phenoxybenzamine, haloperidol, benztropine or naloxone but not by cyproheptadine or propranolol.
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PMID:Alleviation of narcotic withdrawal syndrome by conditional stimuli. 103 8

Clinical use of profound hypothermia and total circulatory arrest has been accompanied by occasional postoperative neurological abnormalities. In a series of infant baboons, surface cooling to 32 degrees C (brain) followed by perfusion cooling by cardiopulmonary bypass with a membrane oxygenator and heat exchanger to 18 degrees C was carried out, after which the circulation was stopped for 30 minutes. The animal was rewarmed to 35 degrees C. Marked alterations in the regional cerebral circulation were observed during perfusion cooling and rewarming. Regional cerebral ischemia was negatively correlated with jugular outflow (total cerebral blood flow) during rewarming, while regional hyperemia showed positive correlation both following perfusion cooling and after rewarming. A higher degree of ischemia in brain ischemic samples was found during rewarming than during cooling. These alterations in regional cerebral perfusion were associated with lactacidosis and hyperglycemia after rewarming, and may be considered potentially responsible for posthypothermic cerebral dysfunction.
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PMID:Cerebral effects of profound hypothermia (18 degrees C) and circulatory arrest. 115 33

1. As reflected by increasing plasma concentrations of cortisol, norepinephrine, epinephrine and dopamine, a marked stimulation of the adrenal cortex and of the sympathetic nervous system occurred in Syrian hamsters during moderate hypothermia induced by helium-oxygen atmosphere and cold. 2. A profound hyperglycemia was observed during hypothermia. 3. All effects due to the helium-oxygen atmosphere and cold exposure (helox-cold) disappeared almost completely after rewarming. 4. The results corroborate the hypothesis of an involvement of the adrenal cortex combined with the sympathetic nervous system in the control of acute induced heat production.
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PMID:Sympathoadrenal activity during helox-cold induced hypothermia in Syrian hamsters. 135 91

The records of 150 consecutive patients undergoing thoracoabdominal aortic replacement from 1980 to 1991 were retrospectively reviewed. There were 89 men and 61 women; mean age was 67.8 years (range: 33 to 88 years). Since June 1989, a multimodality prospective perioperative protocol was used to reduce the risk of spinal cord dysfunction. Ischemia is minimized by complete intercostal reimplantation whenever possible, cerebrospinal fluid drainage, and maintenance of proximal hypertension during cross-clamping. Spinal cord metabolism is reduced by moderate hypothermia, high-dose barbiturates, and avoidance of hyperglycemia. Reperfusion injury is minimized by the use of mannitol, steroids, and calcium channel blockers. Ninety-seven percent of patients survived long enough for evaluation of their neurologic function. Spinal cord dysfunction was reduced from 6 of 108 (6%) in the preprotocol group to 0 of 42 in the protocol group (0%) (p less than 0.01). The overall 30-day operative mortality was not significantly different between the groups (9% versus 12%, p = NS). A multimodality protocol appears to be effective in reducing the risk of spinal cord injury during thoracoabdominal aortic replacement.
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PMID:Risk of spinal cord dysfunction in patients undergoing thoracoabdominal aortic replacement. 141 16


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