Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors compared perioperative neuropsychologic dysfunction in patients participating in two studies conducted in institutions using different strategies to manage cardiopulmonary bypass. These differences included hypothermia versus normothermia, presence versus absence of arterial microfilters, and the presence versus absence of glucose-containing solution in the pump prime. Other differences between the two institutions included the type of surgery (intracardiac v extracardiac), the mean duration of cardiopulmonary bypass, and degree of low perfusion pressure during bypass. Despite these major differences, perioperative neuropsychologic dysfunction measured by the two-part Trail-Making psychometric test was similar in the two institutions. Several factors were analyzed for their possible contribution to development of dysfunction, including institution, anesthetic management, age, sex, degree of low perfusion pressure during bypass, and duration of bypass; only age was significant. These results suggest that differences in surgical procedure and management of cardiopulmonary bypass previously thought to contribute to the development of subtle cognitive deficits after cardiac surgery may have been overemphasized.
 ...
PMID:Neuropsychological dysfunction after cardiopulmonary bypass: a comparison of two institutions. 176 21

A female black rhinoceros calf developed significant hypoglycemia (blood glucose, 30 mg/dL) and hypothermia (97 degrees F) within 48 hours of birth and refused to nurse. Normal gestation of the black rhinoceros is 15 months, but elongated hoof slippers and low birth weight (30 kg) suggested prematurity in this calf. Clinical symptoms of neonatal sepsis including lassitude and poor sucking continued in spite of the aggressive use of antibiotics, and the calf required mechanical ventilatory support on day 7. Nutritional support including enteral gavage feedings (Pedialyte/4 ounces of SMA [Wyeth Ayerst] with sucraflox) had been instituted and was supplemented with total parenteral nutrition on day 5. Central venous access was obtained via a jugular cutdown. The total parenteral nutrition included appropriate electrolytes and vitamins for the neonatal calf but did not include trace elements. The use of total parenteral nutrition by our zoos for therapeutic purposes is increasing. Experience with total parenteral nutrition in exotic animals such as the black rhinoceros is limited, yet this may be an important therapeutic modality in these animals, particularly those in danger of extinction.
 ...
PMID:Total parenteral nutrition in a premature rhinoceros calf. 177 15

Intensity of glucose synthesis from different substrates in the liver slices was investigated in 1-, 13-15-, 30-day old and adult (3-6 month old) rats. Maximal gluconeogenesis activity was observed in the liver tissue of 13-15 day old rats. There was a change in the substrate specificity of gluconeogenesis during ontogenesis. Under cold stress and low body temperature (30 degrees C) a rate of gluconeogenesis from some substrates in young rats increased, while in adults-decreased. The activation of gluconeogenesis in adult rats occurred only at prolonged hypothermia to 3 h and almost complete exhaustion of glycogen reserves in the liver.
 ...
PMID:[Intensity of gluconeogenesis in liver tissue of rats of various age groups]. 181 82

The paradigm of long-term sleep deprivation was used as a model of chronic inescapable stress in rats. Several basic metabolic parameters (body weight changes, food and water intake, rectal temperature, serum glucose and creatinine), adrenal and thyroid secretion, norepinephrine and dopamine content and turnover in discrete brain regions, and open field behaviour were examined in the course of the exposure to experimental stress. Sleep deprivation over 7-9 days caused complete physical exhaustion of the animals. It was accompanied by hypothermia and hyperphagia. Adrenal activity was characterized by significant hypercorticism, but also by a relative decrease of the responsiveness to ACTH. A gradual decrease in the thyroid secretion was observed. Sleep deprivation elicited a depletion of norepinephrine in the hypothalamus and decreased its turnover, whereas hippocampal norepinephrine content decreased without considerable turnover alterations. Striatal dopamine content and turnover remained unaffected. Behavioural depression and altered open field activity were also observed in exhausted animals. Long-term sleep deprivation, therefore, seems to reproduce some of the biological correlates of the depressive illness, and may be useful in studying the development of coping failure as a result of chronic stress exposure.
 ...
PMID:Neuroendocrine and neurochemical consequences of long-term sleep deprivation in rats: similarities to some features of depression. 181 84

The putative 5-HT1A receptor antagonist properties of 1-(2-methoxyphenyl)-4-[4-(2-phtalimmido)butyl] piperazine (NAN-190) were studied in mice. The responses studied were hypothermia- and hyperglycemia-induced by the 5-HT1A agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT). NAN-190 (0.3-3 mg/kg) did not antagonize either response, but rather appeared to be additive with the effect produced by 8-OH-DPAT (0.25 mg/kg) alone, at least with respect to temperature. NAN-190, given alone in similar doses, caused hypothermia and hyperglycemia. These results suggest that NAN-190 has similar properties to 8-OH-DPAT with regard to temperature and glucose effects. Therefore, it does not appear to be a effective antagonist for all 5-HT1A-mediated responses.
 ...
PMID:Is NAN-190 an effective antagonist of the hypothermia and hyperglycemia induced by the 5-HT1A receptor agonist, 8-OH-DPAT? 182 70

Preischemic hyperglycemia aggravates brain damage following transient ischemia, and adds some special features to the damage incurred, notably a high frequency of postischemic seizures, cellular edema, and affectation of additional brain structures, such as the substanta nigra pars reticulata (SNPR). We raised the question whether mild intra-ischemic hypothermia (32-33 degrees C), known to reduce selective neuronal vulnerability in normoglycemic subjects, also ameliorates the characteristic damage observed in hyperglycemic animals. To that end, two series of experiments were performed. In the first, normo- and hypothermic animals were subjected to 10 min of ischemia during hyperglycemic conditions (plasma glucose 20-25 mmol.l-1), and allowed either 15 h or 1 week of recovery. In the second, both normo- and hyperglycemic animals were subjected to 15 min of ischemia (at normal or reduced temperature) and surviving animals were studied after 1 week of recovery. All normothermic, hyperglycemic animals developed postischemic seizures and died within the first 24 h. Mild hypothermia afforded substantial protection. Thus, 6/7 hypothermic animals subjected to 10 min of ischemia survived 1 week of recovery and none developed post-ischemic seizures. Of the hypothermic animals subjected to 15 min of ischemia 6/11 survived for 1 week, only one of which developed seizures. Protection by hypothermia was also shown by the histopathological analysis. Experiments with 10 min of ischemia and 15 h of recovery showed the expected damage in normothermic, hyperglycemic subjects. Hypothermia markedly reduced damage in all vulnerable structures, including the cingulate cortex and SNPR. The protection was most pronounced in the caudoputamen, where no affected neurons were seen in the hypothermic subjects. The experiments with 15 min of ischemia confirmed previous findings that mild hypothermia protects normoglycemic animals against the insult. The results also showed that hypothermia prevented most of the exaggeration of damage caused by hyperglycemia. However, under hypothermic conditions hyperglycemia still augmented damage in the cingulate cortex, medial and lateral venteroposterior thalamic nuclei, and SNPR, structures specifically damaged under hyperglycemic, normothermic conditions. This suggests that hypothermia has less of a protective effect on mechanisms causing such damage than on neuronal damage in the classic selectively vulnerable regions, particularly the caudoputamen.
 ...
PMID:Influence of moderate hypothermia on ischemic brain damage incurred under hyperglycemic conditions. 185 66

The hyperglycemic and hypothermic responses to acute ethanol exposure (0, 2, 4, 6 g/kg, intraperitoneally) were examined in non-fasted mice selectively bred for sensitivity (COLD line) or insensitivity (HOT line) to ethanol-induced hypothermia. Blood samples and rectal temperatures were obtained immediately before injection and hourly for 4 hr after injection. As expected, COLD mice demonstrated greater and more prolonged reductions in body temperature than HOT mice, especially at the 4 g/kg dose (HOT: -2.58 degrees C, COLD: -5.08 degrees C). Ethanol produced significant dose-dependent elevations in blood glucose levels over the 4-hr sampling period in both lines. The greatest elevations in blood glucose levels were seen at 4 g/kg, with COLD mice (mean = 225.1 mg/dl) showing significantly greater elevations in blood glucose levels compared to HOT mice (mean = 177.0 mg/dl). These results support the hypothesis that the thermic and glycemic effects produced by ethanol are due to related neural processes that share a common genetic component.
 ...
PMID:The relationship between ethanol-induced hyperglycemia and hypothermia: evidence of genetic correlation. 192 51

Working rat hearts were perfused for 15 minutes at 37 degrees C before switching to a Langendorff perfusion (60 mm Hg aortic pressure) at 10 degrees C for 40 minutes of hypothermic arrest. Ventricular function was allowed to recover for 15 minutes at 37 degrees C by reestablishing the prehypothermic conditions. The perfusate was Krebs-Henseleit bicarbonate buffer containing 3% bovine serum albumin and either glucose (11 mmol/L) or glucose (11 mmol/L) plus palmitate (1.2 mmol/L) and gassed with 95% O2 and 5% CO2. In hearts receiving glucose alone as substrate, coronary flow was maintained constant during the 40 minutes of hypothermic arrest and returned to prehypothermic rates with rewarming. Ventricular function, as estimated by peak systolic pressure and heart rate, recovered to the prehypothermic level. When palmitate was added, coronary flow decreased continuously throughout the hypothermic perfusion (22% decrease by 40 minutes), and ventricular pressure development was lower throughout the rewarming perfusion. Tissue levels of adenosine triphosphate and creatine phosphate were well maintained and long-chain acyl coenzyme A and acyl carnitine decreased during hypothermia regardless of the substrate provided. With rewarming, tissue levels of adenosine triphosphate and creatine phosphate decreased in those hearts receiving palmitate. Omission of fatty acid either during hypothermia or during the first 5 minutes of rewarming improved recovery of function. Addition of oxfenicine to inhibit fatty acid oxidation, or inhibition of Ca2+ overload by verapamil and low perfusate Ca2+, prevented the effects of palmitate on ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Fatty acids suppress recovery of heart function after hypothermic perfusion. 192 62

1. Two hours of exposure to heat stress, resulted in hyperthermia in rabbits (Oryctolagus cuniculus). 2. This was accompanied by a severe hypocapnia, partly compensated for by a significant decrease in bicarbonate (HCO3-) concentration. 3. The severest hyperthermia (Tb = 43.5 degrees) was followed by a sharp decreased in both PaCO2 (to 20.2 torr) and HCO3- (to 9.2 mM/l), resulting in extreme metabolic acidosis (pH = 7.290). 4. The significant increase in serum osmolality (27%) is interpreted by the cumulative effect of increased electrolyte and metabolite concentrations. 5. The elevation in blood BUN, creatinine, globulin and GOT levels point to a possible damage to muscle cells by hypothermia. 6. The stable cholesterol and alkaline phosphatase levels, suggest that liver tissue was not damaged. 7. The dramatic increase in glucose from 103.8 to 348.8 mg%, and the significant increase (from 22.0 to 39.9 mg%) in BUN, suggest a possible disability of the cells to metabolize carbohydrates, accompanied by a progressive proteolysis as an alternative process for energy production. 8. The data suggest that the emergence of muscle cell damage, severe hyperglycemia and acidosis under heat stress, precedes and amplifies the deteriorating effects of high Tb in heat stressed rabbits, which often lead to mortality.
 ...
PMID:The effect of heat exposure on blood chemistry of the hyperthermic rabbit. 198 37

Hypothermia is a well-known concomitant of hypoglycemia in mammals. We tested the hypothesis that this hypothermia is an important adaptive response to hypoglycemia in 11 normal Sprague-Dawley rats. Twelve-hour fasted, conscious animals received primed, continuous insulin infusions for up to 8 hours. Plasma glucose was clamped between 30 and 40 mg/dL and core body temperature was monitored continuously during the insulin infusions. Five of the animals were maintained in a room temperature environment (22 to 24 degrees C) during the hypoglycemia; all became hypothermic (mean +/- SE nadir core temperature, 31 +/- 0.5 degrees C). Spontaneous activity was reduced in these animals, but they remained conscious and responsive to external stimuli. All five returned to normal behavior after euglycemia was restored at the end of the insulin infusions. In the remaining six animals, hypothermia was prevented during hypoglycemia by warming of the air in their cages (mean of hourly core temperatures, 37 +/- 0.1 degrees C). None of these animals survived more than 7 hours. The severity of the hypoglycemia was no greater in the euthermic than in the hypothermic group, as judged by the mean of individual nadir plasma glucose levels (25 +/- 1 v 24 +/- 1 mg/dl, respectively) and by the mean number of glucose values per animal that were less than 30 mg/dL (2 +/- 1 v 7 +/- 1). Plasma osmolality did not change significantly in either group during the period of hypoglycemia, suggesting that dehydration was not the cause of death in the euthermic animals.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Hypothermia is critical for survival during prolonged insulin-induced hypoglycemia in rats. 200 47


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>