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

The effects of changes in ambient and central temperature, amines, PGEu and pyrogen were investigated with respect to the mechanism of Na+-Ca++ ratio in the posterior hypothalamus of the unrestrained cat. Guide tubes were implanted bilaterally above the posterior hypothalamic area of 23 cats so as to accommodate push-pull cannulae. After a Na+ or Ca++ sensitive site was identified by perfusion at 50 mul/min of an artificial CSF containing 10.4 mM excess Ca++ ions or 13.6 mM excess Na+ ions, several types of experiments were undertaken with the results summarized as follows: if the cat was exposed to a cold or warm environmental temperature as the posterior hypothalamus was perfused with excess cation, the typical hypothermia was produced by Ca++ and hyperthermia by Na+ ions. However, if the cat was exposed to peripheral cooling or warming 30 min prior to the perfusion, the fall or rise produced by Ca++ or Na+ was attenuated or prevented. In other experiments, 1.0 muCi 45Ca++ was injected in the ion sensitive site in the posterior hypothalamus to label stores of the cation. Raising of ambient temperature caused a retention of 45Ca++ in this hypothalmic area, whereas a cold environmental temperature enhanced the efflux of 45Ca++ at the same perfusion site. The magnitude of change in 45Ca++ efflux depended upon the intensity of the thermal challenge. Similarly, warming of the anterior hypothalmic, preoptic area by means of implanted thermodes caused an immediate diminution in 45Ca++ efflux in the posterior hypothalamus, whereas cooling of this anterior region augmented the extrusion of 45Ca++ ions from the posterior area. When substances which produce a temperature change were applied to the same thermosensitive zone, the direction of shift in 45Ca++ flux in the posterior area corresponded to the signal for heat production or heat loss. That is, the microinjection of 5-HT, PGE1 or Salmonella typhosa into the anterior hypothalamus enhanced the efflux of 45Ca++ in the posterior hypothalamus as hyperthermia developed, whereas a similar microinjection of norepinephrine reduced the 45Ca++ output from the same sites. Finally, locally anesthetizing the cells of the anterior hypothalamus by the nerve blocker, procaine, prevented the cold and heat-induced 45Ca++ eflux and retention, respectively. These results suggest that if the Na+-Ca++ ratio in the posterior hypothalamus establishes and maintains the set-point for body temperature of 37 degrees -38 degrees C, the mechanism of lability of Ca++ through changes in binding characteristics, transport, or metabolism of the cation serves two purposes: (1) the active defense of the set-point temperature through gradations in ion shifts; and (2) the upward or downward change in set-point value, pathological or normal, triggered by virtue of impulses relayed from the anterior hypothalamus.
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PMID:Hypothalamic Na+ and Ca++ ions and temperature set-point: new mechanisms of action of a central or peripheral thermal challenge and intrahypothalamic 5-HT, NE, PGEi and pyrogen. 97 10

Hypothermia (4 degrees C) reversibly inhibits metabolism of prostaglandin A1 (PGA1) in the perfused rabbit lung and decreases the transit time of PGA1 through the lung. Co-perfusion of PGA1 (0.28 muM) and PGE1 (2.8 muM) resulted in 48% inhibition of PGA1 metabolism. Ouabain and phenoxybenzamine (10(-5) M) did not significantly affect PGA1 metabolism. We examined the effect of diphloretin phosphate (DPP; 6.0 mu/ml) on the metabolism of prostaglandin A1 (0.28-5.03 muM) and E1 (PGE1;0.28-11.56 muM). The metabolism of both prostaglandins appeared to be saturable processes and, in the case of PGE, the data conformed to Michaelis-Menten kinetics: the apparent Km (muM) and apparent Vmax (nmol/lung X min-1) in control lungs were 9.0 +/- 0.3 and 87.9 +/- 1.4, respectively, and in the DPP-treated lungs were 9.6 +/- 0.5 and 57.7 +/- 1.8. This suggests that DPP acts in a noncompetitive manner. The magnitude of inhibition of PGA1 and PGE1 metabolism (both at 0.28 muM) was linearly related to the DPP concentration, over the range of 0.06 to 25.0 mug/ml. The ID50 values of DPP inhibition of PGA1 and PGE1 metabolism were 2.2 and 8.4 mug/ml, respectively. Perfusion of PGA1 at 2.96 muM or higher concentrations caused reversible vasoconstriction which was significantly inhibited (P less than .05) by DPP (6.0 mug/ml) by an average of 77.2 +/- 5.8% (n = 7).
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PMID:Metabolism of prostaglandins A and E in the perfused rabbit lung and the effects of selected inhibitors. 97 71

1. In unanaesthetized restrained rats kept at an ambient temperature of 21-23degrees C, rectal temperature was continuously monitored and the temperature effects of injections of prostaglandins, endotoxin from Salmonella abortus equi, lipid A, and antipyretics were examined. 2. Fever occurred when prostaglandin E1, E2, F1alpha or F2alpha (PGE1, PGE2, PGF1alpha, PGF2alpha) was injected into the cerebral ventricles in doses of 200 ng and 2 mug. PGE2 was the most potent prostaglandin followed in descending order by PGE1, PGF2alpha, and PGF1alpha. The fever produced by 2 mug of PGE1 and PGE2 was short and followed by a fall in temperature to below the pre-injection level. 3. I.V. injections of endotoxin and lipid A in doses of 3 or 10 mug usually caused a long lasting fall in temperature, but when injected into the cerebral ventricles in doses of 400 ng or 1 mug, they produced long lasting fevers. 4. Injected I.V. or I.P., indomethacin and paracetamol had a hypothermic action of their own. Indomethacin was more potent than paracetamol and both were more potent than injected I.P. 5. I.V. and I.P. injections of indomethacin and paracetamol did not reverse the hypothermia in response to I.V. endotoxin or lipid A, but the fever responses to their injection into the cerebral ventricles were prevented and abolished by the antipyretics. 6. It is concluded that in rats endotoxin and lipid A, or the endogenous pyrogens produced by them, do not readily pass through the blood-brain barrier into the brain tissue. If they do reach brain tissue, as when injected into the cerebral ventricles, they stimulate synthesis and release of prostaglandin in rats as they do in other species, and thereby produce fever. The hypothermia in response to I.V. endotoxin or lipid A, on the other hand, is thought to be independent of prostaglandin synthesis and to result from a direct toxic action on the skin vessels.
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PMID:Prostaglandins, endotoxin and lipid A on body temperature in rats. 117 7

Beta-phenylethylamine on injection into mice (100 mg/kg i.p.) produces a marked hyperthermia which is followed by a prolonged hypothermia. The hyperthermic response was studied in this report. The hyperthermic response was inhibited by p-chlorophenylalanine, methysergide, cyproheptadine, alpha-methyl-tyrosine, propranolol, practolol, phenoxybenzamine, phentolamine, haloperidol, pimozide, protriptyline and desipramine. Lysergic acid diethylamide potentiated the response, while p-chloroamphetamine was without effect. While FLA-63 potentiated the response, disulfiram and reserpine were ineffective in preventing the hyperthermia. Nicotinic acid and prostaglandin E1 did not prevent PE induced hyperthermia. It was concluded from these results that PE induced hyperthermia in mice is blocked by agents that reduce the effective concentration of either DA or 5-HT in the central nervous system (by either synthesis inhibitors or receptor blockers). The involvement with catecholaminergic neurons at least was postulated to be a result of PE induced release of DA from DA neurons.
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PMID:The effect of beta-phenylethylamine on temperature in mice and its possible mechanisms of action. 124 22

Pulmonary preservation is improved by hypothermia, but the optimal preservation temperature is not known. The effects of two different preservation temperatures, 4 degrees and 10 degrees C, on lung function were studied in a canine left lung allograft survival model allowing selective perfusion of either lung. After donor treatment with high-dose prostaglandin E1, (25 micrograms/kg), lungs were flushed with modified Euro-Collins solution (50 ml/kg) and stored in Euro-Collins solution for 18 hours at 4 degrees C in group I (n = 8) and 10 degrees C in group II (n = 6). Pulmonary gas exchange and hemodynamics were compared on the day of transplantation (day 0) and 3 days later (day 3). Rapid, high-flow, low-pressure flush was achieved uniformly in both groups (flush time: group I, 35.1 +/- 2.4 second; group II, 35.3 +/- 3.0 seconds; p = 0.96; flush pressure: group I, 9.8 +/- 0.7 mm Hg; group II, 10.1 +/- 1.1 mm Hg; p = 0.8). Transplanted lungs provided similar excellent oxygenation in both groups on day 0 (arterial oxygen tension, group I, 451 +/- 82 mm Hg; group II, 497 +/- 37 mm Hg; p = 0.61; inspired oxygen fraction = 1.0) and day 3 (arterial oxygen tension, group I, 551 +/- 57 mm Hg; group II, 587 +/- 19 mm Hg; p = 0.55), with a statistically significant improvement from day 0 to day 3 in both groups (group I, p = 0.034; group II, p = 0.038). There was no difference in arterial carbon dioxide tension, base excess, cardiac output, blood pressure or pulmonary artery pressure between the two groups. We conclude that a large bolus of prostaglandin E1 into the pulmonary artery produces a high-flow, low-pressure flush with modified Euro-Collins solution; with this technique, equivalent, reliable 18-hour lung preservation can be achieved at 4 degrees and 10 degrees C flush and storage temperatures.
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PMID:Reliable eighteen-hour lung preservation at 4 degrees and 10 degrees C by pulmonary artery flush after high-dose prostaglandin E1 administration. 159 77

From January 1982 to June 1990, 2730 patients with congenital heart defects (CHDs) were treated. 537 patients had complex lesions. Fifty of them died, a mortality rate of 9.31%. The operative age ranged from 2 days to 11 years (mean 3.16 +/- 1.68 years), and weight from 2.2 kg to 29 kg (mean 12.2 +/- 3.99 kg). Repair with deep hypothermia plus circulatory arrest was performed in 58 patients, moderate hypothermia plus cardio pulmonary bypass in 459, and normal thermic bypass in 8. The clinical experience concludes that an accurate diagnosis should be made promptly in neonates with complex CHDs. In the cyanotic neonates, surgical results can be improved by use of PGE1 and balloon atrial septostomy. For congestive CHDs, operation must be performed earlier to prevent pulmonary hypertension.
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PMID:[Surgical treatment of complex congenital heart defect in children and infants]. 191 91

Intraperitoneal injection of prostaglandin E1 (PGE) produces a transient hypothermia in rats that lasts 1-2 h. Rats exposed to an ambient temperature (Ta) of 26 degrees C displayed a decrease in rectal temperature (Tre) of 0.95 +/- 0.12 degrees C (SE) after injection with PGE (100 micrograms/kg ip). Hypothermia was produced mainly by heat losses, as indicated by increases in tail blood flow. At Ta of 4 degrees C, PGE produced a comparable fall in Tre of 1.00 +/- 0.14 degrees C. However, in the cold the hypothermia was caused solely by decreases in heat production. These results indicate that the PGE-induced hypothermia is not the result of a peripheral vasodilation induced by the direct action of PGE on the tail vascular smooth muscle but is a central nervous system-mediated response of the thermoregulatory system induced by PGE within the peritoneal cavity. Capsaicin injected subcutaneously induces a transient hypothermia in rats because of stimulation of the warm receptors. If administered peripherally in sufficient amounts, it is reputed to impair peripheral warm receptors so that they become desensitized to the hypothermic effects of capsaicin. We measured PGE-induced hypothermias in rats both before and after capsaicin desensitization at Ta of 26 degrees C. Before desensitization the hypothermia was -1.14 +/- 0.12 degrees C, whereas after capsaicin treatment the PGE-induced hypothermia was -0.34 +/- 0.17 degrees C. The biological effects of capsaicin are diverse; however, based on current thinking about the thermoregulatory effects of capsaicin desensitization, our results indicate that peripheral warm receptor pathways are in some manner implicated in the hypothermia induced by intraperitoneal PGE.
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PMID:Effects of cold and capsaicin desensitization on prostaglandin E hypothermia in rats. 238 39

The optimal surgical management (primary or staged repair) of interrupted aortic arch (IAA) with ventricular septal defect (VSD) remains to be determined. A consecutive series of 14 neonates, aged 3-18 days (mean: 10 +/- 6 days) underwent primary complete repair. Mean weight was 3.3 +/- 0.4 kg. Eleven patients had IAA type B, 2 had type A and 1 had type C. Six infants had the Di George syndrome. Preoperative management (mean: 5 +/- 4 days) included prostaglandin E1 (14/14), intubation and ventilation (13/14), and inotropic support (11/14). Surgery was performed under deep hypothermia and circulatory arrest and involved resection of all ductal tissue, direct end-to-side aortic arch anastomosis and patch closure of the VSD. There were 2 early deaths (14%, 70% CL: 5%-31%): low cardiac output (1), residual VSD (1). Four patients (33%, 70% CL: 13%-52%) underwent reoperation for recurrent aortic obstruction (3 patients, 1 death) or left ventricular outflow tract obstruction (LVOTO) (1 patient). The results improved with time: no death and no recurrent aortic obstruction in the last 8 patients. At last follow-up (11 patient, mean follow-up = 24 +/- 9 months), all patients were free of cardiac symptoms; none had persistent aortic obstruction; 4 had LVOTO (gradient greater than 20 mm Hg) and 1 (with the Di George syndrome) had severe mental disorders. Primary complete repair provides satisfactory results in most infants born with IAA and VSD. An adequate direct aortic arch anastomosis should entail a low risk of recurrent obstruction. LVOTO develops in many cases and may require further surgery.
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PMID:Primary definitive repair of interrupted aortic arch with ventricular septal defect. 239 28

Five infants (22-42 days of life) underwent arterial switch operation for simple transposition of the great arteries under deep hypothermic cardio-pulmonary bypass. Three babies required prostaglandin E1 infusion to keep ductus arteriosus opened widely before surgery. Balloon atrioseptostomy was necessary in 0-10 days of life in all babies because of poor condition. Left to right ventricular peak pressure ratio ranged from 0.75 to 0.86, preoperatively. Four of the five survived the operation, and one died of coronary insufficiency because of kinking of the implanted coronary artery. Hypothermic circulatory arrest was used in three (38-41 minutes). Aortic cross clamp time was 70-100 minutes, and cold crystalloid cardioplegia was given only one time just after aortic clamp in 3 babies. Single dose of cardioplegia protected left ventricular muscle well in babies with transposition of the great arteries as same as multiple dose method used in those with ventricular septal defect.
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PMID:[Arterial switch operation for simple transposition of the great arteries in infancy]. 279 90

Effects of continuous prostaglandin E1 (PGE1) infusion 0.03 micrograms.kg-1.min-1 on hemodynamics, body temperature and urine output during cardiopulmonary bypass (CPB) were studied. Systemic vascular resistance was kept significantly lower in PGE1 administration group than control group. Differences between core and peripheral temperature decreased faster in the PGE1 administration group than the control group. Mean arterial pressure was stable at 40mmHg during CPB in the PGE1 group and 60mmHg in the control group. However, there were no significant differences in urine output between the PGE1 administration group (10.8ml.kg-1.h-1) and the control group (9.4ml.kg-1.h-1). This study indicates that continuous PGE1 infusion (0.03 micrograms.kg-1.min-1) is a method of choice for vasodilation and improvement of peripheral perfusion during hypothermia of CPB.
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PMID:[Effects of prostaglandin E1 infusion during cardiopulmonary bypass]. 281 Jun 97


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