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

This study was designed to assess the effects of some key excretory nitrogenous substances on body temperature and selected ambient temperature (Ta) in the mouse. In the first experiment, a dosage-response curve was developed to assess the effects of urea, creatinine, and ammonium chloride on colonic temperature at a Ta of 20 degrees C. All three substances elicited a drop in body temperature at a critical dosage. The threshold dosages were 3280 mg/kg for urea, 1279 mg/kg for creatinine, and 365 mg/kg for ammonium chloride. In a second experiment the selected Ta was monitored using a temperature gradient system. Mice were injected with dosages of the nitrogenous substances that had previously been shown to cause hypothermia at a Ta of 20 degrees C. Urea and ammonium chloride had no significant effect on the selected Ta nor on the colonic temperature after 90 min in the temperature gradient. Creatinine elicited a slight lowering of the selected Ta but had no effect on colonic temperature. The thermoregulatory responses to extremely toxic dosages of the nitrogenous substances appear to be quite dissimilar to that when animals are treated with xenobiotic compounds.
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PMID:Thermoregulatory responses in mice following acute administration of principal nitrogenous excretory substances. 325 Dec 52

The use of high-dose corticosteroids in the treatment of severe sepsis and septic shock remains controversial. Our study was designed as a prospective, randomized, double-blind, placebo-controlled trial of high-dose methylprednisolone sodium succinate for severe sepsis and septic shock. Diagnosis was based on the clinical suspicion of infection plus the presence of fever or hypothermia (rectal temperature greater than 38.3 degrees C [101 degrees F] or less than 35.6 degrees C [96 degrees F]), tachypnea (greater than 20 breaths per minute), tachycardia (greater than 90 beats per minute), and the presence of one of the following indications of organ dysfunction: a change in mental status, hypoxemia, elevated lactate levels, or oliguria. Three hundred eighty-two patients were enrolled. Treatment--either methylprednisolone sodium succinate (30 mg per kilogram of body weight) or placebo--was given in four infusions, starting within two hours of diagnosis. No significant differences were found in the prevention of shock, the reversal of shock, or overall mortality. In the subgroup of patients with elevated serum creatinine levels (greater than 2 mg per deciliter) at enrollment, mortality at 14 days was significantly increased among those receiving methylprednisolone (46 of 78 [59 percent] vs. 17 of 58 [29 percent] among those receiving placebo; P less than 0.01). Among patients treated with methylprednisolone, significantly more deaths were related to secondary infection. We conclude that the use of high-dose corticosteroids provides no benefit in the treatment of severe sepsis and septic shock.
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PMID:A controlled clinical trial of high-dose methylprednisolone in the treatment of severe sepsis and septic shock. 330 74

Five patients who had undergone renal transplantation 3 months to 23 years ago were operated on successfully for an abdominal aortic aneurysm. In the first case, dating from 1973, the kidney was protected by general hypothermia. In the remaining patients, no measure was used to protect the kidney. Only one patient showed a moderate increase of blood creatinine in the postoperative period; renal function returned to normal in 15 days. All five patients have normal renal function 6 months to 11 years after aortic repair. Results obtained in this series show that protection of the transplant during aortic surgery is not necessary, provided adequate surgical technique is used. Such a technique is described in detail. Its use simplifies surgical treatment of such lesions and avoids the complex procedures employed in the seven previously published cases.
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PMID:Abdominal aortic aneurysmectomy in renal transplant patients. 351 May 92

A multicenter survey evaluated the clinical presentation, treatment, and outcome of accidental hypothermia. Data were collected from 13 emergency departments, with 401 of the 428 cases presenting during a two-year study period. Core temperatures ranged from 35 C to 15.6 C (mean, 30.57 C +/- 3.53) with 272 cases (63.6%) less than or equal to 32.2 C. There were no significant differences by age in presenting temperature, rewarming strategies, or mortality. The first hour rewarming rate was significantly (P less than .05) faster in the population less than or equal to 59 years (1.08 +/- 1.39 C/hr) than in those greater than or equal to 60 years (0.75 +/- 1.16 C/hr). Male core temperatures averaged 30.27 +/- 3.44 C versus female temperatures of 31.1 +/- 3.61 C. There were no clinically significant differences in male (N = 296) versus female (N = 132) profiles. High ethanol levels (315 to 800 mg%) did not affect outcome. Nine of 27 (33%) patients who received CPR initiated in the field survived, versus six of 14 (43%) with CPR begun in the ED. The profile of the CPR versus non-CPR population differed significantly (P less than .05) in location (outdoors), initial temperature (24.8 +/- 3.77 C vs 30.94 +/- 3.12 C), third-hour rewarming rate (2.28 +/- 1.53 C vs 1.17 +/- 1.18 C/hr), and numerous laboratory parameters. Tracheal intubation was performed without incident in 117 cases, of which 97 were less than or equal to 32.2 C. There were 73 fatalities (17.1%). Of these, 84.9% (N = 62) were less than or equal to 32.2 C. Predisposing conditions in this group included "serious" illness (30), systemic infection (28), trauma (15), immersion (ten), frostbite (seven), and overdose (two). The initial pulse, hemoglobin, and first-hour rewarming rate was lower in the deceased population, while the potassium, urea nitrogen, creatinine, and phosphorus were elevated. Excluding treatment combinations, outcome with exclusive use of a single rewarming strategy was passive external rewarming, 14 deaths below 32.2 C, 13 above; active external rewarming, six deaths below 32.2 C, two above; active core rewarming, 38 deaths below 32.2 C, none above. Refinements of the American Heart Association's CPR standards in hypothermia and a Hypothermia Survival Index are proposed.
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PMID:Multicenter hypothermia survey. 363 69

To assess the effects of body temperature on renal susceptibility to ischemic injury, rats were rendered acutely hypothermic (90-93 degrees F), normothermic (98-99 degrees F), or hyperthermic (101-103 degrees F) with a heat-controlled surgical board and then were subjected to 25 min of bilateral renal artery occlusion (RAO). Renal high-energy phosphates, their degradation products, and nonprotein sulfhydryl (NPSH) content were assessed at selected times during the peri-ischemic period. The severity of acute renal failure (ARF) was determined for 48 h following RAO by blood urea nitrogen (BUN) and plasma creatinine determinations and by renal histology. Ischemic ATP, ADP, AMP, GTP, GDP, UTP, and NAD levels and postischemic NPSH levels (15 min reflow) inversely correlated with temperature (P less than 0.001). BUN, creatinine concentrations (at 24 and 48 h), and histological injury (at 48 h) directly correlated with temperature (P less than 0.01). Hyperthermia in the absence of RAO had no demonstrable adverse renal effects. We conclude that hyperthermia potentiates ischemic renal injury, whereas hypothermia confers protection. These effects are associated with, and may be influenced by, temperature-induced changes in renal high-energy phosphate availability and oxidant stress during the ischemic/postischemic period.
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PMID:Body temperature: an important determinant of severity of ischemic renal injury. 372 86

To characterize the transport system of cimetidine, an organic cation, in the blood-cerebrospinal fluid barrier, the accumulation of cimetidine by the isolated rat choroid plexus was examined. Accumulation of cimetidine was against a concentration gradient via a saturable process (Km = 53 microM, Vmax = 12 nmol/ml/min) that was inhibited by sulfhydryl reagents (p-hydroxymercuribenzoate), metabolic inhibitors (KCN and 2,4-dinitrophenol) and hypothermia (Q10 = 4.5), but did not require inward Na+ gradient. Organic cations such as 1N-methylnicotinamide, tetraethylammonium, choline, histamine and creatinine did not affect the accumulation of cimetidine at the concentration of 1 mM. Cimetidine did not affect the accumulation of tetraethylammonium. More lipophilic cations such as quinidine and quinine inhibited not only the accumulation of cimetidine but also that of an organic anion, benzylpenicillin, although the inhibitory mechanisms are not known. One millimolar of organic anions, such as 5-hydroxyindoleacetic acid, p-aminohippuric acid, homovanillic acid, salicylic acid and benzylpenicillin, inhibited the accumulation of cimetidine. Furthermore, the accumulation of organic anions (benzylpenicillin and salicylic acid) showed saturability and was inhibited by cimetidine. Cimetidine and the organic anions thus showed a mutual inhibition. Oligopeptides also inhibited the accumulation of cimetidine. These findings suggested that cimetidine transport in the choroid plexus is via carrier-mediated active transport process, but does not require inward Na+ gradient. This transport is inhibited by several compounds with different properties like oligopeptides, lipophilic cations and organic anions, although the inhibitory mechanism is not known.
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PMID:Transport of cimetidine by the rat choroid plexus in vitro. 379 52

The effects of low flow low pressure pulsatile bypass were studied in 90 consecutive patients undergoing coronary artery surgery. Overall pump flow rate (OFR) was 19-49 (mean 31 +/- 7) ml/kg/min at all temperatures. Moderate (28 degrees C) hypothermia was used. When cross-clamped flow was 17-49 (mean 27 +/- 7) ml/kg/min and mean perfusion pressure 50-60 mmHg. Priming volume (PV) was reduced to 1.45 +/- 0.02 L (range 1.2-2.0 L) PV, cardioplegia and volume additions were considered as total bypass crystalloid (TBC) and this correlated positively with increased post-operative positive water balance (r = 0.58, P less than 0.001). Bypass urine output averaged 135 +/- 24 ml (range 0-1,000 ml) was unrelated to OFR and correlated only with TBC (r=0.47, P less than 0.001). In 86 a single cardioplegia dose of 0.7 L (range 0.4-0.8 L) sufficed for this ischaemic period (mean 46 +/- 16 min). Four required a further 0.2-0.3 L. Their ischemic times were 44-74 min (mean 59 +/- 13 PNS). Inotropes were used in only 3 patients. Post-operatively 7 required diuretics for low hourly urine flow. Of the 76 with normal pre-operative renal function urea rose transiently in 15. Three had raised urea for over 9 days. Creatinine rose transiently in 7 but persisted in only one. Plasma cortisol (n=78) rose in 67 and fell in 11, indicating, overall, an adequate metabolic response. Plasma free haemoglobin before and after bypass varied widely and did not correlate with flow rate or perfusion time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of low flow, low pressure pulsatile bypass. 387 61

The effects of chlorpromazine, an agent with inhibitory effects of calcium influx, phospholipase activation, and Na-K-ATPase, on preserving renal function and proximal tubular ultrastructure were evaluated in renal ischemia. After right nephrectomy chlorpromazine (0.025 mg) or 1 ml of 0.9 per cent saline was selectively administered to the rat kidney immediately prior to a sixty-minute occlusion of the remaining renal artery. Pretreatment with chlorpromazine resulted in a significant attenuation in the rise in postischemic serum creatinine. Hypothermia of the kidney during ischemia provided an additional protective effect. Electron microscopic study of the proximal convoluted tubule demonstrated that the structural damage was less severe in chlorpromazine-treated rats and virtually complete preservation of a normal ultrastructure was observed when hypothermia was added.
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PMID:Effects of chlorpromazine on ischemic rat kidney: a functional and ultrastructural study. 398 28

Adriamycin (Adriablastine), administered weekly at the dose of 5 mg/kg i.p. for 3 weeks in rats, produced a general decrease of vitality associated with a decrease of body weight, hypothermia, decreases of stroke volume and cardiac output. Hematocrit was decreased. Renal blood flow decreased whereas pulmonary blood flow increased. Mean blood pressure and heart rate remained unaffected. Biochemical evaluations revealed a decrease of blood urea and serum creatinine, which might be related to decreased food intake and protein metabolism. Morphological changes in the heart tissue could not be appreciated. Venoruton (HR), administered at the dose of 300 mg/kg p.o. daily for 28 days (5 days before and 23 days after the first injection of adriamycin), improved adriamycin-induced clinical signs and symptoms (loss of body weight, hypothermia and decreased general vitality). It tended to increase cardiac output and stroke volume.
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PMID:Protective effects of O-(beta-hydroxyethyl)-rutosides (HR) against adriamycin-induced toxicity in rats. 400 21

An in situ flushing solution was evaluated with regard to the following: (1) its ability to protect the kidney during 60, 90, and 120 minutes of normothermic ischemia; (2) the effects of using an intracellular versus extracellular electrolyte composition in the flushing solution; and (3) the ability of the flushing solution to complement in situ hypothermia as a protective measure during long-term ischemia. Rat kidneys were briefly flushed in situ with an isotonic phosphate buffered solution (pH 7.2) containing 50 milliosmole of sucrose. The left renal pedicle was then immediately clamped to render the kidney ischemic and to hold the flushing solution in the kidney. Following removal of the pedicle clamp, a contralateral nephrectomy of the right kidney was performed and daily serum creatinine levels determined to evaluate postischemic renal function. The results indicate the following: (1) the flushing procedure is very effective in preventing postischemic acute renal failure following 60 minutes of normothermic ischemia, but is considerably less effective for ischemic times of 90 minutes or more; (2) an intracellular electrolyte composition in the flushing solution does not improve the protective effects of this solution; and (3) the flushing procedure can significantly improve on the protection otherwise provided by in situ hypothermia.
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PMID:Evaluation of a flushing solution designed to protect kidneys from in situ ischemia. 402 28


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