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

Whether retrograde coronary sinus cardioplegia adequately preserves right ventricular (RV) function is still a point of concern. Using technetium Tc 99m-labeled red blood cells, we assessed global and segmental RV function by first-pass and gated blood-pool radionuclide angiocardiography before and within 24 hours after aortic valve replacement in 14 consecutive patients (age, 58 +/- 5 years; mean +/- SEM). Coronary sinus cardioplegia was given in a multidose fashion at a flow rate of 50-70 ml/min through a balloon-tipped catheter, with the inflated balloon kept seated around the intra-atrial rim of the coronary sinus orifice. Additional myocardial protection was provided by systemic (25 degrees C) and topical hypothermia. Postoperatively, none of the patients had clinical or hemodynamic patterns suggestive of RV dysfunction. The postoperative global RV ejection fraction (0.49 +/- 0.03) was similar to the preoperative value (0.49 +/- 0.01). Analysis of segmental wall motion did not reveal postoperative abnormalities of new onset in any of the three anatomically defined RV regions (free wall, apex, and septum). Similarly, RV end-diastolic and end-systolic volume indexes (ml/m2) were not significantly affected by coronary sinus cardioplegia, being 71.6 +/- 5.8 and 36.1 +/- 3.5 before, and 67.4 +/- 3.8 and 34.5 +/- 2.3 after aortic valve replacement, respectively. We conclude that retrograde coronary sinus cardioplegia does not cause a detectable impairment of RV function if the balloon catheter does not obstruct the terminal tributaries of the coronary sinus and, hence, does not impede delivery of cardioplegia to right-sided cardiac structures.
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PMID:Adequate preservation of right ventricular function after coronary sinus cardioplegia. A clinical study. 255 1

An important goal in managing patients with respiratory failure using mechanical ventilatory support and positive end-expiratory pressure (PEEP) is to optimize tissue oxygen delivery relative to oxygen consumption. To this end, systemic hypothermia has been reported to reduce oxygen consumption. Cooling, however, may antagonize hypoxic pulmonary vasoconstriction and depress cardiac output. To determine whether these potentially adverse effects of cooling on tissue oxygen delivery would outweigh any potential benefits, we studied the effects of systemic hypothermia and end-expiratory pressure on venous admixture, intrapulmonary blood distribution, and oxygenation variables in 40 dogs with oleic acid-induced pulmonary edema of the right lung. The dogs were randomly assigned to four treatment groups of 10 dogs each: normothermia and zero end-expiratory pressure (ZEEP); normothermia and 10 cm H2O PEEP; hypothermia and ZEEP; hypothermia and PEEP. Hypothermia to 31.9 +/- 0.1 degree C (mean +/- SEM) caused no adverse effects on intrapulmonary blood flow distribution (measured by radioactive microspheres) or on venous admixture. Tissue oxygen delivery and arterial oxygenation did not improve with hypothermia, the latter being 109 +/- 13 mm Hg and 70 +/- 8 mm Hg with PEEP and ZEEP, respectively. However, hypothermia significantly reduced oxygen consumption, so that the coefficient of oxygen delivery (i.e., the ratio of oxygen supply to consumption) increased from 2.5 +/- 0.1 to 3.2 +/- 0.2 (p less than 0.01) with ZEEP and from 2.0 +/- 0.1 to 2.6 +/- 0.3 with PEEP (p = 0.016). Thus, although systemic hypothermia failed to improve arterial oxygenation and tissue oxygen delivery, it decreased systemic oxygen demands, thereby improving the oxygen supply-demand balance.
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PMID:Hypothermia with and without end-expiratory pressure in canine oleic acid pulmonary edema. 266 83

Hypothermia protects tissue function in ischemia. This study determined if selective brain cooling inhibits cerebral cortical lactate accumulation and thus accounts for imporved neurologic outcome after complete cerebral ischemia in dogs. The brain was selectively cooled (hippocampal temperature 33 degrees C) by nasal lavage with water at 5 degrees C. Control dogs received nasal lavage with water at 39 degrees C. Mean +/- SEM rectal temperature in both groups was 39 +/- 1 degree C prior to ischemia. Selective brain cooling before and during 10 minutes of cardiac arrest was associated with significantly improved neurologic function and 100% survival, whereas normothermic cardiac arrest produced marked neurologic dysfunction and 100% mortality. Cerebral cortical lactate accumulation was measured in a complementary series of dogs exposed to the same two treatments but with the addition of six cerebral cortical brain biopsies taken before, during, and immediately after cardiac arrest. Brain and rectal temperatures of dogs in the brain biopsy protocol were similar to those of dogs in the recovery protocol. There was no difference detected in cerebral lactate accumulation during ischemia between brain-cooled and control dogs. Thus, reduction in cortical brain lactate during ischemia cannot account for the postischemic functional protection afforded by preischemic selective brain cooling.
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PMID:Protection from cerebral ischemia by brain cooling without reduced lactate accumulation in dogs. 272 44

A standard murine model was used to determine whether acute pretreatment exposures to hypoxia could alter ultimate hypoxic survival time. Adult male albino mice (Mus musculus) weighing 25-30 g were subjected to three pretreatment hypoxic exposures (4.5% O2, balance N2) of increasing duration (90, 120, and 150 seconds) with 300 seconds of normoxia between each pretreatment exposure and before testing of hypoxic survival time. Acute pretreatment exposures to hypoxia significantly increased mean +/- SEM hypoxic survival time from 108 +/- 4 to 403 +/- 42 seconds. Mean +/- SEM blood glucose concentrations increased significantly from 201 +/- 19 to 397 +/- 10 mg/dl immediately after hypoxic pretreatment. A significant increase in mean +/- SEM blood ketone concentrations, from 0.15 +/- 0.01 to 0.40 +/- 0.08 mM, was detected in the blood 1,800 seconds but not 300 seconds after hypoxic pretreatment. However, pretreatment with exogenous glucose or ketones alone, to mimic the blood levels seen after hypoxic pretreatment, failed to increase hypoxic survival time. In contrast, mice pretreated with hypoxic exposures plus the exogenous substrate beta-hydroxybutyrate had an increased mean +/- SEM hypoxic survival time of 749 +/- 48 seconds and a decreased body temperature. Stepwise Cox regression analyses with body temperature as a fixed covariate suggest that this decrease in body temperature has a partial role in, but can not fully account for, the increased hypoxic survival time. These data suggest that sequential exposures to hypoxia induce metabolic changes that protect against the lethal effects of hypoxia, perhaps by altering substrate mobilization and utilization and/or by inducing a hypometabolic hypothermia.
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PMID:Hypoxia-induced increases in hypoxic tolerance augmented by beta-hydroxybutyrate in mice. 277 83

Postoperative cardiac patients frequently are mildly hypothermic, yet the influence of hypothermia on left ventricular (LV) contractility has received little attention. To study the possible effects of mild hypothermia on LV function, six pigs were placed on partial right ventricular bypass, the hearts were electrically paced to control heart rate, and myocardial temperature was varied between 34 degrees and 38 degrees C. Using two pairs of orthogonally oriented sonomicrometer crystals in the left anterior descending (LAD) and left circumflex (LCX) distributions, we estimated regional work (the area within LV pressure-area loops) over a range of LV preloads. Diastolic function was assessed by measurement of the time constant of LV pressure decay during isovolumic relaxation. Regional work data were expressed as percentages of baseline (38 degrees C and end-diastolic pressure of 10 mm Hg). To control for preload variations, regional work and time constants were calculated from beats with end-diastolic areas within 0.1% of baseline. Regional work (mean +/- SEM) declined from 85.1 +/- 6.7% at 38 degrees C to 31.9 +/- 4.4% at 34 degrees C. Time constants were prolonged from 44.8 +/- 2.5 msec at 38 degrees C to 61.6 +/- 2.7 msec at 34 degrees C. These data demonstrate a marked depression of LV contractility, even at mild levels of hypothermia that may be encountered clinically after cardiac operations.
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PMID:Systolic and diastolic left ventricular dysfunction due to mild hypothermia. 280 6

The mechanisms of ischemia-reperfusion injury in skeletal muscle remain controversial. We investigated the ability of postischemic hypothermia to diminish reperfusion edema and improve skeletal muscle pH in a bilateral, in vivo isolated canine gracilis muscle model. In five anesthetized animals, both gracilis muscles were subjected to 6 hr of ischemia followed by 1 hr of reperfusion. After 5 hr of warm ischemia, one gracilis muscle was cooled to 21 degrees C (cold reperfusion, CR) while the contralateral gracilis muscle was maintained at ambient temperature (warm reperfusion, WR). Reperfusion muscle edema was quantitated by measurement of gracilis muscle weight gain. Interstitial muscle pH was monitored by glass microelectrodes. Vascular permeability was measured by analysis of albumin (125I-Alb) leak. Results are presented as the means +/- SEM. (table; see text) Postischemic hypothermia significantly increased the interstitial muscle pH and significantly reduced postreperfusion muscle edema, without changing the vascular permeability to albumin. These data suggest that hypothermia may provide a clinical method for salvaging ischemic skeletal muscle from the postreperfusion edema that can lead to compartment syndromes, reperfusion injury, and subsequent limb loss.
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PMID:Postischemic hypothermia diminishes skeletal muscle reperfusion edema. 281 55

Thirty-six brain-dead children were managed to allow organ harvesting, which was possible in 21 (7 multi-organ). Optimal ventilation allowed for normal PaO2 and PaCO2 (mean +/- SEM FiO2 = 0.50 +/- 0.05). The management of hemodynamics was quite difficult and cardiac arrest may be due to patient transport, electrolyte disorders and dehydration. Vascular filling was of main importance and required standard solutes (5 or 2.5% glucose, normal saline, Ringer lactate) at a rate of 3.0 +/- 0.5 ml/kg/h, adapted for electrolytes (mainly KCl); sometimes, other solutes may be used: blood (17 patients), human 20% serum albumin (17 patients), plasma (9 patients). This filling was sufficient for 15 patients; the others required inotropic agents: dopamine (17 +/- 8 micrograms/kg/min), dobutamine (42 +/- 18 micrograms/kg/min). Diuresis was more than 3 ml/kg/h in 38% of the patients and desmopressin was used in 3 cases. Hypothermia (minimum 31.2 degrees) had no major consequence. No infection was found. Quality of management of brain-dead patients is of main importance; the possibility of organ harvesting must be evoked in such situations and is the first step in organ transplantations.
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PMID:[Resuscitation of children in the brain death state from the view of organ procurement for therapeutic purposes]. 324 51

Regional hypothermia is known to protect many tissues from ischemic injury. We investigated the relationship between regional hypothermia and skeletal muscle ischemia-reperfusion injury in a bilateral in vivo isolated canine gracilis muscle model. In five anesthetized dogs, one gracilis muscle was subjected to 6 hours of ischemia followed by 1 hour of reperfusion while the contralateral muscle served as a nonischemic control. Localization and quantitation of skeletal muscle injury was determined by histochemical staining with triphenyl tetrazolium chloride (TTC) followed by computerized planimetry of the infarct size. Muscle pH and temperature were monitored continuously in the proximal, middle, and distal segments by using pH electrodes and needle thermistors. Muscle pH was calculated by use of the Nernst equation with temperature correction, and hydrogen ion washout rates (H+) were derived from the observed change in muscle pH during reperfusion. A significant (p less than 0.05) regional hypothermia was observed in the distal third of the muscle. The preischemic temperature in the distal muscle was 27 +/- 2 degrees (SEM) C, compared to 34 +/- 1 degree and 32 +/- 2 degrees C in the proximal and middle segments of muscle, respectively. This temperature gradient was sustained throughout the experiment. The distal third of the ischemic muscle demonstrated significantly less (p less than 0.05) injury than the proximal and middle thirds as measured by TTC infarct size (31 +/- 10%, compared to 71 +/- 3% and 78 +/- 6%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional hypothermia protects against ischemia-reperfusion injury in isolated canine gracilis muscle. 339 82

We tested the hypothesis that isovolemic anemia blunts the thermogenic response to environmental cold stress in 3 to 4-day-old newborn piglets. Eight animals were studied in both thermoneutral (31.6-32.8 degrees C) and cold (19.6-20.2 degrees C) environments, before and after an isovolemic, partial volume exchange transfusion which reduced the hematocrit from 26 to 15%. In the nonanemic phase of study, deep rectal temperatures declined but had plateaued by 30 minutes after onset of cold stress and remained within normal limits for newborn piglets. In the anemic phase of study, deep rectal temperature declined continuously throughout cold stress with true body core hypothermia (less than 38 degrees C) observed at all measurement points beyond 15 min of cold stress. Baseline oxygen consumption did not differ between the two study phases (17.6 +/- 1.8 versus 16.7 +/- 2.1 ml/kg-1/min-1, mean +/- SEM). However, during environmental cold stress, oxygen consumption increased by 64% over baseline in the nonanemic phase of study (p less than 0.05) whereas 21% increase over baseline was observed in the anemic phase (p NS). We conclude that isovolemic anemia limited oxygen consumption and heat production during environmental cold stress, resulting in body core hypothermia.
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PMID:Anemia blunts the thermogenic response to environmental cold stress in newborn piglets. 358 87

The role of hypothermia in the antihypoxic effects of drugs was examined in the present experiments. The effects of environmentally induced hypothermia and drugs were tested by exposing mice to 100% nitrogen gas for 80 sec and counting the number of survivors. In a series of 68 vehicle control groups, the mean of mice surviving the test was 8.6% (SEM = 1.4). Hypothermia induced by lowering the ambient temperature or by isolating mice for a brief period increased the number surviving hypoxia, and the per cent of animals surviving was linearly related to body temperature. When the effects of drugs were compared to that of hypothermia, several drugs were found which protected mice from hypoxia to a greater extent than hypothermia alone. Active substances included the anticonvulsant drugs phenobarbital, phenytoin, carbamazepine and diazepam, but not primidone. Physostigmine and the muscarinic agonist oxotremorine also caused significant protection, while the effects of nicotine could be completely accounted for by hypothermia. Arecoline had a biphasic, time-dependent effect that may be explained by a combination of muscarinic and nicotinic actions. The effects of the muscarinic agonists are centrally mediated, since they could be blocked by low doses of scopolamine HCl, but not by the quaternary analog scopolamine methyl nitrate. Furthermore, the antihypoxic effect of physostigmine was not mimicked by the peripherally acting acetylcholinesterase inhibitor, neostigmine. These results suggest that some drugs do have protective effects against hypoxia which are independent of drug-induced hypothermia and that these effects may be mediated through the CNS.
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PMID:Protection against hypoxia-induced lethality in mice: a comparison of the effects of hypothermia and drugs. 359 68


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