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

The permeability of the rat blood-brain barrier during different levels of hypothermia was examined using a new and more sensitive quantitative radiotracer technique. In contrast to the findings of previous studies, tracer permeation as measured here by the calculated cerebrovascular permeability-area product (PA), did not increase during hypothermia. Rather, rats maintained at specific temperatures between 30-16 degrees C (1 h) by contact surface cooling, displayed lowered permeation (PA) of i.v. injected 14C-sucrose, 125I-bovine serum albumin and 3H-alpha-amino-isobutyric acid in all brain regions examined. This effect was temperature-dependent and reversible on rewarming to normothermic temperature. Elevated plasma tracer concentration vs. time was characteristic of hypothermic rats except those cooled to 30 degrees C. That no elevation in plasma tracer accompanied alterations in tracer permeation at 30 degrees C, indicates hypothermic induced reductions in PA are independent of altered plasma tracer levels. Furthermore, the nature of alpha-amino-isobutyric acid to rapidly distribute to intracellular vs. extracellular sites suggests the effects of hypothermia seen here are due primarily to the condition of cerebrovascular membranes.
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PMID:Hypothermia-induced reduction in the permeation of radiolabelled tracer substances across the blood-brain barrier. 688 Jun 23

A review of 398 neonatal autopsies at Downstate Medical Center revealed 27 cases of kernicterus during the seven-year period from 1971 through 1977. With the current intensive care of the sick newborn, kernicterus continues to occur, mainly in premature infants with relatively low levels of serum bilirubin (mean of 11.5 mg/100 ml). To understand the factors contributing to the development of kernicterus, clinical and pathologic findings in 27 infants with kernicterus were compared to 103 "control" infants with retrospectively. Birth weight, gestational age, sex, and Apgar scores were comparable in both groups. The duration of survival was significantly shorter in infants with kernicterus than in the control infants. The clinical signs and symptoms of kernicterus were nonspecific and the premortem diagnosis of kernicterus was not suspected in most of the cases. There were no significant differences in the peak serum bilirubin values, incidence of hypothermia, hypoglycemia, convulsions, anemia, infection, use of phototherapy, transfusion and exchange transfusion in the two groups. Serum albumin values and bilirubin binding capacity measured by 2-(4-hydroxybenzeneazo)benzoic acid were significantly lower in the kernicteric group although the bilirubin-albumin molar ratio was equal in both groups. The incidences of severe acidosis and hypoxic encephalopathy were significantly higher in the kernicteric infants. In this study, acidosis, hypoxia, hypoalbuminemia, and low bilirubin binding capacity were seen more often in kernicteric infants than in control infants. However, analysis of previously suggested risk factors failed to identify any single factor or combination of factors which could be predictive to the development of kernicterus.
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PMID:Lack of predictive indices in kernicterus: a comparison of clinical and pathologic factors in infants with or without kernicterus. 719 47

The present study was undertaken to investigate the interrelation of nutrition, core temperature, and thyroid function and their influence on survival of patients aged > or = 70 y admitted to the hospital with acute conditions. Sixty-seven patients entered the study. Nutritional state, thyroid function, rectal temperature, and the APACHE II score were recorded at admission. The patients were followed until death or hospital discharge. Patients with a serum albumin concentration < 35 g/L showed a lower triiodothyronine (T3) concentration, a higher reverse triiodothyronine (rT3) concentration, and a higher death rate. Prior weight loss (> or = 10%) did not influence thyroid status but increased the mortality rate. Eleven patients were hypothermic (< 36.5 degrees C) and had a higher mortality, lower total T3 concentration, and higher rT3 concentration than the normothermic or hyperthermic subjects. Serum albumin, body weight, and total T3 concentration were higher in survivors (n = 51) than in nonsurvivors (n = 16). Ongoing weight loss and hypoalbuminemia at admission are highly prevalent in elderly people with acute disease, and influence their clinical outcome. Mild hypothermia was a good predictor of death. Hypoalbuminemia and hypothermia were associated with low T3 and high rT3 values.
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PMID:Influence of nutrition, thyroid hormones, and rectal temperature on in-hospital mortality of elderly patients with acute illness. 766 Nov 30

The unique germfree, colostrum-deprived, immunologically "virgin" piglet model was used to evaluate the ability of lactoferrin (LF) to protect against lethal shock induced by intravenously administered endotoxin. Piglets were fed LF or bovine serum albumin (BSA) prior to challenge with intravenous Escherichia coli lipopolysaccharide (LPS), and temperature, clinical symptoms, and mortality were tracked for 48 h following LPS administration. Prefeeding with LF resulted in a significant decrease in piglet mortality compared to feeding with BSA (16.7 versus 73.7% mortality, P < 0.001). Protection against the LPS challenge by LF was also correlated with both resistance to induction of hypothermia by endotoxin and an overall increase in wellness, as quantified by a toxicity score developed for these studies. In vitro studies using a flow cytometric assay system demonstrated that LPS binding to porcine monocytes was inhibited by LF in a dose-dependent fashion, suggesting that the mechanism of LF action in vivo may be inhibition of LPS binding to monocytes/macrophages and, in turn, prevention of induction of monocyte/macrophage-derived inflammatory-toxic cytokines.
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PMID:The protective effects of lactoferrin feeding against endotoxin lethal shock in germfree piglets. 952 62

Therapeutic cerebral hypothermia is widely used for the treatment of severe head injury and cerebral ischemia. The effects of cerebral hypothermia on the cerebral blood flow (CBF) and metabolism, and cerebral vasculature in the normal brain were investigated. Thirty-four adult cats were divided into four groups. CBF was monitored by hydrogen clearance. Arteriovenous oxygen difference (AVDO2) and cerebral venous oxygen saturation (ScvO2) were measured in blood samples from the superior sagittal sinus. The cerebral metabolic rate of oxygen (CMRO2) and cerebral vascular resistance (CVR) were calculated. The cerebral blood volume (CBV) was measured using technetium-99m-labeled human serum albumin in 12 cats. Deep cerebral temperature was cooled from 37 degrees C to 25 degrees C using a water-circulating blanket. In the hypothermia group (Group A: n = 10), CBF (51.2 +/- 8.3 ml 100 g-1 min-1 at 37 degrees C) decreased with lower brain temperature (6.1 +/- 2.7 at 25 degrees C). CMRO2 (2.24 +/- 0.75 ml 100 g-1 min-1 at 37 degrees C) was also decreased (0.52 +/- 0.20 at 25 degrees C). AVDO2 (4.3 +/- 1.0 ml 100 g-1 min-1 at 37 degrees C) increased significantly at 31 degrees C (6.6 +/- 1.8; p < 0.05) and ScvO2 (67.8 +/- 7.9% at 37 degrees C) decreased significantly at 29 degrees C (53.7 +/- 9.7; p < 0.05). CBV (5.3 +/- 1.2% at 37 degrees C) decreased significantly at 29 degrees C (3.7 +/- 1.0; p < 0.05) and CVR (3.2 +/- 0.7 mmHg ml-1 100 g-1 min-1 at 37 degrees C) increased significantly at 29 degrees C (13.8 +/- 5.2; p < 0.01). The combined effect of hypothermia with vasopressor (noradrenalin) (Group B: n = 6) or barbiturate (thiopental) administration (Group C: n = 6) on the cerebral metabolic parameters were also examined. Hypothermia with noradrenalin administration significantly improved the ischemic parameters (AVDO2 was 4.7 +/- 1.4 ml 100 g-1 min-1 at 31 degrees C and ScvO2 was 72.2 +/- 6.4% at 29 degrees C). However, hypothermia with barbiturate administration did not improve these metabolic parameters. These results suggest that hypothermia may cause vasoconstriction and misery perfusion in the brain. This potential risk of relative ischemia can be avoided by combination with vasopressor administration.
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PMID:Misery perfusion caused by cerebral hypothermia improved by vasopressor administration. 1049 21

In the management of severe pediatric brain injury, attention has previously been paid to brain edema, ICP elevation and low cerebral perfusion pressure (CPP). However, in the acute stage within 3-6 hours after trauma, brain hypoxia and hyperglycemia associated with diffuse brain injury are often observed. We have pointed out brain thermo-pooling (elevation of brain tissue temperature) and brain hypoxia caused by defective release of oxygen from hemoglobin (due to decrease in red blood cell enzyme (DPG)) as a new mechanism of brain injury. To treat these pathologic changes, we have developed a brain hypothermia treatment, the major purpose of which is to prevent brain hypoxia, brain thermo-pooling, neurohormonal changes causing cytokine encephalopathy, and a selective, radical-mediated damage of the dopamine A10 nervous system. The brain tissue temperature is initially adjusted to 35 degrees C with adequate cerebral oxygenation, followed by brain hypothermia at 34 degrees C for 1 weeks to prevent brain hypoxia, free radical reactions, brain edema and ICP elevation. What is most difficult in the pediatric brain hypothermia treatment is to maintain metabolic balance in the injured brain tissue and pulmonary infections associated with an immune crisis. When a rapid elevation of serum glucose is noted it is critical to lower the value because glucose quickly penetrates the blood-brain barrier and increases pyruvate and lactate by inhibiting the TCA cycle metabolism. Thus, hyperglycemia during brain hypothermia treatment is one of the major target of management. Another problem is immune crisis associated with secondary pulmonary infections. To prevent them, early enteral nutrition and replacement of L-arginine were most useful, as well as preconditioning for rewarming as follows: serum albumin > 3.0 g/dl; lymphocyte > 1500/mm3; T-H (CD4) lymphocytes > 55%; serum glucose, 120-140 mg/dl; vitamin A > 50 mg/dl; Hb > 12 g/dl and 2,3 DPG, 10-15 mumol/gHb; O2 ER, 23-25% and AT-III, > 100%. The clinical benefit of this therapy is still controversial.
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PMID:[Brain hypothermia treatment for the management of severe pediatric brain injury]. 1072 86

Changes in brain temperature are known to modulate the marked neuronal damage caused by an approximately 10-min intra-ischemic period. Numerous studies have suggested that the extracellular glutamate concentration ([Glu](e)) in the intra-ischemic period and the initial postischemia period is strongly implicated in such damage. In this study, the effects of intra-ischemic brain temperature (32, 37, 39 degrees C) on [Glu](e) were investigated utilizing a dialysis electrode combined with ferrocene bovine serum albumin (BSA), which allows oxygen-independent real-time measurement of [Glu](e). This system allowed separate quantitative evaluation of intra-ischemic biphasic glutamate release from the neurotransmitter and metabolic pools, and of postischemic glutamate re-uptake in ischemia-reperfusion models. The biphasic [Glu](e) elevation in the intra-ischemic period did not differ markedly among intra-ischemic brain temperatures ranging from 32 to 39 degrees C. Intra-ischemic normothermia (37 degrees C) and mild hyperthermia (39 degrees C) markedly inhibited [Glu](e) re-uptake during the postischemic period, although the intra-ischemic [Glu](e) elevation did not differ from that during intra-ischemic hypothermia (32 degrees C). It was assumed that normothermia or mild hyperthermia in the intra-ischemic period influences intracellular functional abnormalities other than the intra-ischemic [Glu](e) elevation, thereby inhibiting glutamate re-uptake after reperfusion rather than directly modulating intra-ischemic [Glu](e) dynamics.
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PMID:Quantitative evaluation of extracellular glutamate concentration in postischemic glutamate re-uptake, dependent on brain temperature, in the rat following severe global brain ischemia. 1079 87

Isolated hepatocytes in suspension provide a number of advantages for use in bioartificial liver device, however, poor stability of this cell preparation at physiological temperatures is an apparent barrier preventing their use. We therefore investigated the integrity and differentiated function of isolated rat hepatocytes under conditions of mild hypothermia. Isolated hepatocytes were suspended in a bicarbonate buffered saline medium, supplemented with glucose and bovine serum albumin (BSA), and maintained for 48 h at 25 degrees C on a rotary shaker under an atmosphere of 95% O2 and 5% CO2. Under these conditions there was no significant decline in cell viability and good preservation of cellular morphology on transmission electron microscopy for at least 24 h. Isolated hepatocytes in suspension at 25 degrees C were also able to maintain normal Na+ and K+ ion gradients. The cellular energy status ([ATP], ATP/ADP ratio, cytoplasmic and mitochondrial redox potentials), metabolic function (urea synthesis and ammonia removal), albumin synthesis and phase I and phase II drug detoxification activity of these cells were also maintained for at least 24 h post isolation. These observations demonstrate the robust nature of mildly hypothermic isolated hepatocytes in suspension and encourage further studies re-examining the feasibility of using this cell preparation in bioartificial livers.
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PMID:Maintenance of integrity and function of isolated hepatocytes during extended suspension culture at 25 degrees C. 1295 84

Lipopolysaccharide (LPS)-induced systemic inflammation is accompanied by either hypothermia (prevails when the ambient temperature (Ta) is subneutral) or fever (prevails when Ta is neutral or higher). Because platelet-activating factor (PAF) is a proximal mediator of LPS inflammation, it should mediate both thermoregulatory responses to LPS. That PAF possesses hypothermic activity and mediates LPS-induced hypothermia is known. We asked whether PAF possesses pyrogenic activity (Expt 1) and mediates LPS fever (Expt 2). The study was conducted in Long-Evans rats implanted with jugular catheters. A complex with bovine serum albumin (BSA) was infused as a physiologically relevant form of PAF; free (aggregated) PAF was used as a control. In Expt 1, either form of PAF caused hypothermia when infused (83 pmol kg-1 min-1, 60 min, i.v.) at a subneutral Ta of 20 degrees C, but the response to the PAF-BSA complex (-4.5 +/- 0.5 degrees C, nadir) was ~4 times larger than that to free PAF. At a neutral Ta of 30 degrees C, both forms caused fever preceded by tail skin vasoconstriction, but the febrile response to PAF-BSA (1.0 +/- 0.1 degrees C, peak) was > 2 times higher than that to free PAF. Both the hypothermic (at 20 degrees C) and febrile (at 30 degrees C) responses to PAF-BSA started when the total amount of PAF infused was extremely small, < 830 pmol kg-1. In Expt 2 (conducted at 30 degrees C), the PAF receptor antagonist BN 52021 (29 micromol kg-1, i.v.) had no thermal effect of itself. However, it strongly (~2 times) attenuated the febrile response to PAF (5 nmol kg-1, i.v.), implying that this response involves the PAF receptor and is not due to a detergent-like effect of PAF on cell membranes. BN 52021 (but not its vehicle) was similarly effective in attenuating LPS (10 microg kg-1, i.v.) fever. It is concluded that PAF is a highly potent endogenous pyrogenic substance and a mediator of LPS fever.
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PMID:Platelet-activating factor: a previously unrecognized mediator of fever. 1456 87

Isolated oral keratinocytes in suspension provide a number of advantages for use in maxillofacial surgery, however, the poor stability of this cell preparation at physiological temperatures is an apparent barrier preventing their use. The purpose of the present study was to evaluate whether human serum albumin (HSA) could serve as an effective constituent of a storage medium to enhance human oral keratinocyte (HOK) viability under conditions of mild hypothermia. Primary human oral keratinocytes were isolated from small pieces of the non-inflamed gingival tissues obtained during the extraction of the third molars of patients. HOK were cultured on collagen type I-coated culture dishes in keratinocyte growth medium (KGM). After the trypsinization of a culture dish (passage 2 or 3), freshly isolated HOK were stored for 24, 48, and 72 h at 4 degrees C or at room temperature in KGM, saline, Dulbecco's modified Eagle's medium (DMEM), saline supplemented with 10% HSA or DMEM supplemented with 10% (v/v) HSA under one atmosphere pressure. After storage, HOK cell survival was determined by dye exclusion using trypan blue and colony-forming assay and cell cycle change was obtained by flow cytometry. Highest cell viability was obtained in saline supplemented with 10% HSA and DMEM supplemented with 10% (v/v) HSA at 4 degrees C and at room temperature. Under these conditions no significant decline in keratinocyte viability was observed for at least 48 h. The cell cycle profiles of these cells were also maintained for at least 48 h at room temperature. These observations demonstrate that HSA might be better at preserving the viability of HOK stored under hypothermic and mild hypothermic conditions up to 48 h.
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PMID:The effect of human serum albumin on the extended storage of human oral keratinocyte viability under mild hypothermia. 1571 Mar 74


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