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

The commonest adverse reaction of autotransfusion of drain blood is an increase in temperature, probably due to a cytokine-mediated inflammatory reaction. We recorded body temperature in 21 patients operated on with a total knee prosthesis prospectively during the first 18 postoperative hours. The patients had been given an autotransfusion of autologous filtered drain blood (40 events) within the first 8-9 hours. They all had hypothermia at the end of operation, with a continuous increase in temperature during the first 12 hours whereafter the temperature slowly fell. No additional increase in temperature was seen during the first 2 hours after an autologous retransfusion. Autotransfusion of filtered drain blood within the first 8 postoperative hours after arthroplasty thus did not seem to cause an additional increase in temperature above that due to spontaneous recovery after postoperative hypothermia and surgical trauma.
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PMID:Fever and autologous blood retransfusion after total knee arthroplasty: a prospective study of 40 autotransfusion events in 21 patients. 1214 81

beta 2 microglobulin knockout (beta2M-/-) mice lack CD8+ T and natural killer T cells. We hypothesized that beta 2M-/- mice are resistant to lethal intraabdominal sepsis. To test this hypothesis, mortality, cytokine production, and physiologic function were assessed in beta 2M-/- mice during sepsis caused by cecal ligation and puncture (CLP). beta 2M-/- mice survived significantly longer than wild-type mice after CLP but ultimately exhibited 100% mortality. Treatment of beta 2M-/- mice with anti-asialoGM1 to deplete natural killer cells conferred greater than 70% long-term survival. Compared with wild-type mice, beta 2M-/- mice treated with anti-asialoGM1 produced decreased amounts of proinflammatory cytokines and did not exhibit hypothermia or metabolic acidosis after CLP. Adoptive transfer of CD8+ T and natural killer cells into beta 2M-/- mice treated with anti-asialoGM1 re-established CLP-induced mortality. CD8 knockout mice treated with anti-asialoGM1, which are specifically deficient in CD8+ T and natural killer cells, exhibited 40% long-term survival after CLP. Furthermore, treatment of wild-type mice with antibodies to CD8 and asialoGM1 conferred a significant survival benefit compared with wild-type mice treated with nonspecific IgG. These findings demonstrate that beta 2M-/- mice treated with anti-asialoGM1 are resistant to CLP-induced mortality and that depletion of CD8+ T and natural killer cells largely accounts for the survival benefit observed in these mice.
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PMID:Beta 2 microglobulin knockout mice are resistant to lethal intraabdominal sepsis. 1498 27

Claude Bernard in the late 19th century, was one of the first who recognized that acute injury was associated with the development of hyperglycemia. In 1942 David Cutherbertson introduced the terms ebb and flow to describe the phases of hypo- and hypermetabolism, which follow traumatic injury. Hyperglycemia during the ebb phase is promoted by hepatic glycogenolysis secondary to catecholamine release, as well as by direct sympathetic stimulation of glycogen breakdown. Hyperglycemia is a prominent feature of the flow phase in patients who sustain more severely injured or in whom septic complications develop. It results from augmented glucose production in the presence of insulin resistance in peripheral tissues. The flow phase is clinically expressed as a syndrome consisting of: hypermetabolism (manifested by hyperglycemia, hyperlactatemia and protein catabolism), hyperdynamic cardiovascular state and clinical manifestations of fever or hypothermia, tachycardia, tachypnoea and leucocytosis. The hypermetabolic response to stress may be prolonged when there is stimulus for continuous formation of mediators--a persistent focus of injury or infection. Three systems are responsible for translating the initial insult into the stress response: nervous, endocrine and humoral (cytokine). These systems are interrelated. Maximal metabolic response to stress requires the participation of all three systems. Although glycogenolysis increases hepatic glucose output during the ebb phase, this effect is transient because glycogen stores are rapidly depleted. In contrast, the flow phase is characterized by a sustained increase in gluconeogenesis, which in turn promotes hyperglycemia. Hyperglycemia is common following stress, despite the fact that many tissues exhibit increased cellular uptake and utilization of glucose. Peripheral insulin resistance is central to this process by limiting insulin-mediated glucose uptake in skeletal muscles. In addition, hepatic insulin resistance also plays a role in the genesis of hyperglycemia during stress. In general, the degree of hyperglycemia and insulin resistance are directly proportional to the severity of the stress response. Hyperlactatemia and oxygen consumption also increase concurrently with the severity of stress. Modest hyperglycemia during stress may be of potential benefit by promoting cellular glucose uptake, however, severe hyperglycemia may be associated with complications, this in turn could result in organs dysfunction.
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PMID:[Alterations of blood glucose homeostasis during septic or injury stress--hyperglycemia]. 1271 56

We recently reported that hypothermia protects against intrapulmonary nitric oxide overproduction and nitric oxide-mediated lung injury in endotoxemic rats. Few studies have been performed to investigate whether hypothermia reduces inflammation by affecting favorable changes in chemokine and pro- and anti-inflammatory cytokine profiles. In this study, we tested the hypothesis that hypothermia decreases concentrations of growth-related oncogene/cytokine-induced neutrophil chemoattractant-1 (GRO/CINC-1), interleukin (IL)-1beta, IL-6, and myeloperoxidase and increases concentration of IL-10 in the lungs endotoxemic rats. Twelve rats were anesthetized and randomized to treatment with either hypothermia (T = 18-24 degrees C; n = 6) or normothermia (T = 36-38 degrees C, n = 6). Endotoxin (15 mg/kg of Escherichia coli lipopolysaccharide) was administered intravascularly and lung tissue was harvested 150 min later. Three additional rats were sham instrumented and maintained as normothermic but not given endotoxin. Hematoxylin & eosin staining was performed for qualitative inspection of tissues. Quantitative analyses of lung homogenates were performed using enzyme-linked immunosorbent assays for IL-1beta, IL-6, IL-10, and GRO/CINC-1. Myeloperoxidase concentrations were determined using a colorimetric assay. Hypothermia attenuated the induction of intrapulmonary IL-1beta (P < 0.05), IL-6 (P < 0.05), GRO/CINC-1 (P < 0.05), and myeloperoxidase (P < 0.05) caused by endotoxin. Inspection of the lungs revealed that hypothermia similarly attenuated histological signs of injury, such as interstitial edema and neutrophil accumulation. Hypothermia increased the intrapulmonary concentration of IL-10 more than 3-fold over that measured in the normothermia (endotoxin-exposed) group (P < 0.05). Hypothermia inhibits neutrophil recruitment in the lungs of endotoxemic rats in part by decreasing proinflammatory cytokine expression. Additionally, hypothermia induces intrapulmonary IL-10 expression. Further studies are needed to investigate whether IL-10 mediates the anti-inflammatory effects of hypothermia.
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PMID:Hypothermia induces interleukin-10 and attenuates injury in the lungs of endotoxemic rats. 1281 67

Accidental hypothermia is a common companion of trauma/haemorrhage, and several clinical studies have identified reduced body temperature as an independent risk predisposing to increased morbidity and mortality. Accordingly, the majority of trauma care guidelines prescribe early and aggressive rewarming of hypothermic patients. Enzyme reactions are generally downregulated at temperatures below 37 degrees C, including most of those responsible for the inflammatory response. The rationale for adhering to these recommendations uncritically may therefore be questioned. In a rat model of mild hypothermia and haemorrhagic shock we wanted to compare the influence of rapid rewarming with persistently reduced temperature on the synthesis of early inflammatory mediators and organ function. Thirty-four male albino Sprague-Dawley rats were studied. Withdrawal of 2.5 ml blood/100 g body weight was performed over 10 min, with simultaneous reduction of body temperature to 32.5-33.5 degrees C. Seventy-five minutes after initiation of bleeding, two-thirds of the shed blood was retransfused. One group (n=17) was rewarmed to normothermia, the other (n=17) was kept hypothermic. The study was terminated after an observation period of 2 h. At the end of the study the rewarmed animals had a significantly lower mean arterial pressure, higher heart rate, higher synthesis of reactive oxygen species from peritoneal phagocytes, increased circulating levels of nitric oxide, and higher values of the organ markers aspartate aminotransferase and urea. The pro-inflammatory cytokines TNF-alpha and IL-6, the anti-inflammatory cytokine IL-10, the organ markers alanine aminotransferase, alpha-glutathione S-transferase and creatinine, as well as organ injury scores were equal in both groups. Three rewarmed rats died prematurely, versus one hypothermic animal. In conclusion, the results suggest that during the early stages after haemorrhagic shock, rapid rewarming from mild hypothermia may have unfavourable effects both on basic haemodynamic variables, and on the internal inflammatory environment of cells and tissues.
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PMID:Rapid rewarming after mild hypothermia accentuates the inflammatory response after acute volume controlled haemorrhage in spontaneously breathing rats. 1286 16

Interleukin-10 (IL-10)-deficient (IL-10(-/-)) mice infected with Plasmodium chabaudi (AS) suffer a more severe disease and exhibit a higher rate of mortality than control C57BL/6 mice. Here, we show that a drop in body temperature to below 28 degrees C and pronounced hypoglycemia of below 3 mM are reliable indicators of a lethal infection. Elevated inflammatory responses have been shown to accompany pathology in infected IL-10(-/-) mice. We show that neutralization of tumor necrosis factor alpha (TNF-alpha) in IL-10(-/-) mice abolishes mortality and ameliorates the hypothermia, weight loss, and anemia but does not affect the degree of hypoglycemia. These data suggest that TNF-alpha is involved in some of the pathology associated with a P. chabaudi infection in IL-10(-/-) mice but other factors play a role. IL-10(-/-) mice that survive a primary infection have been shown to control gamma interferon (IFN-gamma) and TNF-alpha production, indicating that other cytokines or mechanisms may be involved in their down-regulation. Significantly higher levels of transforming growth factor beta (TGF-beta), a cytokine with such properties, are present in the plasma of infected IL-10(-/-) mice at a time that coincides with the disappearance of IFN-gamma and TNF-alpha from the blood. Neutralization of TGF-beta in IL-10(-/-) mice resulted in higher circulating amounts of TNF-alpha and IFN-gamma, and all treated IL-10(-/-) mice died within 12 days with increased pathology but with no obvious increase in parasitemia. Our data suggest that a tight regulation of the balance between regulatory cytokines such as IL-10 and TGF-beta and inflammatory cytokines such as IFN-gamma and TNF-alpha is critical for survival in a mouse malaria infection.
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PMID:Pathology of Plasmodium chabaudi chabaudi infection and mortality in interleukin-10-deficient mice are ameliorated by anti-tumor necrosis factor alpha and exacerbated by anti-transforming growth factor beta antibodies. 1293 25

We studied the effects of hypothermia on mortality rate, concentrations of tumor necrosis factor alpha and interleukin 6 in plasma, and the end products of nitric oxide (NO) in endotoxemia. It was found that moderate and mild hypothermia improved the mortality rate and attenuated cytokine responses and the elevation of the end products of NO after endotoxin injection and that these beneficial effects were similar for moderate and mild hypothermia.
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PMID:Effects of hypothermia on mortality and inflammatory responses to endotoxin-induced shock in rats. 1296 30

Aging is accompanied by an altered stress response that underlies increased susceptibility of the elderly patients to physiological stress such as infection and sepsis. In the present study, we investigated the effects of aging on mortality, hypothermia, and cytokine induction in mouse models of intra-abdominal sepsis and endotoxemia. Systemic inflammation associated with either cecal ligation/puncture (CLP) or injection with bacterial endotoxin, lipopolysaccharide (LPS), resulted in a significantly elevated mortality rate in aged (24 months) compared to young (4 months) mice. The aged mice also showed profound hypothermia during these inflammatory stresses; the severity of hypothermia at the early phase of sepsis or endotoxemia could predict the mortality of individual animals. The stress-mediated induction of interleukin-1beta, interleukin-6, and interleukin-10 (IL-1beta, IL-6, and IL-10) in the circulating blood tended to be higher with aging in both CLP and LPS models, and in particular, the induction of IL-6 was significantly augmented with aging. The serum level of IL-6 showed a strong correlation with degrees of hypothermia. In the heart and lungs, the induction of mRNA for IL-6 and IL-10 was also significantly enhanced with aging. These results clearly demonstrate an age-associated increase in mortality, hypothermia, and induction of IL-6 during endotoxemia and sepsis.
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PMID:Effects of aging on mortality, hypothermia, and cytokine induction in mice with endotoxemia or sepsis. 1465 93

The aches and pains that accompany fever appear to be mediated, at least in part, by the peripheral release of cytokines such as interleukin-1beta (IL-1beta). The objective of this study was to determine, whether changes in nociceptive sensitivity produced by IL-1beta administration are temporally linked to changes in core body temperature. Experiment 1 examined nociceptive responsiveness for a period of 3 h following systemic administration of IL-1beta (1, 3, 10 and 20 microg/kg). The two highest doses of IL-1beta produced a drop in temperature beginning approximately 60 min after cytokine administration. This hypothermia lasted 90 min and was associated with hyperalgesia. Experiment 2 examined changes in temperature and nociception for 12 h following administration of IL-1beta (10 microg/kg). An early, short-lived hypothermia was followed by a significant hyperthermia from 3.25 to 6.5 h following IL-1beta administration. This late-occurring fever was accompanied by hyperalgesia. Both the hypo- and hyperthermia phases were associated with a reduction in locomotor activity. Given that repeated nociceptive testing may confound assessment of temperature and activity, Experiment 3 examined the effects of IL-1beta (10 microg/kg) administration on temperature and activity in rats that remained in their home cages. The biphasic change in temperature and the reduction in activity were nearly identical to that reported in Experiment 2, indicating that repeated nociceptive testing did not confound these data. The results of this study demonstrate that, two phases of hyperalgesia occur and coincide with the periods of altered thermoregulation produced by systemic administration of IL-1beta.
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PMID:Simultaneous analysis of the time course for changes in core body temperature, activity, and nociception following systemic administration of interleukin-1beta in the rat. 1469 96

Hypothermia is a thermoregulatory response to systemic inflammation that is often regarded as maladaptive to the host. However, rodents show regulated hypothermia (that is, a selection of cool ambient temperature) during systemic inflammation that correlates with enhanced survival, supporting an adaptive value to this response. The mechanisms regulating hypothermia are not fully understood, but cytokines such as tumor necrosis factor-alpha (TNF-alpha), interleukins (ILs) and interferon-gamma have been shown to induce or modulate hypothermia. A review of the literature suggests that TNF-alpha functions as an endogenous cryogen (i.e., induces hypothermia), whereas IL-10 modulates TNF-alpha production and/or release as a mechanism of hypothermia attenuation. IL-1beta and IL-6 are typically regarded as endogenous pyrogens, but may induce hypothermia during viral and bacterial inflammation. A role for endogenous IFN-gamma in hypothermia has not been demonstrated, but injection of this cytokine potentiates hypothermia through augmented production of other cytokines. It is clear that additional research is required in this area. Suggested areas for future research include a determination of the final mediator of hypothermia and its specific anatomical site of action as well as the role of cytokines in the regulation of hypothermia under non-inflammatory conditions.
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PMID:Hypothermia in systemic inflammation: role of cytokines. 1497 94


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