Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Prazosin (PRA) was used in febrile (LPS; 1 mcg/kg; i.v.) and normothermic rabbits at ambient temperatures (Ta) of 5, 19 and 28 degrees C. This drug was given i.v. in the form of an infusion at a rate of 0.75 mg/kg/3 hr. 2. In normothermic animals, PRA produced significant hypothermia mainly at Ta of 5 and 19 degrees C. In a cold environment, the hypothermic effect of PRA was associated with inhibition of metabolic rate and evaporative heat loss. 3. Infusion of this drug significantly prevented the LPS-induced fever in all experimental conditions. In the cold environment, a drop in body temperature was correlated with an inhibition of metabolic rate; in the thermoneutral environment, antipyresis was associated with an increase in heat dissipation from the ear-skin area; in the hot environment, the correlation between antipyresis and mechanisms of heat dissipation was much less clear. 4. The possible action of PRA on the effector part of the central thermoregulatory system is discussed.
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PMID:Do central mechanisms participate in the thermoregulatory activity of prazosin? 148 22

We examined the effects of intravenous (IV) or intracerebro-ventricular (ICV) injection of prostaglandin E2 (PGE2) on the rectal temperature of restrained rats. The IV injection of PGE2 (0.5 mg/kg) caused hypothermia in rats with high initial rectal temperatures, but caused an elevation in rectal temperature in those animals whose starting temperatures were low. In contrast, the ICV injection of PGE2 induced fever, regardless of the rectal temperature at the time of injection. We also examined whether temperature changes due to the IV injection of endotoxin (lipopolysaccharide, LPS, 10 micrograms/kg) or interleukin-1 beta(IL-1 beta, 0.2 micrograms/kg) were dependent upon the rats' initial rectal temperatures. Rats with low rectal temperatures developed fevers in response to LPS, while animals with high starting temperatures showed hypothermia. In contrast, the IV injection of IL-1 beta produced fever regardless of initial rectal temperature. These data suggest that PGE2 acts centrally to cause fever and peripherally to cause hypothermia, and that following the injection of LPS, these opposing actions of PGE2 may act together to determine the thermoregulatory response.
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PMID:The effect of prostaglandin E2 on the body temperature of restrained rats. 194 25

Hypothermia may contribute to serious life-threatening infections. An experimental model has been established in pigs in order to study the effects of hypothermia on host bacterial defenses. The function of blood neutrophils from pigs and humans was examined in vitro at 37 and 29 degrees C. Bacterial killing of Staphylococcus aureus 502A by human neutrophils after 90 and 180 min incubation at 29 degrees C was reduced to 76 +/- 6% and 83 +/- 7% of killing at 37 degrees C. Porcine neutrophil killing was similarly reduced at 90 min (72 +/- 9%) and remained significantly impaired after 180 min (52 +/- 11%). Phagocytosis of ORO-DP-LPS particles by human neutrophils after 5 min at 29 degrees C was 40 +/- 5% of that at 37 degrees C and only 55 +/- 7% after 15 min by which time maximum phagocytosis had occurred at 37 degrees C. Porcine neutrophils ingested significantly less ORO (68 +/- 8%) after 5 min at 29 degrees C and reached normal values by 15 min. Stimulation of hexose monophosphate pathway in human neutrophils for 20 min at 29 degrees C was only 13 +/- 5% of that at 37 degrees C and required 2 h of stimulation to reach normal values. Porcine cells were reduced to 74 +/- 9% after 20 min incubation and reached normal values by 30 min. Directed neutrophil migration as assessed under agarose was impaired for both human (39 +/- 6%) and porcine (20 +/- 4%) neutrophils at 29 degrees C compared to 37 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Susceptibility of human and porcine neutrophils to hypothermia in vitro. 405 77

The cytogenetic effects of hyperthermia resulting from climatic influences as well as from infections were studied. Whole-body exposure of NMRI mice to an elevated environmental temperature induced a high frequency of micronucleated polychromatic erythrocytes in bone marrow. Hyperthermia at high relative humidity was more effective in increasing body temperature and cytogenetic damage than at low RH. A sex-related difference in response to heat stress was observed. Hyperthermia on pregnant mice induced a significant increase in the incidence of micronucleated PEs in fetal blood cells. Parenteral administration of bacterial endotoxin, lipopolysaccharides, induced either hypothermia or hyperthermia. However, LPS-induced hypothermia as well as fever does not so far appear to produce cytogenetic damage.
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PMID:The mutagenic potential of hyperthermia and fever in mice. 663 51

1. Thermal responses to sodium nitroprusside (SNP, 3 mg/kg/hr) and arginine vasopressin (AVP, 3 micrograms/kg) were investigated in normothermic and febrile rabbits (LPS, 1 microgram/kg) at ambient temperature of 20.0 +/- 1.0 degrees C. Furthermore, blood pressure after these drugs was tested on a separate group of animals. 2. I.v. infusion of SNP produced hypothermia and attenuated pyrogen fever. On the other hand, AVP increased body temperature and intensified the febrile response. 3. Both drugs affected in an opposite way blood pressure, i.e. SNP produced falls and AVP increases in this parameter. 4. The relationship between the activity of the vascular and thermoregulatory systems in normothermic or febrile state is discussed.
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PMID:Thermoregulatory activity of sodium nitroprusside and arginine vasopressin. 759 93

1. Previous studies suggest that arginine vasopressin (AVP) is released into the ventral septal area (VSA) of the rat brain during the antipyresis induced by the cyclo-oxygenase inhibitor indomethacin. In addition, there is evidence for increased AVP transmission in the VSA of animals having a reduced pyretic response following three intravenous injections of bacterial endotoxin (LPS) (endotoxin tolerant). Since ventral septal AVP receptors can also become 'sensitized' following exposure to AVP, we questioned whether the antipyretic action of indomethacin would increase, via an action involving central AVP, if this drug were administered into LPS-tolerant rats. 2. Intraperitoneal indomethacin (7.5 mg kg-1) was effectively antipyretic when administered 2 h after an intravenous challenge with LPS (50 micrograms kg-1) into conscious unrestrained rats. This dose of indomethacin had no effect on the core temperature of non-febrile rats given intravenous 0.9% pyrogen-free saline. 3. Three intravenous injections of LPS over a period of 3 days resulted in rats that were tolerant to the pyrogenic effects of LPS. When indomethacin was administered 2 h following the third LPS injection, a dose-dependent hypothermia was observed. This effect was age dependent, as profound hypothermia was seen in 8 week but not 20 week old rats. 4. A mortality rate of 41% (P = 0.02) was observed within 24 h of indomethacin treatment in 8 week old tolerant rats compared with 0% in 8 week old non-tolerant and 20 week old tolerant rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alteration of the physiological responses to indomethacin by endotoxin tolerance in the rat: a possible role for central vasopressin. 783

At a subthermoneutral ambient temperature of 24 degrees C, intravenous administration of bacterial endotoxin (lipopolysaccharide, LPS) to rats resulted in hypothermia associated with a fall in oxygen consumption followed by fever. At the thermoneutral ambient temperature of 30 degrees C, animals only responded to LPS with fever. The hypothermia and reduction in oxygen consumption were attenuated in rats with eliminated peripheral macrophages. By contrast, macrophage elimination did not affect the febrile response to LPS. Both the hypothermia and the febrile response to LPS were prevented by peripheral administration of the cyclooxygenase inhibitor indomethacin. We conclude that hypothermia in response to LPS is caused by reduced thermogenesis, involves antipyretic products released from peripheral macrophages, and is mediated by prostaglandins. In addition, the febrile response likewise involves prostaglandins, but in contrast to the hypothermia appears to be independent of pyrogens released from peripheral macrophages. Previously, we reported the induction of the pyrogen interleukin-1 in the brain during the time course of the febrile response to LPS (34). The latter observations support the hypothesis that the second phase of biphasic fever is mediated by synthesis and action of pyrogens inside the blood-brain barrier.
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PMID:Hypothermia to endotoxin involves reduced thermogenesis, macrophage-dependent mechanisms, and prostaglandins. 830 29

Previously, we have reported that intravenous administration of bacterial endotoxin (lipopolysaccharide, LPS) in rats kept at a subthermoneutral ambient temperature of 24 degrees C results in a fall in colonic temperature that involved the release of antipyretic products by peripheral macrophages. Here, we demonstrate that treatment of rats with a biologically active antiserum to tumor necrosis factor (TNF) markedly attenuates the hypothermia in response to administration of LPS (0.5 mg/kg). Moreover, this hypothermia was prevented by central injection of a selective antagonist of V1 vasopressin receptors, dPTyr(Me) arginine vasopressin (AVP; 2 micrograms icv). AVP is thought to act as an antipyretic in the ventral septal area (VSA) of the brain. Because the AVP content of this area has been shown to be eliminated after long-term castration, we have tested the hypothesis that castration would attenuate the hypothermia in response to administration of LPS. Castrated rats displayed a markedly less hypothermic response than age-matched controls in response to administration of LPS. We conclude that hypothermia in response to intravenous injection of LPS involves the release of TNF from peripheral macrophages. Moreover, our results are consistent with the possibility that androgen-dependent vasopressinergic neurons in the VSA are mediating the hypothermia in response to intravenous administration of LPS.
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PMID:Hypothermia to endotoxin involves the cytokine tumor necrosis factor and the neuropeptide vasopressin in rats. 830 60

Thermoregulatory and plasma corticosterone responses to peripheral LPS and TNF alpha were compared and correlated with brain FOS protein expression. TNF alpha mimicked the corticosterone response evoked by LPS and the increase in FOS expression in the hypothalamic PVN. TNF alpha also mimicked LPS-activation of central noradrenergic and adrenergic neurones. TNF alpha did not induce a hypothermia which might reflect its failure to activate the vasopressin neurones of the BNST.
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PMID:TNF alpha mimics the endocrine but not the thermoregulatory responses of bacterial lipopolysaccharide (LPS): correlation with FOS-expression in the brain. 878 97

In sum, our results indicate that LPS shock-associated hypothermia involves the following major mechanisms: 1) a decrease in the threshold Tb for activation of cold thermogenesis; 2) the resultant widening of the interthreshold zone; and 3) cold-seeking behavior. We speculate that, in severe systemic inflammation, this hypothermia constitutes an adaptive response.
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PMID:Endotoxin shock-associated hypothermia. How and why does it occur? 910 Sep 63


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