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

The effects of NiCl2 on the colonic temperature and thermoregulatory behavior (TRB) of rats were examined. TRB was evaluated in an instrumental (operant) setting in which rats were required to press a level to obtain convectional heat (SEEK) or to avoid heat (ESCAPE). Orthogonal polynomial regression was used to describe the response patterns in both the SEEK and ESCAPE situations. Two milligrams per kilogram of Ni (ip) caused rapid, transient hypothermia at an ambient temperature of 21 degrees C. When given access to heat reinforcement, rats responded for heat at a lower rate immediately after 2 or 5 mg/kg of Ni (up to 5-15 min) than after saline. Subsequently, response rates rose 30 min or more after Ni injection. A converse pattern was found with the heat escape situation. These observations, confirmed by two contrasting procedures, indicate that the changes were thermoregulatory in nature and cannot be explained by nonspecific suppressive or excitatory effects of Ni. They further suggest that Ni-induced hypothermia results from an altered body temperature set point. The subsequent reversal in behavior probably arises from a direct action of Ni on autonomic effector mechanisms. The origin and biological significance of these findings require further investigation. Physical requirements and response topography are discussed as critical variables in the interpretation of experiments requiring similar responses under different ambient temperatures.
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PMID:Modification by nickel of instrumental thermoregulatory behavior in rats. 234 Sep 85

1. The purpose of this study was to examine the interaction between ambient temperature (Ta) and the effects of nickel chloride on the thermoregulatory system of the mouse. 2. Male mice of the BALB/c strain were injected with nickel chloride at dosages of 0, 0.1, 1.0, 2.5, 5.0 and 10.0 mg/kg intraperitoneally and placed in an environmental chamber set at a Ta of either 10, 20, 30 or 35 degrees C for 60 min. Colonic temperature was then measured after one hour of exposure at a given Ta. 3. The thermoregulatory effects of nickel chloride were highly dependent on Ta. Nickel chloride had no effect on body temperature at Ta's of 30 and 35 degrees C. 4. 10 mg/kg dosage of nickel chloride caused a significant reduction in colonic temperature at a Ta of 20 degrees C. At a Ta of 10 degrees C the 5 and 10 mg/kg dosages of nickel chloride caused a significant lowering of body temperature. 5. Using segmented linear regression techniques it was shown that the threshold dose of nickel chloride for causing hypothermia was 9.6 and 3.3 mg/kg at Ta's of 20 and 10 degrees C, respectively. 6. This study has shown that two stressors, low Ta and nickel chloride intoxication, when applied independently have no effect on body temperature; however, when applied simultaneously, they have a significant toxic effect on thermoregulation.
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PMID:Temperature regulation following nickel intoxication in the mouse: effect of ambient temperature. 256 48

This study was designed to assess the effects of acute nickel chloride administration on behavioral and autonomic thermoregulation in the rat. In one experiment, male rats of the Fischer 344 strain were injected with nickel chloride (IP) at dosages of 0 to 24.0 mg/kg and placed in an environmental chamber maintained at an ambient temperature (Ta) of 10 or 20 degrees C. Colonic temperature was measured 60 min postinjection. Nickel chloride caused a dose-related decrease in colonic temperature, and the hypothermia was accentuated at the cooler Ta. In a second study, rats injected with 0, 6.0, 12.0, or 24.0 mg/kg nickel chloride were placed in a temperature gradient which allowed the rats to select their preferred thermal environment. Nickel chloride at dosages of 12.0 and 24.0 mg/kg caused a significant reduction in the selected Ta. At these dosages the rats were also significantly hypothermic at 60 min postinjection. In a third experiment, whole-body oxygen consumption (i.e., metabolic rate) was measured at Ta's of 10, 20, and 30 degrees C following a 12.0 mg/kg injection of nickel chloride. Nickel chloride caused an initial depression in metabolic rate and hypothermia at Ta's of 10 and 20 degrees C but not at 30 degrees C. In conclusion, (a) nickel chloride affects both behavioral and autonomic control of thermoregulation in the rat and appears to induce a regulated decrease in body temperature and (b) the behavioral thermoregulatory response of the rat is less sensitive to nickel chloride when compared to the mouse.
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PMID:Effect of nickel chloride on body temperature and behavioral thermoregulation in the rat. 275 27

To quantify the immediate hypothermic response to an injection of NiCl2, and to delineate the ensuing derangements of circadian rhythms, the core body temperature and physical activity of rats were monitored by radiotelemetry from a thermistor probe implanted in the peritoneal cavity. The rats were housed in individual cages in a quiet room at 20 +/- 1 degrees C with 12 h light/dark cycles. After an injection of NiCl2 (e.g., 250 mumol/kg), the core body temperature diminished to a nadir at 1.5 h and returned to the baseline at 4 h; core body temperature at 1.5 h post-dose averaged 3.0 +/- 0.5 degrees C below the simultaneous value in control rats. During the period from 8 to 80 h post-dose, the mean body temperature of NiCl2-treated rats did not differ from controls, but the amplitude of the diurnal cycle of body temperature was dampened and the acrophase of the temperature cycle was delayed from 10:32 pm to 3:00 am. These parameters returned towards the control values during the period from 80 to 152 h post-dose. Physical activity of rats was reduced during the period from 8 to 80 h post-dose and the amplitude of the diurnal cycle of physical activity was dampened, but the acrophase of the activity cycle was not retarded in synchrony with the temperature cycle. This study shows that, in addition to causing prompt hypothermia that lasts 4 h, injection of NiCl2 deranges the circadian rhythm of thermoregulation during 3 days after recovery from hypothermia, causing 4.5 h delay of the temperature acrophase. Thus, the transient bout of hypothermia evidently sets back the biological clock of thermoregulation.
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PMID:Hypothermia and deranged circadian rhythm of core body temperature in nickel chloride-treated rats. 322 27

Various types of preconditioning including the main hypoxia (hypoxic, circulatory, hematic/hypemic and tissue/histotoxic), agonists of adenosine A-receptors and openers of K(ATP)-channels induce a hypothermia. A-agonists act through A1-receptors, CoCl2 and NiCl2--via endogenous adenosine and activation by it A1-receptors. The developing hypothermia correlates with neuroprotective effect and is important, but not the only mechanism of tolerance increase to global ischemia. At the similar hypothermia the preconditioning effect excels more frequently an influence of external cooling.
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PMID:[The importance of hypothermia in the preconditioning increase of ischemic tolerance to global cerebral ischemia]. 1686 90

Different types of hypoxia, including several new models, protect the brain against complete global ischemia. Hypoxic (stay in hermetic chamber without or with consumption of CO2 and H2O exhaled), circulatory (bleeding), hematic (injections of NaNO2, CoCl2, NiCl2) and tissue (histotoxic) hypoxia (K2-malonate injection) increases cerebral ischemic tolerance in early terms (in hours). Intracerebroventricular injections of NaNO2, CoCl2, NiCl2 and K2-malonate in nontoxic doses have weak effects. These substances act by peripheral mechanisms. Increased ischemic tolerance is accompanied by pronounced hypothermia which closely correlates with a neuroprotective effect. This shows using tolerant strategy.
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PMID:[Different types of hypoxic preconditioning protect the brain against complete global ischemia]. 1894 7