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)

Small lesions in the brain stem (including the hypothalamus) of the European hamster were effective with respect to food intake, hibernatory disposition and thermogenic power (oxygen consumption) as well. Hyperphagia was accompanied by depression of hibernation mostly. Moreover, hibernation was hindered by impairment of the thermogenic capacity. Entrance into hibernation depended on the integrity of the middle and caudal hypothalamic areas and the rostral portions of the pons and midbrain. Hyperphagia resulted from destruction of the middle (ventromedial) hypothalamic and caudal hypothalamic areas, including transition structures to the pons. A depression of thermogenesis against cold was observed after destruction of supramammillary and neighbouring mesencephalic areas. Supplementary results: An annual metabolic rhythm characterized by a minimum in december has been established once more. Urethane anesthesia did not abolish cold thermogenesis, despite the development of a slight hypothermia. Poikilothermia resulting from brain stem damage disappeared during a three-day period. Furthermore, diencephalic lesions did not suppress arousal from hibernation significantly.
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PMID:[Effect of brain stem lesions on hibernation of the hamster (Cricetus cricetus L.)]. 119 40

1. The effects of two anaesthetics, sodium pentobarbital and urethane, and the effects of anaesthesia-associated hypothermia on acid-base status and blood gases were studied in rats without assisted ventilation. 2. Manipulation of conscious rats produces a progressive increase in arterial lactate associated with slight hyperventilation. 3. Sodium pentobarbital anaesthesia produces mild respiratory acidosis accompanied by increase in lactate arterial values. Urethane anaesthesia leads to partially compensated metabolic acidosis. 4. Hypothermia reduces metabolic acidosis and hypercapnia induced by sodium pentobarbital anaesthesia. No difference between hypothermic and normothermic values was observed in urethane anaesthesia.
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PMID:Differential effects of hypothermia upon blood acid-base state and blood gases in sodium pentobarbital and urethane anaesthetised rats. 139 74

Urethane-anesthetized rats were used to study the mechanism of cocaine-induced death. Continuous recording of the changes in five physiological parameters, including respiratory rate (RR), electroencephalogram (EEG), blood pressure (BP), electrocardiogram (ECG), and body temperature (BT), were conducted after intraperitoneal (IP) administration of a single dose of cocaine HCl (70 mg/kg). In the control group (normothermic with core body temperature 37.7 +/- 0.1 degree C and spontaneously breathing), the death rate was 88% (15/17), and the average time to respiratory arrest was 12.99 +/- 1.40 min (mean +/- SEM). The first set of experiments investigated the contribution of hypothermia to cocaine-induced death. The hypothermic group (core body temperature 33.9 +/- 0.3 degrees C and spontaneously breathing) had a death rate of 81.5% (22/27), and an average time to respiratory arrest of 16.70 +/- 1.24 min, which was significantly (p les than 0.05) prolonged. A substantial decrease in respiratory rate was seen in normothermic group, while all the other measured parameters remained relatively stable until respiratory arrest. Sequential arterial blood gas data in this group showed a decrease in PaO2 from 116.0 +/- 5.7 mmHg to 57.7 +/- 4.6 mmHg, an increase in PaCO2 from 27.7 +/- 2.2 mmHg to 42.7 +/- 3.0 mmHg, and a decrease in pH from 7.467 +/- 0.039 to 7.357 +/- 0.003. To confirm that respiratory depression was an important mechanism of cocaine-induced death in this model, ten normothermic rats underwent mechanical ventilation, and all survived cocaine exposure. This study points to the important role of respiratory depression as a cause of cocaine-induced death.
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PMID:Cocaine-induced respiratory depression in urethane-anesthetized rats: a possible mechanism of cocaine-induced death. 178 91

The blood flow rates of 14 tissues in the body were determined by microsphere method using normal and tumor-bearing rats kept conscious or under urethane anesthesia. The effects on the blood flow rate in the tissues were assessed for multimodal therapy, systemic hypothermia for ischemic brain injury, and local hyperthermia and angiotensin II-induced hypertensive chemotherapy for cancer. Urethane anesthesia showed no effect on cardiac output, while there was a tendency of decrease of blood flow rate and % of cardiac output in each tissue other than muscle tissue, in which they increased as a counterbalance, in normal and tumor-bearing rats. Systemic hypothermia gave results similar to those of urethane anesthesia in normal rats, but for tumor-bearing rats, it decreased cardiac output, and consequently the blood flow rate in most tissues. Brain blood flow rate was about half of that in the conscious rats. Local hyperthermia also decreased the cardiac output and blood flow rate in each tissue, including the tumor tissue. Angiotensin II-induced hypertension showed no effect on cardiac output, had various effects on blood flow rate in each tissue, and led to no increase in the tumor blood flow rate. Simulations based on the physiological pharmacokinetic modeling suggested that intramuscular injection of a lung-specific derivative of ceftazidime would provide the ideal biodistribution to ensure its optimal therapeutic efficacy during systemic hypothermia. This methodology, namely the pharmacokinetic simulation based on the physiological values of the body, will provide a useful piece of information on drug delivery systems under various conditions.
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PMID:Blood flow rate in normal and tumor-bearing rats in conscious state, under urethane anesthesia, and during systemic hypothermia. 989 94

The present study attempted to ascertain whether hypothermia attenuated the heat stroke-induced dopamine overload and gliosis in rat brain. Urethane-anesthetized rats were exposed to water blanket temperature (T(blanket)) of 42 degrees C until mean arterial pressure (MAP) began to decrease from their peak levels, which was arbitrarily defined as the onset of heat stroke. Extracellular concentrations of dopamine in brain were assessed by microdialysis methods. Hypothermia was accomplished by decreasing T(blanket) from 42 to 16 degrees C. The animals exposed to T(blanket) of 26 degrees C served as the normothermic controls. The values of MAP in heat stroke rats without hypothermia were all significantly lower than those in normothermic controls. However, the extracellular levels of dopamine and the number of glial fibrillary acidic protein-reactive cells in brain were greater. Hypothermia immediately after the onset of heat stroke reduced the heat stroke-induced circulatory shock as well as dopamine overload and gliosis in brain. The data demonstrate that hypothermia attenuates both dopamine overload and gliosis in rat brain associated with heatstroke.
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PMID:Hypothermia attenuates cerebral dopamine overloading and gliosis in rats with heatstroke. 1249 89