Effect of water temperature on isoproterenol-induced water intake.
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Biomedical subjects
Publications and source records attributed to C C Barney.
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The spontaneous water intake of rats increases when they are transferred abruptly from a cold (5 degrees C) to a neutral (25 degrees C) environment. This has been termed thermogenic drinking. Treatment of cold-acclimated rats with SQ 14,225, an angiotensin converting enzyme inhibitor, at 10-50 mg/kg of body weight prior to removal from cold, inhibited the thermogenic drinking response in a dose-dependent manner. Plasma for determination of plasma renin activity (PRA) was obtained by cardiac puncture from methoxyflurane anesthetized rats maintained chronically at both 25 degrees and 5 degrees C. In addition, plasma was obtained from cold-acclimated rats 15 min after removal from 5 degrees to 25 degrees C. PRA values were 2.2 +/- 0.4 (S.E.) ng/ml/h for control rats; 1.9 +/- 0.8 ng/ml/h for cold-acclimated rats and 8.5 +/- 1.7 ng/ml/h for cold-acclimated rats removed from cold for 15 min. Thus, PRA was significantly increased in rats removed acutely from cold. These data suggest that thermogenic drinking may be mediated by the renin-angiotensin system.
Female rats exposed to air at 5 +/- 1 degree C for 12 weeks had a greater increase in heart rate in response to s.c. administration of d,l-isoproterenol (8 microgram/kg body weight) than warm-acclimated controls when both were tested in air at 25 +/- 1 degree C. After removal from cold for 24, 48, or 72 h, cold-acclimated rats still showed a greater responsiveness of heart rate to s.c. administration of isoproterenol (8 microgram/kg body weight) when compared with warm-acclimated controls. However, by 96 h after removal from cold, the responsiveness of heart rate to isoproterenol in the cold-treated group no longer differed from that of the warm-acclimated group. Hence, the increased beta-adrenergic responsiveness of heart rate in cold-acclimated rats was lost at some time between 72 and 96 h after removal from cold.
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Prostaglandin E1 (PGE1) hyperthermia (fever) was studied at ambient temperatures (Ta) of 18, 27, and 35 degrees C in four male unanesthetized rhesus monkeys (Macaca mulatta) implanted with four guide tubes and one reentrant tube within the preoptic anterior hypothalamus (PO/AH). Rectal, hypothalamic, and mean weighted skin temperatures, O2 consumption, CO2 production, and respiratory and total evaporative water losses were measured continuously before and during PGE1 fever at each Ta. The febrile reponse to PO/AH PGE1 injection was dose responsive and was less at a Ta of 35 degrees C than at the other Ta's. At a Ta of 18 degrees C, fever was brought about primarily by an increase in metabolic rate. At a Ta of 27 degrees C, fever was produced by an increase in metabolic rate and by skin vasoconstriction. At a Ta of 35 degrees C, fever was the result of an increase in metabolic rate and a decrease in sweating evaporative heat loss. At each Ta some generalized skin vasconstriction also occurred. During the plateau phase of the fever, the measured heat losses and gains returned to near control levels. The data indicate that the rhesus monkey shows specific thermoregulatory responses to PO/AH PGE1 injection and would be a good model for the study of thermoregulation during fever in higher primates.
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A technique is presented for preparing a durable thermode implant in the hypothalamus of the rhesus monkey. In unanesthetized monkeys implanted with thermodes in the anterior hypothalamic area of the brain, a linear relation was found between local sweat rates on the general body surface and clamped hypothalamic temperature. Changes in skin temperature were found to shift the hypothalamic set-point temperature at which sweating began but did not alter the gain of the hypothalamic temperature-sweat rate relationship. This study provides direct support for the concept that central brain temperature and skin temperature interact additively in the control of sweating in higher primates. Due to the very close similarity between these responses and those seen with indirect measurements of brain temperature in men, the rhesus monkey is seen as an excellent experimental analogue for studying human thermoregulation.
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The effect of cycloheximide, an inhibitor of protein synthesis, on temperature regulation in afebrile rats was studied to determine whether its reported antipyretic effect might be attributable to a non-specific antimetabolic effect. Within 60 min after administration of cycloheximide (5 mg/kg IP) to female rats at ambient temperatures of 34, 25 and 15 degrees C, a significant decrease in colonic temperature was observed as compared with control rats administered saline IP. Measurements of rate of oxygen consumption showed that cycloheximide (5 mg/kg IP) significantly depressed the ability of rats to increase their heat production during a cold stress (15 degrees C). In the cold the rate of oxygen consumption increased 8.7 +/- 0.8 ml/min/kg0.75 in the control rats but only 1.8 +/- 0.9 ml/min/kg0.75 in the cycloheximide-treated rats. Since the thermoregulatory changes accompanying cold stress are similar to those observed during the genesis of fever, these data suggest that cycloheximide may have a general depressant effect on heat production rather than a specific antipyretic effect.
The dose of thyroxine (0-150 micrograms/kg body weight) administered subcutaneously daily to surgically thyroidectomized male rats was correlated significantly with their metabolic activity as assessed by rate of oxygen consumption and colonic temperature. There was a significant dose-dependent increase in total serum thyroxine, triiodothyronine and reverse-triiodothyronine concentrations with increasing doses of thyroxine administered. The cardiostimulatory response to administration of isoprenaline (8 micrograms/kg body weight s.c.) was also correlated directly with the dose of thyroxine administered. The concentration of cardiac beta-adrenoceptors in these animals was correlated significantly with total serum thyroxine and triiodothyronine concentrations, basal heart rate, and the chronotropic response to administration of isoprenaline.