Thermoregulation around a new  set-point' established in the monkey by altering the ratio of sodium to calcium ions within the hypothalamus.
1. The cerebral ventricles of the unanaesthetized monkey were perfused at a rate of 50-100 mul./min with artificial cerebrospinal fluid (c.s.f.) containing 11.0-34.0 mM excess sodium or 23.9-47.9 mM excess calcium ions. By repeated perfusions, a marked hyperthermia elicited by excess sodium or deep hypothermia by excess calcium was sustained for up to half a day.2. During the sodium-induced hyperthermia or calcium-induced hypothermia, the monkey thermoregulated adequately around the new level of temperature in response to either 50 or 150 ml. water heated to 58 degrees C or chilled to 0 degrees C and given by the intragastric route. Cold water produced a transient hypothermia after which temperature returned to the pre-load level; hot water given in the same way evoked a short-lasting hyperthermia, and again the temperature returned just to the new setpoint level.3. Perfusions at 50 mul./min of isolated areas of the diencephalon by means of push-pull cannulae with a solution containing 11.0-34.0 mM excess sodium ions or 11.3-47.9 mM excess calcium ions altered the body temperature of the monkey only when the sites of perfusion were located in the mammillary region of the posterior hypothalamus. Following the prolonged hyperthermia produced by excess sodium ions or the deep hypothermia evoked by excess calcium ions in the push-pull perfusion fluid, the monkey thermoregulated around the new temperature level again in response to 150 ml. of either hot or cold water given in the stomach.4. Chelation of calcium ions within the ventricles by perfusing EGTA through the cerebral ventricles caused a long-lasting elevation in temperature. When EGTA was perfused directly in the posterior hypothalamus by means of push-pull cannulae, a profound hyper-pyrexia ensued which could be abolished immediately by perfusing a solution of excess calcium at the same diencephalic site.5. During the calcium-induced hypothermia, the heart rate declined but the electrical activity of the cortex was relatively unchanged. Feeding was also elicited in the hypothermic monkey by noradrenaline microinjected at a site in the hypothalamus at which eating was evoked when the body temperature was normal.6. The evidence supports the hypothesis that in the primate, the inborn mechanism which establishes the set-point for body temperature at 37 degrees C is the constancy in the intrinsic ratio between sodium and calcium ions within the posterior hypothalamus. If the set-point is elevated or lowered by a disturbance of the balance between these two cations, the monkey nevertheless can thermoregulate normally around the new level of body temperature.
D000818:Animals; D001833:Body Temperature Regulation / Q000187:drug effects*; D002118:Calcium / Q000494:pharmacology*; D002552:Cerebral Ventricles; D002555:Cerebrospinal Fluid; D003080:Cold Temperature; D004569:Electroencephalography; D004987:Ethers / Q000494:pharmacology; D005247:Feeding Behavior; D005334:Fever / Q000139:chemically induced; D000882:Haplorhini; D006358:Hot Temperature; D007031:Hypothalamus / Q000187:drug effects*; D007035:Hypothermia / Q000139:chemically induced; D007094:Imides / Q000494:pharmacology; D008251:Macaca; D010477:Perfusion; D012964:Sodium / Q000494:pharmacology*; D014867:Water
D004987:Ethers; D007094:Imides; D014867:Water; D012964:Sodium; D002118:Calcium