Body temperature effects of opioids administered into the periaqueductal grey area of rat brain

Six adult white-tailed deer (Odocoileus virginianus borealis) were exposed to 165 periods of 12 consecutive hours of controlled constant ambient temperature in an indirect respiration calorimeter. Temperatures among periods varied from 38 to 0 (summer) or to −20C (fall, winter, spring). Traits measured were energy expenditure (metabolic rate), proportion of time spent standing, heart rate, and body temperature, the latter two using telemetry. The deer used body posture extensively as a means of maintaining body energy equilibrium. Energy expenditure was increased at low ambient temperature to combat cold and to maintain relatively constant body temperature. Changes in heart rate paralleled changes in energy expenditure. In a limited number of comparisons, slight wind chill was combatted through behavioral means with no effect on energy expenditure. The reaction of deer to varying ambient temperatures was not the same in all seasons of the year.

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Vasopressin release within the ventral septal area of the rat brain during drug-induced antipyresis

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1993.264.6.r1133 ◽

1993 ◽

Vol 264 (6) ◽

pp. R1133-R1138 ◽

Cited By ~ 4

Author(s):

M. F. Wilkinson ◽

N. W. Kasting

Keyword(s):

Body Temperature ◽

Rat Brain ◽

Extracellular Fluid ◽

Subsequent Treatment ◽

Septal Area ◽

Nerve Terminals ◽

Perfusion Fluid ◽

Drug Induced ◽

Vasopressin Release ◽

Neuronal Mechanisms

The techniques of push-pull perfusion and radioimmunoassay were used to determine concentrations of arginine vasopressin (AVP) in extracellular fluid derived from the ventral septal area (VSA) of the rat brain following antipyresis elicited by acetaminophen or indomethacin in conscious and unrestrained rats. Reduction of bacterial lipopolysaccharide (LPS)-induced fever by intraperitoneal indomethacin resulted in significant increases in AVP levels in VSA perfusion fluid (P < 0.05). In contrast, antipyresis after acetaminophen treatment was without significant effect on AVP output from VSA nerve terminals. In control animals (non-pyrogen treated), body temperature rose in apparent response to the perfusion procedure. Despite this elevation in core temperature, subsequent treatment with acetaminophen or indomethacin did not result in significant changes in AVP release from VSA perfusates. We conclude that AVP release into VSA extracellular fluids following intraperitoneal indomethacin is dependent upon the neuronal sequelae inherent to pyrogen-evoked fever and not nonspecific rises in body temperature. These results support the hypothesis that endogenous AVP, acting within the VSA, participates in the neuronal mechanisms mediating indomethacin-induced antipyresis.

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Temperature Transition of Human Hemoglobin at Body Temperature: Effects of Calcium

Biophysical Journal ◽

10.1016/s0006-3495(01)76232-7 ◽

2001 ◽

Vol 80 (6) ◽

pp. 2622-2630 ◽

Cited By ~ 36

Author(s):

Christina Kelemen ◽

Shu Chien ◽

G.M. Artmann

Keyword(s):

Body Temperature ◽

Temperature Effects ◽

Human Hemoglobin ◽

Temperature Transition

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