Search PubMed⌕ Search

Biomedical subjects

P R Marques

Publications and source records attributed to P R Marques.

26 records · Page 2Linked to original sources
PubMed1984

Behavioral thermoregulation, core temperature, and motor activity: simultaneous quantitative assessment in rats after dopamine and prostaglandin E1.

These studies were designed to determine the dose-response autonomic and behavioral thermoregulatory effects and the motor effects of dopamine (DA) and prostaglandin E1 (PGE1) injected into the lateral cerebral ventricles of rats. These studies were made possible with a computer-controlled thermocline that permits freely moving rats to select preferred ambient temperatures ranging between 7 and 39 degrees C. All rats were studied with the thermocline gradient both on and off to control for nonspecific effects. PGE1 (0, 0.1, 0.2, 0.5, 1.0 micrograms) produced a dose-related increase in core temperature and produced a dose-related selection of warmer ambient temperatures. Dopamine (0, 50, 100, 200, 400 micrograms) produced a dose-related hypothermia and cold-seeking behavior. Without the gradient, DA-injected rats did not become as hypothermic as in the gradient-on condition. When the gradient was available, rats showed a significant rebound increase in core temperature 50-80 min after DA which did not occur when the gradient was off. Overall, DA induced increases in motor activity, but, during the first 10 min after injection while the gradient was on, the rats made stable selections of cool ambient temperatures and showed reduced activity. Conversely, the behavioral effect of PGE1 did not facilitate the autonomically mediated heat gain. These results emphasize the necessity of creating behavioral options for animals in order to fully evaluate drug effects on thermoregulation.

Alprostadil↗
PubMed1983

Restraint alters the thermic response to morphine by postural interference.

The effects of morphine on body temperature have been shown to be altered by restraint. The purpose of this study was to determine how the type of restraint alters body temperature measurements and whether restraint alters the effects of morphine on body temperature by interfering with the ability of the rats to adjust their posture. The thermic effects of 5 doses of morphine (3.8 to 45 mg/kg) were compared in two types of restraint and confinement to a 13 X 20 X 20 cm pan without restraint. In unrestrained rats, morphine caused predominantly hyperthermia, but with restraint morphine caused hyperthermia at low doses and hypothermia at higher doses. Morphine hypothermia was greater in rats restrained in a wire-mesh restrainer which prevented heat and humidity build-up than in the commonly used plastic restrainer. In the unrestrained rats, morphine treatment was associated with a posture characterized by exophthalmos, immobility, a hunched position and increased muscle tone. Restrained rats could not assume a compact posture. These results suggest that restraint alters the thermic effect of morphine mainly by interfering with postural mechanisms which reduce heat loss.

Animals↗
PubMed1981

Hypothalamic control of endocrine thermogenesis.

Hypothalamic and ruminal cooling raised serum thyrotropin (TSH), adrenocorticotropin (ACTH), norepinephrine (NE), and glucose in conscious goats in 20 degree C ambient temperature. Cooling of the preoptic anterior hypothalamus (POAH) for 2 h initially evoked shivering and vasoconstriction, leading to 1.5 degree C rise in rectal temperature (Tr). Pituitary-thyroid activation by POAH cooling was shown by peak rises in TSH of 60% at 40 min, in triiodothyronine (T3) of 54% at 80 min, and in thyroxine (T4) of 40% at 140 min. At 60 min, ACTH and NE peaked at 57 and 65%, respectively. TSH, ACTH, and NE declined during the 2nd h of POAH cooling as Tr plateaued; when POAH cooling was stopped, these hormones fell below basal level as vasodilation and panting restored Tr to normal. In contrast to the core hyperthermia evoked by POAH cooling, ruminal intubation with O degree C water (1 liter/10 kg) led to general hypothermia, Tpoah and Tr falling 1.6 degree C at 40 min. Pituitary-thyroid responses were less but ACTH and NE more, compared with POAH cooling. TSH peaked at 37% at 20 min, T3 at 55% at 60 min, and T4 at 18% at 200 min. ACTH peaked at 250% at 30 min and NE at 120% at 20 min. Thermosensitive neurons in the POAH seem to mediate more sensitive and complete control over TSH than over ACTH, or NE release, whereas extrahypothalamic core thermosensitivity (e.g., brain stem, spinal cord, abdomen) may influence ACTH and NE more than TSH release.

Adrenocorticotropic Hormone↗
PubMed1979

Parathyroid hormone release is not associated with acute sympathetic arousal in goats.

Physiological activation of the sympathetic adrenomedullary (SAM) axis following both thermal and non thermal stress was assessed by changes in serum norepinephrine, glucose and/or protein as well as indices of peripheral blood flow. The occurrence of elevated serum parathyroid hormone (PTH) did not reliably reflect SAM activation as might be predicted from pharmacological studies that document a beta adrenergic receptor mechanism in the parathyroid gland that mediates catecholamine stimulated release of PTH into the circulation. The beta agonist isoproterenol at 1 microgram/min for 60 min did produce a transient increase in serum PTH at 20 min. Overall, the data raise doubts about the physiological significance of the adrenergic receptor in the parathyroid gland. Significant increases in serum PTH of 67% and 109% above basal respectively were seen following ruminal loading with cold and thermoneutral water. Associated with the PTH change were increased serum phosphorus and elevated or constant serum protein and serum total calcium.

Animals↗