POSSIBLE MECHANISMS FOR REDUCTION OF CIRCULATING CONCENTRATIONS OF PROGESTERONE BY INTERFERON-ALPHA IN COWS - EFFECTS ON HYPERTHERMIA, LUTEAL CELLS, METABOLISM OF PROGESTERONE AND SECRETION OF LH

Experiments were performed to determine the mechanism by which recombinant bovine interferon-alpha(I)1 (rbIFN-alpha) causes an acute reduction in plasma concentrations of progesterone. In experiment 1, administration of a prostaglandin synthesis inhibitor blocked rbIFN-alpha-induced hyperthermia but did not prevent the decline in plasma concentrations of progesterone. The decline in progesterone concentrations caused by rbIFN-alpha was, therefore, not a direct consequence of the associated hyperthermia or of pathways mediated through prostaglandin synthesis. It is also unlikely that rbIFN-alpha acts to increase the clearance of progesterone since injection of rbIFN-alpha did not decrease plasma concentrations of progesterone in ovariectomized cows given an intravaginal implant of progesterone (experiment 2). In experiment 3, rbIFN-alpha did not affect basal and LH-induced release of progesterone from cultured luteal slices, indicating that rbIFN-alpha is unlikely to affect luteal function directly. Injection of rbIFN-alpha did, however, cause a decrease in plasma concentrations of LH in ovariectomized cows (experiment 4) that coincided temporally with the decrease in progesterone concentrations seen in cows having a functional corpus luteum. The present results strongly suggest that rbIFN-alpha acts to reduce secretion of progesterone by interfering with pituitary support for luteal synthesis of progesterone. The finding that rbIFN-alpha can inhibit LH secretion implies that interferon-alpha molecules should be considered among the cytokines that can regulate hypothalamic or pituitary function.

Role of brain nitric oxide in the thermoregulation of broiler chicks

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Food deprivation and hypothermia in desynchronized sleep-deprived rats

Reports of the effect of desynchronized sleep (DS) deprivation on body temperature (Tb) of rats in the literature are contradictory. Since conspicuous body weight loss is common in such deprivation, the effect of food plus DS deprivation on Tb of adult male Wistar rats was studied. DS deprivation carried out by the small platform method with food ad libitum(N = 8) induced hyperthermia (Tb above 38.5 degrees C) in 1 to 3 rats daily until the 8th day, when a case of discrete hypothermia (Tb below 36.9 degrees C) appeared. Food deprivation alone started to induce hypothermia on the third day in one (20%) out of five rats. Fasting imposed from the 5th to the 8th day of DS deprivation (N = 12) caused hypothermia in 33% and 67% ofthe animals on the second and third day of starvation, respectively. DS compensatory manifestations in 6 starved rats intensified (N = 2) or precipitated (N = 2) hypothermia after the end of sleep deprivation. It is concluded that the hypothermia is not a primary effect of DS deprivation, and this state of sleep seems to have its particular functional role which is independent of thermoregulation.

HIPERTERMIA EM RATOS INDUZIDA PELA LESAO ELETROLITICA DO MESENCEFALO: PARTICIPACAO DAS PROSTAGLANDINAS

The present studies were conducted to determine the role of prostaglandins in the etiology of a rise of body temperature observed in rats after electrolytic lesion made on the dorsal mesencephalic areas. This hyperthermia was abolished by intraperitoneal administration of indomethacin, an inhibitor of prostaglandins synthesis. These results strengthen the suggestion of a similar mechanism for both neurogenic hyperthermia and the fevers produced by pyrogens. However, until further experiments are carried out, the possibility of lesion in producing hyperthermia by different mechanisms cannot be ruled out.

Nonthermal activation of transient receptor potential vanilloid-1 channels in abdominal viscera tonically inhibits autonomic cold-defense effectors

An involvement of the transient receptor potential vanilloid (TRPV) 1 channel in the regulation of body temperature (T b) has not been established decisively. To provide decisive evidence for such an involvement and determine its mechanisms were the aims of the present study. We synthesized a new TRPV1 antagonist, AMG0347 [(E)-N-(7-hydroxy-5,6,7,8-tetrahydronaphthalen-1- yl)-3-(2-(piperidin-1-yl)-6-(trifluoromethyl)pyridin-3-yl)acrylamide], and characterized it in vitro. We then found that this drug is the most potent TRPV1 antagonist known to increase T b of rats and mice and showed (by using knock-out mice) that the entire hyperthermic effect of AMG0347 is TRPV1 dependent. AMG0347-induced hyperthermia was brought about by one or both of the two major autonomic cold-defense effector mechanisms (tail-skin vasoconstriction and/or thermogenesis), but it did not involve warmth-seeking behavior. The magnitude of the hyperthermic response depended on neither T b nor tail-skin temperature at the time of AMG0347 administration, thus indicating that AMG0347-induced hyperthermia results from blockade of tonic TRPV1 activation by nonthermal factors. AMG0347 was no more effective in causing hyperthermia when administered into the brain (intracerebroventricularly) or spinal cord (intrathecally) than when given systemically (intravenously), which indicates a peripheral site of action. We then established that localized intra-abdominal desensitization of TRPV1 channels with intraperitoneal resiniferatoxin blocks the T b response to systemic AMG0347; the extent of desensitization was determined by using a comprehensive battery of functional tests. We conclude that tonic activation of TRPV1 channels in the abdominal viscera by yet unidentified nonthermal factors inhibits skin vasoconstriction and thermogenesis, thus having a suppressive effect on T b. Copyright © 2007 Society for Neuroscience.

Infecção experimental com Salmonella Dublin em bezerros bubalinos: estudo clínico, laboratorial e terapêutico

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

TRPV4 activates autonomic and behavioural warmth-defence responses in Wistar rats

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Effect of indomethacin on hyperthermia induced by heat stress in broiler chickens

An investigation was carried out to verify whether the heat stress hyperthermia response of broilers is prostaglandin-dependent. Male broiler chickens of the Hubbard-Petterson strain, aged 35-49 days, were used. Chickens were injected with indomethacin (1 mg/kg intraperitoneally) 15 min before or 2 h after heat exposure (at 35 degrees C for 4 h), and rectal temperature was measured before injection and up to 4 h thereafter. Birds were separated into two groups with and without access to water during heat stress. The increase in rectal temperature was lower (P<0.05) in birds with access to drinking water during heat exposure. All birds injected with indomethacin exhibited an increase in rectal temperature, irrespective of whether indomethacin was administered before or in the course of the rise in temperature. The results revealed that the increase in rectal temperature during heat exposure is not prostaglandin-dependent, and that the use of cyclooxigenase inhibitors is not recommended to attenuate heat stress hyperthermia in broiler chickens.