Biomedical subjects

O Shido

Publications and source records attributed to O Shido.

57 records · Page 4Linked to original sources

PubMed1985

Contributions of baroreceptor reflex to the hypothermic effect of intraventricular angiotensin II in rats.

The mechanisms of the hypothermic effect of angiotensin II (AII) injected into the lateral ventricle were investigated in unanesthetized rats at an ambient temperature of 18 degrees C. Mean blood pressure (BP), heart rate (HR), metabolic rate (M), colonic temperature (Tcol), and temperatures of the interscapular brown adipose tissue (TBAT), and the tail skin (Tsk) were continuously monitored. AII at a dose of 5 micrograms produced a sharp and marked elevation in BP accompanied by bradycardia, and a decrease of M and Tco1 in the sinoaortic baroreceptor intact rats. The difference between TBAT and Tcol decreased significantly, which suggests a suppression of nonshivering thermogenesis of the BAT. Tsk was not changed by the AII injection. After sinoaortic denervation, however, the decrease in Tcol and M with AII injection was significantly reduced despite a marked elevation in BP. In addition, intravenous arginine-vasopressin antagonist pretreatment suppressed the elevation in BP and the decrease in HR, Tcol, and M after AII injection. From these results, it is concluded that the hypothermia which occurred after AII injection into the lateral ventricle can be largely attributed to the baroreflexive suppression of M, and to some extent to the direct effect on the thermoregulatory center in rats.

Adipose Tissue, Brown↗

PubMed1985

Effects of intraventricular neurotensin on blood pressure and heat balance in rats.

The effects of intraventricular neurotensin (NT) at doses of 0.1, 1.0, and 10.0 micrograms on blood pressure (BP), heart rate (HR), heat production (M), heat loss (H), and colonic temperature (T co1) were investigated in conscious rats in a direct calorimeter at 18 and 28 degrees C. At 18 degrees C, a 10.0 micrograms of NT significantly increased BP for several minutes after injection with prolonged bradycardia. The larger two doses (1.0 and 10.0 micrograms) significantly reduced M and T co1. In sinoaortic denervated rats, a 1.0 microgram of NT elevated BP and decreased HR. The decrease in HR was significantly smaller than that in nerve intact rats, which indicates the occurrence of baroreflex with intraventricular NT. The changes in M and T co1 in the denervated rats were, however, not statistically different from the intact rats. The baroreflexive suppression of metabolism seems to play a minimum role in the NT-induced hypothermia. H slightly increased for several minutes after central NT (1.0 and 10.0 micrograms) and significantly decreased thereafter. Thermal conductance significantly increased for a longer period of time after NT injection. At 28 degrees C, 1.0 microgram of NT increased H and M. It is concluded that central NT produced hypothermia by reducing M and enhancing H in the cool environment, but not at 28 degrees C.

Animals↗

PubMed1984

Baroreflexive suppression of heat production and fall in body temperature following peripheral administration of vasopressin in rats.

Intravenous injection of vasopressin (lysin-8-vasopressin, LVP) in unanesthetized rats at an ambient temperature of 18 degrees C caused a decrease in heat production (M) followed by a fall in colonic temperature (Tco1). These changes were preceded by an elevation of aortic blood pressure (BP) and bradycardia, and were related to the dosage of LVP administered. Temperature of the interscapular brown adipose tissue (BAT) significantly fell after LVP injections. Therefore, it can be said that the decrease in metabolism by the peripheral LVP is at least partly due to suppression of BAT thermogenesis. After bilateral sino-aortic deafferentation, however, the changes in these variables were greatly but not completely reduced except for the elevation of BP. LVP of 0.25 micrograms, more than sufficient to cause a significant elevation of BP when administered peripherally, had no effect on M and Tco1 when injected into the anterior hypothalamus. From these results, we conclude that the hypothermic effect of vasopressin administered peripherally is largely attributed to the baroreflexive suppression of nonshivering thermogenesis, and is not due to the action on the temperature regulatory centers. The slight but insignificant suppression of metabolism in the sinoaortic denervated rats following injection of LVP may be caused by a decreased blood flow to the thermogenic tissues.

Adipose Tissue, Brown↗