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钒酸盐诱导猫出现少尿和血管收缩。

Vanadate-induced oliguria and vasoconstriction in the cat.

作者信息

Larsen J A, Thomsen O O

出版信息

Acta Physiol Scand. 1980 Dec;110(4):367-74. doi: 10.1111/j.1748-1716.1980.tb06682.x.

Abstract

The effect of sodium orthovanadate (vanadate) on kidney function and hemodynamics was tested in chloralose anesthetized, fasting cats. Vanadate given i.v. caused a reversible, marked decrease in glomerular filtration rate and urine production without significantly affecting the fractional water excretion rate. In the recovery period, after administration of vanadate, urine flow and the urinary excretion rate of electrolytes were only slightly different from control values. This action of vanadate appears to be due mainly to constriction of the renal blood vessels leading to a fall in glomerular capillary pressure. Vanadate likewise caused a dose dependent decrease in arterial conductance and blood flow of other vessels in the splanchnic area, whereas the femoral and carotid arteries were reversely and less affected. The vascular effect appears to be caused by a direct action of vanadate on vascular smooth muscle, but the mechanism of action is still unsettled.

摘要

在水合氯醛麻醉、禁食的猫身上测试了原钒酸钠(钒酸盐)对肾功能和血流动力学的影响。静脉注射钒酸盐会导致肾小球滤过率和尿量产生可逆性显著下降,而对水排泄分数率没有显著影响。在注射钒酸盐后的恢复期,尿流量和电解质尿排泄率与对照值仅有轻微差异。钒酸盐的这种作用似乎主要是由于肾血管收缩导致肾小球毛细血管压力下降。钒酸盐同样会导致内脏区域其他血管的动脉传导和血流呈剂量依赖性下降,而股动脉和颈动脉受到的反向影响较小。血管效应似乎是由钒酸盐对血管平滑肌的直接作用引起的,但其作用机制仍未明确。

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