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造影剂诱导的肾血管收缩与内源性血管收缩激素

Contrast medium-induced renal vasoconstriction and endogenous vasoconstrictor hormones.

作者信息

Katzberg R W, Meggs L G, Schulman G, Hollenberg N K

出版信息

Br J Radiol. 1982 Apr;55(652):266-8. doi: 10.1259/0007-1285-55-652-266.

Abstract

Hypertonic solutions, such as contrast media (meglumine/sodium diatrizoate-76%; Renografin-76), induce vasoconstriction in the renal vascular bed via an unknown mechanism. We assessed a possible role of two vasoconstrictor hormones known to be released by the kidney, angiotensin II (AII) and the prostaglandin, thromboxane. Specific inhibition of AII at the smooth muscle receptor level by saralasin (0.33-0.75 microgram/kg/min, IA) did not attenuate the response. Inhibition of prostaglandin formation by indomethacin (4 mg/kg, IV), likewise, did not prevent the decrease in renal perfusion. We conclude that neither AII nor the prostaglandin system mediate the contrast medium-induced renal vasoconstriction.

摘要

高渗溶液,如造影剂(76%的葡甲胺/泛影酸钠;泛影葡胺-76),通过一种未知机制在肾血管床中诱导血管收缩。我们评估了已知由肾脏释放的两种血管收缩激素——血管紧张素II(AII)和前列腺素血栓素的可能作用。沙拉新(0.33 - 0.75微克/千克/分钟,静脉注射)在平滑肌受体水平对AII的特异性抑制并未减弱这种反应。同样,吲哚美辛(4毫克/千克,静脉注射)对前列腺素形成的抑制也未能阻止肾灌注的降低。我们得出结论,AII和前列腺素系统均不介导造影剂诱导的肾血管收缩。

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