Kitamura S, Yoshida T, Said S I
Proc Soc Exp Biol Med. 1975 Jan;148(1):25-9. doi: 10.3181/00379727-148-38469.
The role of the liver and the lung in the inactivation or potentiation of the biological activity of the vasoactive intestinal polypeptide (VIP) was examined in five anesthetized dogs. Infusions of the peptide were made into the right ventricle, the left ventricle, and the portal vein. Each animal received 4 doses, ranging from 0.29 to 2.23 mug/kg. Systemic arterial blood pressure, tidal volume, breathing frequency, and minute ventilation were continually monitored. The biological effects of the peptide were measured in terms of (a) the fall in arterial blood pressure; and (b) respiratory stimulation. Infusions of the peptide into the portal vein produced either no effect or significantly weaker effects (p smaller than 0.01) than infusions into the right ventricle. The latter infusions were moderately more potent (p smaller than 0.05) than infusions into the left ventricle VIP thus appears to be effectively inactivated during passage through the liver. The apparent increase in biological potency of the peptide during its passage through the lung may be attributable to the release of additional vasodilator substances, or to further activation of the peptide.
在五只麻醉犬中研究了肝脏和肺在血管活性肠肽(VIP)生物活性失活或增强中的作用。将该肽分别注入右心室、左心室和门静脉。每只动物接受4剂,剂量范围为0.29至2.23微克/千克。持续监测体循环动脉血压、潮气量、呼吸频率和分钟通气量。根据以下方面测量该肽的生物学效应:(a)动脉血压下降;(b)呼吸刺激。将该肽注入门静脉要么没有效果,要么比注入右心室的效果明显更弱(p小于0.01)。后者的注入比注入左心室的效力稍强(p小于0.05)。因此,VIP在通过肝脏的过程中似乎有效地失活了。该肽在通过肺的过程中生物学效力的明显增加可能归因于额外血管扩张物质的释放,或该肽的进一步激活。