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以往的实验发现,外源性PGE_1在蟾蜍膀胱及兔游离肾的集合管中可抑制AVP刺激尿流作用,这表明AVP和PGE间的互相作用;消炎痛及其他类阿斯匹林药物,促进AVP在蟾蜍、大白鼠、犬和人膀胱中的影响更支持了上述的设想,为了确定AVP对肾内PGE合成的影响,本实验选用了游离兔肾灌注的方法,在这个模型中排除了在完整动物中因给予AVP而改变了尿中水盐电解质的平衡,从而引起PGE分泌的可能性,并用AVP及无升压作用的类似物dD′-AVP(1-去氨-8-D-精氨酸加压素)来灌注游离兔肾,及在肾静脉血中的PGE_2用RIA测定并用生物测定法证实。 AVP的剂量按20、200及2,000ng加入,其灌注
Previous experiments have found that exogenous PGE 1 inhibits AVP-induced urinary flow in the collecting duct of toad bladder and rabbit free kidney indicating the interaction between AVP and PGE; indomethacin and other aspirin-like drugs that promote The influence of AVP in toads, rats, dogs and human bladder more supports the above hypothesis. In order to determine the effect of AVP on renal PGE synthesis, a method of free rabbit renal perfusion was chosen for this experiment. In this model, AVP in intact animals altered the balance of water and salt electrolytes in the urine, resulting in the possibility of PGE secretion and was treated with AVP and an analog of non-pressure-boosting dD’-AVP (1-desamino-8- Vasopressin) to perfuse free rabbit kidney, and PGE 2 in renal venous blood was assayed by RIA and confirmed by bioassay. The doses of AVP were added at 20, 200 and 2,000 ng, which were perfused