Prasad C M, Adamski S W, Svensjö E, Grega G J
J Pharmacol Exp Ther. 1982 Feb;220(2):293-8.
In dogs anesthetized with pentobarbital, 60 min local i.a. infusions of prostaglandin E1 (4 micrograms/min) together with bradykinin (10 micrograms base/min) into forelimbs perfused at a constant pump controlled flow rate produced decreases in perfusion pressure and very marked increases in lymph flow, lymph total protein concentration, total protein transport and weight (266 g). Pretreatment with indomethacin did not significantly reduce the very marked increases in these parameters produced by the combined prostaglandin E1-bradykinin infusions. Treatment with diphenhydramine completely prevented the increases in lymph flow, lymph total protein concentration, total protein transport, weight and vasodilation produced by infusions of histamine, but not those produced by infusions of prostaglandin E1 or bradykinin. Pretreatment with methylprednisolone prevented the increases in lymph flow, lymph total protein concentration, total protein transport and weight produced by infusions of prostaglandin E1, but not those produced by infusions of high doses of histamine or bradykinin. Treatment with either methylprednisolone or diphenhydramine significantly reduced the very marked increases in these parameters produced by combined infusions of prostaglandin E1 and bradykinin to levels produced by infusions of bradykinin alone. Vasopressin or isoproterenol treatment essentially prevented the very marked increases in lymph flow, lymph total protein concentration, total protein transport and weight produced by combined infusions of prostaglandin E1 and bradykinin. These data suggest that the potentiation of the bradykinin edema formation produced by prostaglandin E1 results from an endogenous release of histamine and that treatment with vasopressin or isoproterenol essentially prevents the development of edema produced by combined infusions of these autacoids. Moreover, the potentiation is not dependent on the vasodilator action of prostaglandin E1 as it may be demonstrated under constant controlled flow conditions.
在戊巴比妥麻醉的犬中，以恒定的泵控流速灌注前肢，局部动脉内60分钟输注前列腺素E1（4微克/分钟）并同时输注缓激肽（10微克碱基/分钟），可导致灌注压降低，淋巴流量、淋巴总蛋白浓度、总蛋白转运及重量（266克）显著增加。用吲哚美辛预处理并不能显著降低前列腺素E1与缓激肽联合输注所引起的这些参数的显著增加。用苯海拉明治疗可完全阻止组胺输注所引起的淋巴流量、淋巴总蛋白浓度、总蛋白转运、重量及血管舒张的增加，但不能阻止前列腺素E1或缓激肽输注所引起的增加。用甲泼尼龙预处理可阻止前列腺素E1输注所引起的淋巴流量、淋巴总蛋白浓度、总蛋白转运及重量的增加，但不能阻止高剂量组胺或缓激肽输注所引起的增加。用甲泼尼龙或苯海拉明治疗可显著降低前列腺素E1与缓激肽联合输注所引起的这些参数的显著增加，使其降至单独输注缓激肽所引起的水平。血管加压素或异丙肾上腺素治疗基本可阻止前列腺素E1与缓激肽联合输注所引起的淋巴流量、淋巴总蛋白浓度、总蛋白转运及重量的显著增加。这些数据表明，前列腺素E1所引起的缓激肽水肿形成的增强是由组胺的内源性释放所致，并且血管加压素或异丙肾上腺素治疗基本可阻止这些自分泌物质联合输注所引起的水肿的发展。此外，这种增强并不依赖于前列腺素E1的血管舒张作用，因为在恒定的受控流速条件下也可观察到这种现象。
