Background: Although postischemic cardiac or pulmonary dysfunction can relate to the impact of remotely generated oxygen stress mediators on the heart, their direct effect on the vascular bed remains unresolved. Thus, we tested these remote effects in an ex-vivo double organ model.
Methods: After stabilization With Krebs-Henseleit solution, isolated rat livers were either perfused or made ischemic for 2 hours. Aortic rings were stabilized, immersed in postischemic liver perfusates and their functions were tested. Some organs originated from donors fed with tungstate, whereas others had mannitol (0.25 g/kg) in the buffer.
Results: Incubation of aortic rings with postischemic hepatic effluent resulted in protracted contraction. Spasm was slightly lesser when the livers were pretreated with tungstate or exposed to mannitol, but worse in pretreated rings. The return to basal tone was abrupt in all ischemia-reperfusion aortae. The response of the rings to phenylephrine under the influence of the ischemia-reperfusion hepatic effluent was deficient. Mannitol prevented most abnormal responses.
Conclusions: Aortal tone impairment can occur by direct influence of the ischemia-reperfusion liver. It cannot be attributed entirely to xanthine oxidase, but also to other hepatic-released factors.
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