Effects of XXXX on levels of @entity4770 and thromboxane A2 in cerebral arteries of the monkey.

@entity2871 @entity510 @entity5434 @entity1426 @entity4770 @entity1410 @entity2473 @entity4461 @entity2553
To determine whether cerebral arteries in @entity2473 have an altered capacity to synthesize the vasoactive substances @entity4770 and @entity2871 A2, we measured levels of these @entity1426 metabolites using a primate model of @entity2553 . Twenty-four @entity5434 were assigned at random to one of three groups designated sham, clot, or clot-removal. All animals underwent base line cerebral angiography and bilateral dissection of the major cerebral arteries from the arachnoid. The clot and @entity4461 had autologous @entity1410 placed around the vessels to simulate @entity510 . The sham group had a similar volume of saline instilled into the subarachnoid space. Twenty-four hours later, the clot-removal group underwent a second craniotomy to remove the @entity1410 . Seven days after the initial operation, angiography was repeated on all animals. The animals were then killed, and the cerebral arteries were removed. Basal levels of @entity4770 and @entity2871 in the cerebral vessels were measured after incubation in vitro by radioimmunoassay. No detectable leukotriene C4 release by these arteries was measurable using radioimmunoassay. Angiography revealed severe @entity2553 in the clot group, but not in the clot-removal or sham groups. There were no statistical differences among the groups in @entity2871 release, but @entity4770 levels were significantly lower in the clot group than in the clot-removal group (P less than 0.05). It thus seems that, if an imbalance in constrictor and dilator eicosanoids occurs in association with @entity2553 , this is more likely to arise from a relative lack of the vasodilator component @entity4770 than from a surplus of the vasoconstrictor @entity2871 .(ABSTRACT TRUNCATED AT 250 WORDS)
