Changes in cerebral microcirculation during and after abdominal aortic cross-clamping in rabbits: the role of thromboxane A2 receptor.

Abstract

Little is known about any changes in cerebral hemodynamics, during and after abdominal aortic cross-clamping and unclamping, especially in the cerebral microcirculation. We studied the effects of abdominal aortic cross-clamping and unclamping on cerebral pial vessel diameter in the presence or absence of the thromboxane (Tx)A(2) receptor antagonist using a closed cranial window in 27 rabbits. Although infrarenal aortic cross-clamping did not affect pial vessel diameter, release of a 20-min aortic cross-clamp caused pial arterioles to dilate and then constrict. A significant constriction persisted for at least 60 min (maximum, -17% for large [> or =75 micro m] and -28% for small arterioles [<75 micro m] compared with baseline). Topical administration of a TxA(2) receptor antagonist, seratrodast, at 10(-7) M and 10(-6) M, significantly attenuated the constriction of large and small arterioles (at 60 min, -9% and -13% constriction for 10(-7) M, and -6% and -7% for 10(-6) M). Release of a 20-min aortic cross-clamp induced a sustained pial arteriolar constriction. Because this unclamping-induced vasoconstriction was attenuated by topical administration of seratrodast, it was likely partially mediated via the washout of TxA(2) produced in the ischemic region during the clamp and after cross-clamp release. Abdominal aortic unclamping after a 20-min clamp caused an initial dilation followed by a sustained constriction of pial arterioles. Seratrodast, a thromboxane A(2) receptor antagonist, attenuated the vasoconstriction suggesting that it is at least partly mediated by thromboxane A(2) washed out from the region rendered ischemic by clamping.