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Departments of *Anesthesiology and Critical Care Medicine and
Internal Medicine, Gifu University School of Medicine, Gifu City, Japan
Address correspondence and reprint requests to Hiroki Iida, MD, Department of Anesthesiology and Critical Care Medicine, Gifu University School of Medicine, 40 Tsukasamachi, Gifu City, Gifu 5008705, Japan. Address e-mail to iida{at}cc.gifu-u.ac.jp
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)A2 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 [
75 µm] and -28% for small arterioles [<75 µm] compared with baseline). Topical administration of a TxA2 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 TxA2 produced in the ischemic region during the clamp and after cross-clamp release.
IMPLICATIONS: Abdominal aortic unclamping after a 20-min clamp caused an initial dilation followed by a sustained constriction of pial arterioles. Seratrodast, a thromboxane A2 receptor antagonist, attenuated the vasoconstriction suggesting that it is at least partly mediated by thromboxane A2 washed out from the region rendered ischemic by clamping.
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