Summary:We documented the hemodynamic conse quences of nonocclusive common carotid artery throm bosis (CCAT) and tested the hypothesis that vasoactive substances capable of altering local CBF (LCBF) are re leased into the systemic circulation following cerebrovas cular injury. Ten minutes after photochemically induced CCAT, an autoradiographic determination of LCBF was conducted with [14C]iodoantipyrine. In blood transfusion studies using donor and recipient rats, a I-ml sample of thrombogenically activated blood (TAB) collected down stream from the forming thrombus was reinjected into a recipient rat 15 or 60 min before CBF study. A heteroge neous pattern of abnormal LCBF was documented in the ipsilateral hemisphere of CCAT rats and recipient rats receiving TAB 15 min before CBF study. Acute hemody namic abnormalities included ischemic «35% of control) and hyperemic (> 125% of control) foci and more globalThe pathogenesis of transient ischemic attacks (TIAs) and acute ischemic stroke remains incom pletely understood. Possible mechanisms underly ing these conditions include microembolism, hemo dynamic disturbances, and platelet hyperaggrega bility (Powers and Raichle, 1985;Toole, 1990). To examine cerebral ischemic mechanisms, alterations in local CBF (LCBF) following periods of cerebral Received February 27, 1991; revised May 13, 1991; accepted May 23, 1991. Address correspondence and reprint requests to Dr. W. D. Dietrich at Department of Neurology (04-5), University of Mi ami School of Medicine, P.O. Box 016960, Miami, FL 33101, U. S. A.Abbreviations used: BBB, blood-brain barrier; CCA, common carotid artery; CCAT, CCA thrombosis; ECA, external carotid artery; LCBF, local CBF; MCA, middle cerebral artery; TAB, thrombogenically activated blood; TIA, transient ischemic at tack.
957reductions (50-80% of control) in cortical and subcortical LCBF. Border zone hyperemia exceeding 2.0 mllglmin was associated with focal sites of severe LCBF reduc tions. Although recipient rats that received TAB 15 min before CBF study displayed similar hemodynamic abnor malities, LCBF values in 60-min recipient rats were not significantly different from control despite ischemic foci. Humoral factors generated during CCAT appear to be responsible for the acute LCBF consequences of cerebro vascular thrombosis. Vasoactive substances released from a thrombotic site, capable of regionally affecting vascular reactivity in a time-dependent fashion, might be expected to participate in the pathogenesis of transient ischemic attacks and acute stroke. Key Words: Cerebral blood tlow-Platelets-Stroke-Thrombosis-Transient ischemic attacks.ischemia have been documented in various animal models. Thus, transient periods of global and focal cerebral ischemia produce consistent patterns of hemodynamic abnormalities within the postisch ernie brain, the characteristics of which are depen dent on ischemic duration and severity (Hossmann et al., 1973;Ginsberg et al., 1978;Tamura et al., 1981; Pulsinelli et a1. , 1982;Traupe et al. , 1982; Kagstrom et a...