Intravascular RBC Aggregation and Transient Diminution of Cerebrovascular Volume Following Middle Cerebral Artery Occlusion in Cats

Abstract

Cerebral arterial occlusion and the resultant hemodynamic changes in the microvasculature of the local cerebral tissue supplied by the artery are important issues that are not only of scientific interest but also of clinical significance. Clarification of the pathophysiology seems relevant to a better understanding of transient ischemic attack (TIA) and reversible ischemic neurological deficit (RIND). Recently, we found by our photoelectric method [5] that a rapid but transitory decrease in optical density of the cerebrocortical tissue of the suprasylvian gyrus in cats occurred unfailingly following middle cerebral artery (MCA) occlusion [4]. The decrease in tissue optical density was interpreted by us as a decrease in cerebral blood volume (CBV) [=diminution of cerebrovascular volume (CVV)] brought about by an abrupt fall in the intramicrovascular pressure. However, against this interpretation, it might be argued that CVV could not shrink since it was effectively protected by the autoregulatory mechanism, and that the decrease in tissue optical density could be attributed to intravascular aggregate formation of red blood cells (RBCs) since RBC aggregation also causes a decrease in optical density of the blood [3, 6]. The importance of RBC aggregation in the development of the “no-flow” phenomenon in the ischemic microvasculature was emphasized by Fischer [1]. He considered that one hemorheological consequence of RBC aggregation was an increase in viscous resistance to flow leading to further circulatory impairment. So far no correlative observations on such vascular and hemorheological factors have been carried out because of the lack of appropriate methods for following rapidly changing RBC aggregation and hemodynamic impairment.