Abstract
The mechanism of no-reflow phenomenon (NRP) is still in dispute. The present study was undertaken to evaluate the role of the intravascular component, i.e., platelets and red blood cells (RBC) in the post-ischemic period. Cerebral ischemia was induced in mechanically ventilated dogs by infusion of physiological saline into the cisterna magna at the pressure of 150-200 mmHg for 10-20 minutes. The local cortical CBF (1 CBF) was recorded with a double-needle type thermocouple. The systemic arterial pressure, cisterna magna pressure and cerebral impedance were also monitored.
Blood samples were obtained from the superior sagittal sinus (SSS) and the femoral vein. The three dimensional changes of platelets and RBC were observed by scanning electron microscope and the platelet aggregability to ADP was recorded by Evans aggregometer. The course of 1 CBF was divided into two patterns in the post-ischemic period. In the first, reactive hyperemia was pronounced and in the second, it was only slight or none.
In the latter group with apparent NRP, the changes of platelets and RBC were remarkable especially in the SSS.
Platelets took the activated forms, i.e., pseudopod formation, spreading, surface folds and irreversible membrane fusion (platelet aggregation). Concerning RBC, discocytic shapes were transformed into echinocyte, keratocyte, schizocyte and so on, but no RBC aggregates were found. Platelet aggregability to ADP became lower after cerebral ischemia, being especially prominent in the no-reflow group.
It is concluded that activation of platelet aggregability as well as the morphological change of platelets and RBC are induced by cerebral ischemia, both of which may contribute to the pathogenesis of no-reflow phenomenon.
