In cats subjected to middle cerebral artery occlusion, the resulting ischemia was unaffected by the blood pressure at the time of occlusion when arterial P-CO2, was normal or low. At normal and elevated blood pressures, hypercapnia established prior to occlusion minimized the ischemia and hypocapnia aggravated it, Re-occlusion during postischernic reactive hyperemia resulted in ischemia of the same severity as during the initial occlusion, provided P-CO2 and blood pressure were not changed. These observations suggest that a general determinant of the severity of immediate ischemia in this preparation is the competence of the collateral circulation. This conclusion suggests that proper analysis of the pathogenesis of cerebral infarction requires consideration of immediate ischemia separately from the subsequent course of the ischemic lesion. There are so many variables bearing on the pathogenesis of cerebral infarction that a rational therapy of acute stroke can only be visualized when there is knowledge of the specific arterial lesion, frequent or continuous measurement of regional cerebral blood flow, regional metabolism or neuronal activity, intracranial pressure, and some way of distinguishing paralyzed but viable tissue from infarction.
