The Cerebral Collateral Circulation: 1. Factors Influencing Collateral Blood Flow

TLDR: The present study was undertaken to analyze factors influencing the efficiency of the cerebral collateral circulation as measured by means of the polarographic technic, to clarify the circumstances whereby collateral blood flow fails to prevent infarction, and to determine whether any aspects ofinfarction are reversible.

Abstract: CLINICAL INVESTIGATION of syndromes due to atherosclerotic occlusion or stenosis of the internal carotid, middle cerebral, and basilar arteries has shown that many of the transient symptoms characteristic of such disorders are due to temporary failure of the cerebral collateral circulation. In a recent paper on this subject,' cerebrovascular insufficiency was defined as a state where the local or general blood flow was unable to maintain the metabolic requirements of the brain during physiologic stresses. Examples of stress situations commonly producing symptoms are reduction of cardiac output due to blood loss, postural hypotension, and cardiac dysrhythmia. The syndrome of cerebrovascular insufficiency was considered to be due to a discrepancy between supply of arterial blood and tissue demand for oxygen. It is apparent that measures which tend to promote the development of the cerebral collateral circulation following occlusion of a cerebral vessel are of considerable therapeutic importance. The present study was undertaken to analyze factors influencing the efficiency of the cerebral collateral circulation as measured by means of the polarographic technic, to clarify the circumstances whereby collateral blood flow fails to prevent infarction, and to determine whether any aspects of infarction are reversible. Experimental studies with the polarographic technic in monkey cortex24 and later in man5 have demonstrated the high oxygen consumption and small oxygen reservoir of healthy cerebral tissue. Early consequences of cerebral isschemia appear to be due to local hypoxic damage to neurons,3-6 which may be reversible if a minimal blood flow is preserved. Cerebral anoxia results first in slowing of the electroencephalogram and later in an injury potential (S.P. shift). Once neuronal injury has occurred, the tissue demand for oxygen is greatly reduced, since metabolically paralyzed or infarcted brain has a minimal oxygen consump-