Cerebral blood flow and damage markers during ischemia/reperfusion of brain against a background of modulation of the kinin system’s activity

Abstract

Cerebral hemodynamics’ status under condition of experimental ischemia and following reperfusion of brain against a background of pharmacological modulation of kinins’ formation, the kinin system’s inhibition and depression of kinins’ disruption was investigated by the method of hydrogenous clearance. The brain damage intensity during hypoperfusion of reperfusion period was measured by analyzing its damage markers. It was determined that the activation of kinins’ formation by tripsin has a detrimental effect during ischemia/reperfusion of brain, producing an early development of hypoperfusion in reperfusion period, aggravating a brain damage. The depression of kinins’ disruption by ACE-inhibitors leads to superfluous decreasing of local cerebral blood flow during hypoperfusion of reperfusion period. The inhibition of kinins’ formation by contrykal improves the flow of reperfusion period, preventing the appearance of hypoperfusion and decreasing the brain damage intensity in comparison with a control group. On the whole an activation of the kinin system during ischemia/reperfusion of brain plays mostly pathogenetic role making worse the flow of reperfusion period and aggravating a brain damage.