The kallikrein-kinin system as mediator in vasogenic brain edema: Part 2: Studies on kinin formation in focal and perifocal brain tissue

摘要: Vasogenic edema was induced in mongrel cats by cold injury to study uptake and activation of the plasma-kallikrein-kinin system central nervous (CNS) tissue. A method developed for quantitative assessment kinin formation affected brain tissue areas. Gross disruption blood-brain barrier focal trauma causes marked penetration plasma kininogens into necrotic edematous Moreover, kallikrein-kinin (KK) activated both perifocal areas, markedly enhanced additional cerebral ischemia. Formation kinins led consumption approximately 60% 80% amount being taken up. In tissue, less pronounced, or even absent. However, if ischemia evolved after severe intracranial hypertension, were also formed brain. The intravascular origin found pathological areas secondary deduced from observation that contralateral hemisphere with an intact had no measurable quantities kininogens. Consumption assessed as difference total up minus at postmortem examination. data indicate plasma-KK might occur under all conditions which damage permits proteins, such contusion, ischemia, tumors. potent pathophysiological mechanisms CNS edema, microcirculatory dysfunction, enhancement permeability, together their provide further support a mediator function KK system. Methods specifically interfere damaged should therefore be expected attenuate vasogenic edema.