Activation of the tissue kallikrein–kinin system in stroke

Abstract

Edema formation is a major problem in large ischemic infarcts, and the underlying breakdown of the blood–brain barrier is only incompletely understood. Here, we report that the tissue kallikrein–kinin system, which influences the permeability of the blood–brain barrier, is activated in stroke. In 22 patients with large infarcts in the territory of the middle cerebral artery, we found elevated plasma concentrations of the tissue kinin kallidin. The data suggest that further studies on a possible role of kinin receptor antagonists on edema after stroke are warranted.