title: 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.
authors.affiliation: Department of Neurology, University of Heidelberg, Im Neuenheimer Feld 400, 69120, Heidelberg, Germany.
authors.forename: Simone
authors.initials: S
authors.lastname: Wagner
authors.forename: Pamela
authors.initials: P
authors.lastname: Kalb
authors.forename: Martina
authors.initials: M
authors.lastname: Lukosava
authors.forename: Ulrich
authors.initials: U
authors.lastname: Hilgenfeldt
authors.forename: Markus
authors.initials: M
authors.lastname: Schwaninger
mesh_terms: D005260:Female; D006801:Humans; D020244:Infarction, Middle Cerebral Artery / Q000378:metabolism*; D007609:Kallidin / Q000097:blood*; D016234:Kallikrein-Kinin System; D008297:Male; D008875:Middle Aged; D020842:Plasma Kallikrein / Q000378:metabolism; D020840:Tissue Kallikreins / Q000378:metabolism*
chemical_list: D007609:Kallidin; D020842:Plasma Kallikrein; D020840:Tissue Kallikreins