Evaluation of the kinin-induced pathomechanisms in the development of ARDS by kallikrein inhibition in vivo.
Our findings indicate that the kallikrein-kinin system might participate in the development of acute respiratory failure. They were assessed by measurements of plasma kininogen levels, blood pressure recordings and lung morphology. Aprotinin plasma concentrations ranging from 4 to 7 KIU/ml proved sufficient to inhibit effectively the hemodynamic and morphologic effects caused by tissue kallikrein infusion.
D000818:Animals; D007611:Aprotinin / Q000097:blood / Q000494:pharmacology*; D007610:Kallikreins / Q000097:blood / Q000494:pharmacology*; D007704:Kininogens / Q000097:blood; D011654:Pulmonary Edema / Q000473:pathology / Q000517:prevention & control*; D012128:Respiratory Distress Syndrome / Q000201:enzymology* / Q000473:pathology / Q000503:physiopathology; D013552:Swine
D007704:Kininogens; D007611:Aprotinin; D007610:Kallikreins