Vasoactive effects of aprotinin.
The protease inhibitor aprotinin was given a) in experimental septic shock, and b) in patients with hepatic cirrhosis and ascites, since in both conditions, activation of the plasma kallikrein-kinin system is associated with pathological systemic vasodilatation, which may trigger reflex neuroendocrine activation and renal solute retention. Given early in experimental sepsis, aprotinin maintained the arterial pressure, systemic vascular resistance (SVR), creatinine clearance and sodium excretion, all of which fell in controls. Aprotinin also blocked increases in pulmonary artery pressure and plasma renin activity (PRA). Given late in sepsis, aprotinin caused a rapid rise in arterial pressure and SVR towards baseline levels. In cirrhosis, aprotinin increased SVR in patients with low baseline values, and improved glomerular filtration rate, renal plasma flow and sodium excretion in all subjects; PRA was suppressed by aprotinin. Aprotinin reverses pathological systemic vasodilatation in these two conditions, and this is associated with a reduction in renin release and improved renal function.
D000818:Animals; D007611:Aprotinin / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D007610:Kallikreins / Q000652:urine; D008103:Liver Cirrhosis / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D012083:Renin / Q000097:blood; D012756:Sheep; D012772:Shock, Septic / Q000188:drug therapy* / Q000503:physiopathology; D014655:Vascular Resistance / Q000187:drug effects
D007611:Aprotinin; D007610:Kallikreins; D012083:Renin