In vitro approach to 'uremic cardiomyopathy'

Cardiovascular complications determine the prognosis of patients with chronic renal failure. The contribution of compounds retained during uremia to specific myocardial lesions is controversial. We investigated the contractility of spontaneously beating mouse cardiac myocytes in culture under perfusion with sera derived from patients on maintenance hemodialysis and test solutions containing possible toxins. Cellular contractility under defined environmental conditions is determined by a computer-assisted digital image analysis. 'Uremic sera', creatinine, urea, and combinations of these compounds reduce inotropy of the cultured heart cells, induce arrhythmias or asynchronies in a concentration-dependent manner. We propose the myocyte perfusion technique as an in vitro approach to identify cardiotoxins in the body fluids of chronically uremic patients.