Changes of electromechanical activities in human cardiac tissues following endocardial damage

Role of endocardial endothelium in the electromechanical activity of human heart was studied in isolated human atrial and ventricular muscle fibers obtained at cardiac surgery. The endocardial endothelium was damaged by brief exposure to a bolus of the detergent Triton X-100 (0.25-1 vol%). Triton at concentrations of up to 1 vol% reduced twitch force by one-fifth and one-fourth in guinea-pig sinoatrial and ventricular tissues, respectively, but did not change the action potential configuration. In human atrial tissues, however, a brief exposure to 20 microliters of Triton (0.25-1 vol%) depressed the excitability of both fast and slow response action potentials and reduced markedly the twitch force. The effects of Triton were less potent in human ventricular tissues but Triton still decreased significantly the twitch force (-37 +/- 6.4%) at a concentration of 0.25 vol%. Also, the positive inotropic response to phenylephrine (10-100 microM) was shifted to the higher concentrations by Triton treatment. The present findings indicate that the diseased human atrial and ventricular tissues were more sensitive to the effects of endocardial damage induced by Triton exposure than the healthy animal cardiac tissues were. In addition, the electromechanical responses to the adrenergic agonist phenylephrine were decreased in human cardiac tissues with defective endocardial endothelium.