Tension development of normal and hypertrophied-failing papillary muscles following rapid stimulation.

Recent studies have shown that numerous cellular alterations exist in hypertrophied-failing (HF) cardiac muscle. Of particular interest is the finding of an altered ability of the Na-K pump to regulate membrane potential in this tissue during periods of transient stimulation. The present study was designed to determine if this altered Na-K pump function is in any way related to the ability of this tissue to develop force. Along these lines the rate of stimulation (6/min) of normal and hypertrophied-failing right ventricular papillary muscles from cats was increased to 60/min for 90 sec. This procedure was repeated in solutions with low Na+, low Na+ and Ca++, and Ouabain. These solutions were utilized to vary the ionic load on the Na-K pump and the Na-Ca exchanger. The results demonstrate that the pattern of changes in tension in HF papillary muscles seen following periods of rapid stimulation are significantly different from those of normal muscles. The pattern of changes in mechanical performance were found to be similar to the membrane potential changes described in previous studies. In addition, lowering the Na+ load presented to HF muscles returned the characteristic pattern of changes in tension, following drive, toward normal. Ouabain was found to inhibit the changes in tension development following increased rates of stimulation that are thought to be produced by activation of the Na-K pump. The results suggest that the ability of the Na-K pump to maintain normal transmembrane ionic gradients may be altered in HF muscles. This alteration appears to be capable of affecting cellular Ca++ possibly through the Na-Ca exchange system.