Ventricular function and Na+,K+-ATPase activity and distribution with chronic supraventricular tachycardia

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Abstract
Study objective – The molecular and cellular mechanisms responsible for the dilated cardiomyopathy associated with chronic supraventricular tachycardia are not well understood. The purpose of this study was to examine Na+,K+-ATPase activity and distribution in a pacing induced model of dilated cardiomyopathy. Design – Left ventricular function and Na+,K+-ATPase activity and distribution were examined in two groups of pigs: (1) atrially paced for 3 weeks (supraventricular tachycardia 240 beats·min−1); (2) sham operated controls. Subjects-10 Yorkshire male swine (23-25 kg) were randomly assigned to the control group or the supraventricular tachycardia group. Measurements and main results – Left ventricular function was examined using simultaneous pressure echocardiography. Na+,K+-ATPase activity was determined in tissue homogenates by measuring the rate of p-nitrophenol-phosphate (pNPP) hydrolysis. Changes in content and distribution of Na+,K+-ATPase were examined immuno-histochemically in tissue sections. Left ventricular fractional shortening decreased significantly with supraventricular tachycardia as compared to controls at 15 (SEM 3)% v 31(3)% respectively pv 3.5(0.2) cm respectively pv 6(2)mm Hg respectively p+,K+-ATPase activity (μg pNPP·mg−1 protein·h−1) was significantly lower with supraventricular tachycardia than in controls at 0.45(0.12) v 0.64(0.06) respectively p+,K+-ATPase activity was inhibited by 68% in control and by 45% in supraventricular tachycardia homogenates (p+,K+-ATPase whereas a focal loss of staining was observed in myocytes from the supraventricular tachycardia group. Conclusions – The congestive cardiomyopathy produced by supraventricular tachycardia was associated with a reduction in sarcolemmal Na+,K+-ATPase activity and changes in enzyme distribution. The findings also suggest a reduction in digitalis sensitivity with chronic supraventricular tachycardia. These alterations in Na+,K+-ATPase activity may be one potential mechanism responsible for the depressed left ventricular function associated with chronic supraventricular tachycardia.

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