Prazosin has been used in the treatment of congestive heart failure. It is, however, not known whether prazosin gives only haemodynamic benefit or if it also produces a decrease in the cardiac sarcolemmal Na+-K+-ATPase which has been reported to be increased in the failing heart. The present investigation deals with the effect of 3 months of prazosin treatment in dogs with 3 months of induced mitral insufficiency (MI) on the sarcolemmal Na+-K+-ATPase activity. The dogs were divided into four groups each comprising of five dogs. A--normal; B--3 months of MI; C--6 months of MI; D--3 months of prazosin treatment after 3 months of MI. Three months of MI produced a decrease in the dp/dt and an increase in the end-diastolic pressure of left ventricle but no change in the index of left ventricular contractility and cardiac index. Also there was no change in the sarcolemmal Na+-K+-ATPase. There was a significant decrease in the index of left ventricular contractility and cardiac index and an increase in the LVEDP associated with a significant increase in the left ventricular sarcolemmal Na+-K+-ATPase at 6 months of MI. Sarcolemmal Mg2+-ATPase of both ventricles increased after 6 months of MI the significance of which is not known as yet. There was no change in the sarcolemmal Na+-K+-ATPase of the nonfailing right ventricle. Prazosin treatment prevented the deterioration of the left ventricular contractility and function and also prevented the increase in the sarcolemmal Na+-K+-ATPase observed in failing heart.(ABSTRACT TRUNCATED AT 250 WORDS)
A decrease in the cardiac function and intracellular calcium, and an increase in the cardiac sarcolemmal ATPase have been reported in aortic stenosis of 6 to 9 months duration in dogs. The present investigation deals with the effect of 3 months of digoxin treatment on cardiac function, electrolytes and ATPase in dogs with 3 months of aortic stenosis in order to determine whether digoxin treatment gives only haemodynamic improvement or if it also improves the condition of the myocardium in terms of contractility and biochemical changes. There were no significant changes in any of the haemodynamic parameters of left and right ventricles except the left ventricular end-diastolic pressure which increased significantly at 3 months of aortic stenosis. All the hearts developed left ventricular hypertrophy. Concomitant with these changes, there was a tendency for a decrease in the total tissue Ca2+, intracellular Ca2+ and K+, and a tendency for an increase in the sarcolemmal ATPase. There were no significant differences in any of the haemodynamic parameters between the aortic stenotic and digoxin treated aortic stenotic dogs indicating that digoxin was at least maintaining the haemodynamics close to the pretreatment level. Although digoxin treatment prevented the changes in the sarcolemmal ATPase and extracellular space, it did not prevent the further decrease in the total or intracellular Ca2+. The total and intracellular Ca2+ was still significantly higher than previously observed after 6 to 9 months of aortic stenosis. These results suggest that digoxin treatment not only tended to prevent further deterioration of cardiac function but also tended to prevent further changes in the sarcolemmal ATPase and electrolytes.
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