To determine the effect atherosclerosis has on myocardial contractility, we studied the contractile properties of right ventricular papillary muscles from 34 atherosclerotic and 17 control rabbits. We produced atherosclerosis by feeding for 2 to 8 months a diet of 5% lard, 5% peanut oil, 0.5% cholesterol, and 89.5% rabbit pellets. The controls received only rabbit pellets during the same time interval. Contracting isometrically 12 times per minute at 25 degrees C, muscles from the atherosclerotic rabbits developed tension at a lower maximum rate (max dT/dt), had a longer latency, and required longer to develop tension at the maximum rate and to develop peak tension. In isotonic contractions, they shortened with lower maximum velocities and required longer to accelerate to maximum velocity and to shorten maximally. We found no evidence that developed tension or distance shortened differed between the two groups of muscles. Raising the contraction frequency to 24 contractions per minute between the two groups of muscles. Raising the contraction frequency to 24 contractions per minute brought performance of the two groups of muscles closer in both types of contraction. Norepinephrine (1.5 x 10-5 M) nearly abolished differences between performance of the two groups. The loss of contractility correlates poorly with coronary and aortic atherosclerosis. It occurred early in the feeding of the atherogenic diet. We think it was due to a lipid-induced defect in the cardiac cell's handling of calcium.

Pressure-induced homeometric autoregulation (HAR) has been demonstrated by many investigators in the mammalian ventricle; In isolated cardiac muscle, however, several investigators have reported the opposite effect (anti-HAR); namely, that the first beat after a transition from isotonic to isometric contraction is the most forceful, with a decline over several beats to a steady state. In the present study we find that trabeculae from the canine right ventricle demonstrate either HAR or anti-HAR, depending on the rate of stimulation, the calcium level, and the temperature. Higher calcium, higher temperature, and lower rate of stimulation produce either less HAR or more anti-HAR. When only temperature and rate of stimulation are varied, in each muscle there is a unique rate for each temperature above which HAR occurs and below which anti-HAR occurs.