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Division of Circulatory Physiology, College of Physicians and Surgeons, Columbia University, New York, New York 10032
Isovolumic
contractions were imposed by intraventricular balloon in 39 isolated,
blood-perfused canine hearts to investigate the effects of myocardial
stretch on contractile force. After stabilization at 37°C, left
ventricular volume was increased so that end-diastolic pressure
increased from 0 to 5 mmHg. After the immediate increase in developed
pressure [DP; from 37 ± 14 to 82 ± 22 mmHg (means ± SD)], there was a slow secondary rise in DP (97 ± 27 mmHg)
that peaked at 3 min. However, DP subsequently decreased over the next
7 min back to the initial value (84 ± 25 mmHg). Light emission from
macroinjected aequorin (n = 10 hearts) showed that changes in intracellular calcium [3 min: 124 ± 15% (P < 0.01); 10 min: 99 ± 18% of baseline] paralleled DP changes. Increases in myocardial
adenosine 3',5'-cyclic monophosphate (cAMP) content
(n = 12) accompanied the secondary
rise in DP. In contrast, the gradual elevation of DP after the stretch
was not exerted during continuous 
-adrenergic stimulation by
isoproterenol. Thus, in contrast to isolated muscle, stretch only
transiently increases intracellular calcium and contractile strength in
intact hearts. The findings of changes in cAMP and abolition of the
phenomena by -stimulation suggest that a primary stretch-mediated
influence on cAMP metabolism may underlie these phenomena.
adenosine 3',5'-cyclic monophosphate; contractility
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