Preservation of myocardial compliance and reversal of contracture (“Stone heart”) during ischemic arrest by applied intermittent ventricular stretch |
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Authors: | JDavid Ogilby Carl S Apstein |
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Institution: | 1. From the Cardiac Muscle Research Laboratory, Housman Medical Research Center, Boston University School of Medicine Boston, Massachusetts USA;2. From the Department of Medicine and Thorndike Memorial Laboratory, Boston City Hospital, Boston, Massachusetts USA |
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Abstract: | The hypothesis was tested that intermittent myocardlal stretch could prevent or reverse the increased stiffness or contracture that occurs during severe ischemia. Isolated rabbit hearts with a fluid-filled left intraventricular balloon underwent 90 minutes of ischemie arrest at 35 °C. In the “no stretch” group (n = 10), the intraventricular balloon remained collapsed during the period of arrest; in the “stretch” group (n = 10) the balloon was expanded every 5 minutes to apply intermittent stretch to the arrested myocardium. Intermittent stretching completely prevented contracture during ischemia. In the no stretch group severe ischemic contracture developed, which increased the pressure in the arrested ventricle to 110 ± 14 mm Hg (mean ± standard error of the mean) after 90 minutes of ischemic arrest; in contrast, no contracture (0 ± 1 mmHg) developed in the stretch group during the period of ischemic arrest (p <0.001 versus the no stretch group). After 60 minutes of reperfusion, the stretch group continued to have less contracture (20 ± 4 mmHg versus 42 ± 7 mmHg, p <0.001). Recovery of contractile function was not impaired by the application of intermittent myocardial stretch. Developed pressure and the first derivative of left ventricular pressure () recovered to a greater extent in the stretch group (38 ± 3 versus 27 ± 5 percent and 54 ± 1 versus 35 ± 7 percent, respectively, in the stretch versus the no stretch group), although these differences were not statistically significant (p = 0.10 to 0.05). Both groups had the same degree of tissue lactate accumulation during the ischemic period and the same levels of tissue edema, adenosine triphosphate and creatine phosphate at the end of the reperfusion period. The results indicate that intermittent myocardial stretch during ischemic arrest can prevent a decrease in diastolic compliance without decreasing recovery of contractile function; the intermittent stretch probably ruptured the rigor or contracture bonds that form during prolonged ischemia. |
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Keywords: | Address for reprints: Carl S Apstein MD Director Cardiac Muscle Research Laboratory Boston University School of Medicine 80 East Concord Street Boston Massachusetts 02118 |
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