Abstract
Compared to other muscular organs, there is very little collagen in the left ventricle of the heart. Only about 1% of the wet weight of the left ventricle is due to collagen (1) and most of this collagen is found in the coronary vessel walls and the valvular apparatus. Although there are only a few collagen fibers among the muscular fibers, it is generally assumed that these collagen fibers exert a large effect upon the passive (or diastolic) compliance of the musculature of the left ventricle (2).
Experiments designed to test collagen's contribution to the mechanical properties of the left ventricle have yielded conflicting results. Rabbit hearts incubated in collagenase-containing solutions (1.5 mg/ml) were reported to have increased left ventricular distensibility (3). However, Grimm and White-horn (4) bathed beating hearts with solutions containing from 0.003 to 0.20 mg/ml collagenase and concluded that collagen was not responsible for any diastolic mechanical properties of the heart. Both these experiments were attempts to remove collagen in vitro and both may be criticized: the first cited used dead hearts; the second used levels of enzyme which might have been inadequate. The experimental protocols would have been improved had the collagen been altered in vivo beforehand. A metabolic disease known as “lathyrism” provides a means for altering the collagen beforehand. In many immature laboratory animals, lathyrism can be induced by feeding a lathyrogen such as beta-amino-proprionitrile (BAPN). Lathyritic collagen is weaker than normal and tissues become more extensible (5). The turkey poult is susceptible to lathyrism (6) and its heart is of a size convenient for experimental manipulation. If collagen is important in the passive distensibility characteristics of the left ventricle, and if cardiac collagen is as susceptible to the biochemical lesion as the collagen of other tissues, hearts of lathyritic poults should have markedly altered pre- and postmortem pressure-volume characteristics.
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