The effects of acutely increased ventricular cavity pressure on intrinsic myocardial connective tissue.

Studies of normal hearts have revealed a variety of intrinsic connective tissue structures that surround and interconnect myocytes and ventricular mural layers. Among these structures, springlike coiled perimysial fibers, arrayed parallel to myocytes in the interstitial space, have been described in papillary muscle and ventricle. To evaluate the role of the coiled perimysial fibers under perturbed conditions, rat ventricles were filled with barium-gelatin under different pressures and fixed, and then the myocardium was impregnated with silver to visualize the connective tissue. Ventricles were filled at 30, 70 and 100 to 120 mm Hg. The coiled perimysial fibers were studied for their orientation, stretch, integrity and relation to sarcomere length. The coils were noted to embed within the fibrous anulus and to knot into an umbilical-like mass at the apex, thus anchoring them at both ends of the ventricle. They underwent focal straightening even at 30 mm Hg, with generalized straightening and disruption at the highest pressure; changes were most pronounced in the midventricle. Sarcomeres were maintained below 2.2 micron at 30 and 70 mm Hg of cavity pressure in regions of coiled perimysial fiber stretch; only with fiber disruption at 100 to 120 mm Hg were sarcomeres significantly lengthened. Other findings included connective tissue disruption between ventricular wall layers that allowed slippage of myocytes and mural thinning. These observations suggest that coiled perimysial fibers may act as a buffer to protect myocytes from damage under the effects of high cavity pressure.