Abstract

The present study was conducted to determine the physiological and ultrastructural effects of hyperbaria on the mammalian myocardium. Isolated rat hearts were perfused in vitro for 20 minutes on a Langendorff apparatus, chilled to +5°C and subjected to hydrostatic pressures of 10,000 or 15,000 psi for periods of time of 10–40 minutes. After warming the hearts were reperfused for an additional 30 minutes. Contractile function was recorded during both perfusion periods and declines in contractile strength after high pressure were calculated. A control group of hearts was kept refrigerated at atmospheric pressure for 45 minutes between perfusion periods. Hearts could tolerate 10,000 psi for up to 20 minutes and 15,000 psi for 10 minutes. Alteration of atrial ultrastructure was found in all groups studied but was most prominent in hearts exposed to 10,000 psi for more than 20 minutes and in all hearts subjected to 15,000 psi regardless of time. Disruption of myocardial fine structure resembled that known to result from ischemia. Mitochondria were severely altered as evidenced by swelling, loss of cristae, and ruptures of the mitochondrial envelope. Specific atrial granules were depleted, edema was prominent in the perinuclear and interfibrillar regions, at the lateral cell junctions, and at the interealated dises whose interspaces were significantly widened; sarcotubular elements were also swollen. Nuclear changes included aggregation of chromatin, increased size of the perinuclear cisteae, and rarely, rupture of the outer nuclear membranes. Contractile elements were apparently passively distorted as a result of mitochondrial swelling and generalized interfibrillar edema. Control hearts not subjected to high pressure also showed marked disruption of fine structure, suggesting that ischemic injury played an important role in producing lesions in all hearts.