The central hypothesis of this investigation is that a shortening myocyte generates a time-varying transmural pressure, or intracellular pressure. A mathematical model was formulated for a single myocyte, consisting of a fluid-filled cylindrical shell with axially arranged contractile filaments, to quantitate the fiber-fluid interaction. In this model, the intracellular pressure mediates the interaction between myofilament force, cell shortening, and the mechanical properties of the sarcolemma. Shortening of myofibrils, which are embedded in the fluid-filled myocytes, deforms the myocyte, thereby altering its transmural fluid pressure. This increase in transmural pressure counteracts fiber shortening, hence constituting an internal load to shortening. The shortening of the myocyte is accompanied by thickening, due to the incompressible nature of its contents. Consequently, the overall contractile performance of the cell is integrally linked to the generation of intracellular pressure. The model manifests a positive transmural pressure during shortening, but not without shortening. The pressure in the myocyte, therefore, is not a direct function of the force generated, but rather of shortening. Intracellular pressure was measured through a fluid-filled glass micropipette (5 mu ID) employing a servo-nulling pressure transducer in a standard micropuncture technique. Measured intracellular pressure in a contracting isolated skeletal myocyte of the giant barnacle is observed to be dynamically related to shortening, but not to tension without shortening. The relation between the force of contraction, cell shortening, and intracellular pressure was assessed during both isotonic and isometric contractions. The results support the prediction that isometric, or nondeforming, contractions will not develop intracellular pressure and identify a reason for relengthening of the myocytes during relaxation.

Right atrial collapse (RAC) and right ventricular diastolic collapse (RVDC) have been shown to be useful two-dimensional échocardiographie signs in well-established cardiac tamponade. To assess the value of these signs in cardiac tamponade of varying severity, we studied 8 closed-chest spontaneously breathing dogs with twodimensional echocardiography during varying grades of tamponade induced by intrapericardial saline infusion via a preplaced catheter. Early tamponade was defined as the state when pericardial effusion caused a 20% decline in cardiac output but with normal systolic arterial pressure and a pulsus paradoxus less than 10 mm Hg. Moderate and severe tamponade were stages with progressively decreasing cardiac output and systolic arterial pressure and increasing pulsus paradoxus over 10 mm Hg. Neither RAC nor RVDC was present in any animal in the control state. Sensitivity of RAC was 50% during early tamponade and 100% during moderate and severe tamponade; the specificity was 100% during all grades of tamponade. The sensitivity of RVDC was 38, 63 and 75% during early, moderate and severe tamponade; the specificity was 88% during all stages. Thus, presence of RAC and RVDC in pericardial effusion indicates that hemodynamic deterioration has begun even though conventional signs such as pulsus paradoxus may be absent. As tamponade progresses, the sensitivity of both signs increases. At all grades of tamponade, RAC tends to be more sensitive than RVDC.

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