CARDIAC CONTRACTILITY AND STRUCTURE ARE NOT SIGNIFICANTLY COMPROMISEDEVEN DURING THE LATE, HYPODYNAMIC STAGE OF SEPSIS

Although cardiac function is depressed during endotoxic shock, it rema ins controversial whether the ventricular contractility and structure are altered during sepsis. To resolve this issue, rats were subjected to polymicrobial sepsis by cecal ligation and puncture (CLP). At 2, 5, and 10 h after CLP (i.e., the early, hyperdynamic stage of sepsis) or 20 h after CLP (the late, hypodynamic stage of sepsis, based on the d epressed tissue perfusion), in vivo left ventricular contractility par ameters such as maximal rate of the left ventricular pressure increase (+dP/dt(max)) and decrease (-dP/dt(max)), maximal rate of ''pressure- normalized'' change in ventricular pressure (dP/dt(max)/P), and ventri cular peak systemic pressure were determined using a Digi-Med(R) Heart Performance Analyzer(TM). In additional groups of animals, ultrastruc ture of the cardiac muscle in the left ventricle was examined at 5, 10 , or 20 h after CLP, using a transmission electron microscope. The res ults indicate that +dP/dt(max) and dP/dt(max)/P increased significantl y at 2-10 h after CLP. The values of -dP/dt,, and ventricular peak sys temic pressure increased significantly at 2 and 5 h after the onset of sepsis, respectively. These in vivo ventricular contractility paramet ers, however, were not significantly different from shams at 20 h afte r CLP. Ultrastructural examination showed that enlarged T-tubules were prominent during the hyperdynamic stage of sepsis, which was correlat ed with the increased cardiac contractility. Although focal and modera te hypertrophy as well as expanded intermyocyte junctions could be obs erved occasionally, myocardial cells did not appear to be compromised at 20 h after CLP. Thus, the transition from the hyperdynamic to hypod ynamic circulation during sepsis does not appear to be due to any depr ession in myocardial function because cardiac contractility and struct ure are not compromised even during the late, hypodynamic stage of sep sis. However, further investigation is required to determine whether c ardiac function is depressed at the terminal stage of polymicrobial se psis.