Issn Print: 1073-2322
Publication Date: 2006/06/01
SEPSIS-INDUCED MYOCARDIAL DYSFUNCTION
Excerpt
Despite the fact that septic patients exhibit altered cardiac function, it is not considered a major pathology during sepsis. Thus, the molecular mechanisms underlying sepsis-induced myocardial dysfunction have not been studied extensively. The workshop II in the Annual Meeting of the Shock Society is organized to present recent advances in the pathophysiological mechanisms responsible for sepsis-induced myocardial dysfunction. Clinically, left ventricular contraction and relaxation changes are not evident during early sepsis. In a polymicrobial septic rat model, +dP/dt and -dP/dt on day 1, were not altered but found depressed later, i.e., at 3 and 7 days post sepsis. Diastolic dysfunction characterized by an elevation of the time constant of left ventricular relaxation, tau, was evident at 1, 3- and 7-days post-sepsis. Recent data from our laboratory demonstrated that sepsis-induced cardiodynamic alterations correlated with upregulation of TRADD, Bax, Smac (both mitochondrial and cytosolic fractions), total NfkB expression, p38-MAPK and JNK phosphorylation, and cytochrome C levels in the rat heart at 3 and 7 days post sepsis. Data from various laboratories emphasized that molecular myocardial alterations, which occur during early and late stage of sepsis need to be elucidated thoroughly. A poor understanding of myocardial signaling during early sepsis could be one of the main reasons for limited success of pharmacotherapeutic options for sepsis. We anticipate that an increased understanding of pathophysiological mechanisms leading to sepsis-induced myocardial dysfunction during this workshop would generate new enthusiasm among various research groups in this area of research.
This work in Dr. Sharma's laboratory was supported by NHLBI # 66016.
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