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1 Department of Physiology and Pathophysiology, Peking University Health Sciences Center, Beijing 100083; 2 Institute of Cardiovascular Diseases, Peking University First Hospital, Beijing 100034, China; and 3 Department of Pharmacological and Physiological Science, Saint Louis University School of Medicine, St. Louis, Missouri 63104
Altered phosphorylation and
Ca2+ sensitivity of cardiac myofibrillar proteins during
different phases of sepsis were investigated. Sepsis was induced by
cecal ligation and puncture (CLP). The results show that
phosphorylation of troponin I (TnI) was increased by 268% during the
early phase (9 h after CLP) but decreased by 46% during the late phase
(18 h after CLP) of sepsis. Phosphorylation of C protein was increased
by 76% during the early phase but decreased by 41% during the late
phase of sepsis. Phosphorylation of myosin light chain-2 (MLC-2)
remained unaltered during the early phase but was decreased by 38%
during the late phase of sepsis. Phosphorylation of TnT was unaffected
during the progression of sepsis. The increases in the phosphorylation
of TnI and C protein during early sepsis were associated with the
decrease in the Ca2+ sensitivity of myofilaments and the
increases in myocardial changes in tension development
(+dP/dtmax) and cAMP level. The
decreases in the phosphorylation of TnI and C protein during late
sepsis coincided with the declines in the activities of myofibrillar ATPase, Ca2+ sensitivity of myofilaments, myocardial
±dP/dtmax, and cAMP content. The increases and
the decreases in the phosphorylation of TnI and C protein,
±dP/dtmax, and the tissue cAMP level were
sensitive to isoproterenol stimulation and propranolol inhibition.
These findings suggest that alterations in the phosphorylation of
myofibrillar proteins, such as TnI, C protein, and MLC-2, and changes
in the activities and the Ca2+ sensitivity of myofibrillar
ATPase may contribute to the altered cardiac function during the
progression of sepsis. Furthermore, the sepsis-induced alterations in
the phosphorylation and Ca2+ sensitivity of cardiac
myofibrillar proteins were mediated via a 
-adrenergic receptor pathway.
myofibrillar Mg2+-adenosinetriphosphatase; myosin light chain; protein phosphorylation; troponin
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