McDonough K H, Burke E C, Smith L W
Department of Physiology, Louisiana State University Medical Center, New Orleans.
J Med. 1990;21(1-2):27-49.
The involvement of the myocardium in the injury resulting from bacteremia has been somewhat controversial. Recently, some investigators have suggested that the transition from an early stage of sepsis, in which the cardiovascular system is stable and mortality is relatively low, to the late or preterminal stage of sepsis is a result of cardiac dysfunction. Here, however, data are presented to show that contractile defects and loss of myocardial reserve occur even early during a septic episode, i.e., at a time when cardiac output is elevated or normal. Efforts to determine the mechanism of the cardiac dysfunction are described. These entail studies of whole heart performance under conditions of varying the calcium availability for contraction and assessment of subcellular organelle function. The data indicate that calcium dyshomeostasis may at least partially contribute to the cardiac dysfunction of sepsis. The in vivo adequacy of cardiac function probably results from the capacity of the myocardium in early sepsis to respond to catecholamine support of chronotropy and inotropy.
菌血症所致损伤中心肌的受累情况一直存在一定争议。最近，一些研究人员提出，从脓毒症早期（此时心血管系统稳定且死亡率相对较低）过渡到脓毒症晚期或终末期是心脏功能障碍的结果。然而，本文的数据表明，即使在脓毒症发作早期，即心输出量升高或正常时，就已出现收缩功能缺陷和心肌储备丧失。文中描述了确定心脏功能障碍机制的相关研究。这些研究包括在改变收缩时钙可用性的条件下对全心功能的研究以及对亚细胞器功能的评估。数据表明，钙稳态失调可能至少部分导致了脓毒症的心脏功能障碍。早期脓毒症中心脏功能在体内的正常可能源于心肌对儿茶酚胺支持变时性和变力性的反应能力。
