Myocardial dysfunction in septic shock.
Myocardial depression is a major but poorly understood component of septic shock. This study investigates the morphologic and biochemical abnormalities associated with septic shock. Myocardial cells are incubated in normal and septic plasma in a nutrient-, oxygen-, pH-, electrolyte-, and temperature-controlled environment. Cells and media are tested for basal- and epinephrine-stimulated cyclic adenosine monophosphate (cAMP), lactic dehydrogenase (LDH), and creatine kinase. Electron microscopic studies are done at the end of incubation. Septic LDH and creatine kinase levels in the media are increased substantially, and septic cAMP levels are reduced significantly. Septic cells beat irregularly and arrest along with exhibiting abnormal electron microscopic structure. Septic myocardial dysfunction occurs independently of previously postulated causes that are controlled for in this experiment and therefore may be due to endogenously produced or accumulated toxic factor(s).
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D000818:Animals; D003402:Creatine Kinase / Q000378:metabolism; D003470:Culture Media; D000242:Cyclic AMP / Q000378:metabolism; D004837:Epinephrine / Q000494:pharmacology; D006321:Heart / Q000503:physiopathology*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism* / Q000648:ultrastructure; D051381:Rats; D012772:Shock, Septic / Q000378:metabolism / Q000503:physiopathology*; D013268:Stimulation, Chemical
D003470:Culture Media; D000242:Cyclic AMP; D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase; D004837:Epinephrine