MYOCARDIAL-FUNCTION IN SEPTIC SHEEP

There is an ongoing discussion whether the heart is the primary target organ responsible for the development of cardiovascular failure durin g septic shock as well as its onset. We tried to study the reaction of the heart to sepsis in the early phase of 8 h, using a sublethal mode l of sepsis in six awake cross-bred Austrian mountain sheep. Sepsis wa s induced by infusion of a live Escherichia coli suspension at a dose of 5 x 10(7) colony-forming units per kg body weight over 8 h. Standar d hemodynamic, hematologic and serum tumor necrosis factor (TNF) measu rements were obtained. For evaluation of left ventricular performance we used the following methods, tested in five pilot experiments: 1) Th e shift of the end-systolic pressure-diameter relation. This was chara cterized by the calculated shift of the transverse external end-systol ic diameter of the left ventricle at a ''midrange'' end-systolic press ure of 100 mmHg (end-systolic ventricular diameter deviation, ESVDD100 ). Calculations were performed using a second order regression functio n of the end-systolic pressure diameter points obtained by variation o f afterload by a cuff occluder on the aorta; 2) The shift of the (dP/d t)max over end-diastolic diameter ratio compared to control values est imated by a graphical approach. Mean pulmonary pressure increased from 21 +/- 1 to 36 +/- 2 mmHg in the first hour after starting the E. col i infusion and remained elevated during the entire 8 h observation per iod. Serum TNF was found to peak 1 hour after start of E. coli infusio n and was hardly detectable after 3 hours of bacteremia. Mean aortic p ressure showed minor changes (maximum 105 +/- 3 mmHg, minimum 91 +/- 2 mmHg) and there were no statistically significant alterations of the cardiac index. ESVDD100 showed an ''oscillatory'' reaction in the firs t phase and a statistically significant decrease of contractility in t he second phase (at 4 h). This was confirmed by the graphical method o f the (dP/dt)max over end-diastolic diameter ratio. We may therefore c onclude that there is no early depression of myocardial function or if so, it may be masked by adrenergic stimulation. In the later phase of the 8 h experiment there is a significantly decreased contractility o f the heart. This may be compensated (e.g., ''Starling'' mechanism or heart rate increase) in this sublethal model.