Increased inotropic state during splanchnic artery occlusion shock in the dog.

Myocardial function during various forms of shock and its assessment remain the subjects of continuing controversy. Dogs were instrumented for the measurement of a lead II ECG, systemic arterial pressure, LV pressure, LVdP/dt, and LV anterior wall thickness. Afterload was varied with a snare occluder around the aorta. Contractility was assessed by the end-systolic pressure-wall thickness relationship. After taking control measurements, shock was induced by occluding the celiac and the superior and inferior mesenteric arteries for 2 hr followed by reperfusion. The end-systolic pressure-wall thickness relationship was determined at 1 and 2 hr postocclusion and then at 15, 30, 45, and 60 min postrelease and hourly thereafter. The slope of this relationship was either unchanged or increased (ie greater negative slope) during occlusion. Over the first hour of reperfusion of the splanchnic bed the slope averaged 204 +/- 17% of control, and it reached 221 +/- 41% of control by 3 hr postrelease. Myocardial depression was seen only as an agonal event (39 +/- 6% of control). Sham control dogs were stable over a 4 hr period following sham occlusion. Thus, myocardial contractility was increased during splanchnic artery occlusion shock except as a terminal event. Early depression of circulatory performance was a result of decreased venous return and not cardiac dysfunction.