THE FALL OF CARDIAC-OUTPUT IN ENDOTOXEMIC RATS CANNOT EXPLAIN ALL CHANGES IN ORGAN BLOOD-FLOW - A COMPARISON BETWEEN ENDOTOXIN AND LOW VENOUS RETURN SHOCK

During endotoxin shock mean arterial pressure (MAP) and cardiac output (GO) fall, and the latter is redistributed. To evaluate whether these changes are solely caused by the low output, or are also based on end otoxin itself, we compared regional hemodynamic changes during endotox emia with those in a nonendotoxemic state of decreased CO in anestheti zed rats. In group E (n = 10) endotoxin Escherichia coli 0127:B8 (8 mg kg(-1)) was infused from t = 0 till t = 60 min. In group B (n = 10) t he same decrease of CO and MAP was obtained as in group E by inflating a balloon in the inferior caval vein, distal to the renal veins, from t = 0 till t = 60 min. We measured MAP, CO (thermodilution), central venous pressure, heart rate, organ blood flow, and redistribution of C O (microspheres), arterial lactate and glucose, and hematocrit. MAP an d CO decreased (p <.05) in both groups (by 30 and 50%, respectively at t = 60). Heart rate, hematocrit, arterial lactate, and arterial gluco se were significantly higher (p <.05) in group E (by 17, 12, 180, and 55%, respectively), Blood flow to most organs had similarly decreased in both groups. The decreased intestinal blood flow lead to macroscopi c damage only in group E, Blood flows (absolute or as percentage of CO ) to heart, hepatic artery, and diaphragm, however, had significantly increased in group E while blood flows to skin, skeletal muscle, and s tomach had decreased more in group E. Except for the heart these diffe rences could be explained by increased work load (detoxification: live r; hyperventilation: diaphragm, muscle) and thus to a more pronounced redistribution at the expense of skin and muscle blood flow. Regional hemodynamic changes during endotoxemia thus could largely be attribute d to decrease of CO and redistribution of the circulating blood volume . In the heart, endotoxin seemed to exert effects independent of the h ypodynamic state. This was also true for the intestinal damage and the rise in hematocrit and arterial lactate.