Effects of granulocytopenia on the hemodynamic responses of dogs during E. coli bacteremia.

In both neutropenic and normal dogs a significant and sustained fall in mean arterial pressure (MAP) occurred within 2 h (P less than .01) of the onset of E. coli bacteremia. The MAP remained depressed (P less than .001) in the neutropenic dogs while it increased to normal by 4 h in the control dogs. The fall in MAP was primarily related to a fall in total peripheral resistance (TPR). Although myocardial performance curves declined in both groups over the 4-h period, cardiac index (CI) and left ventricular stroke work index (LVSWI) were not significantly different from baseline in either group; nor was LV filling as assessed by the pulmonary artery wedge pressure (PAWP). No significant differences between groups were demonstrated between the mean pulmonary vascular resistance (PVR), dead space, shunt, or oncotic pressure for either group. A significant (P less than .01) percent reduction of arterial PO2 (PaO2) occurred in the neutropenic dogs. The pH of both groups fell during the course of the experiment and was significantly lower (P less than .02) in the neutropenic dogs at the termination of the study. A similar percent fall in platelet count, factor VIII, and fibrinogen levels was observed in both groups. Circulating endotoxin levels were paradoxically higher in normal animals and did not correlate with any hemodynamic alteration in either group--except that the earlier, higher endotoxin levels in the normal animals were associated with a more rapid decline in myocardial performance. However, the vasodilation of the neutropenic group was clearly related to the higher level of E. coli circulating since the concentration of E. coli in both groups at 4 h was significantly inversely correlated with the MAP (P less than .001).