ANALYSIS OF ENDOTOXIN EFFECTS ON PULMONARY CIRCULATION IN TERMS OF PRESSURE-FLOW CHARACTERISTICS

The purpose of the present work was to explore the hypothesis that pul monary vasoconstriction secondary to endotoxin insult results mainly f rom an increase in the critical closing pressure of the pulmonary vess els. Specifically, we reasoned that in the face of a Starling resistor located between pulmonary arteries and left atrium. upstream transmis sion of increased left atrial pressure (Pla) would be inversely relate d to the level of the pressure intercept (Pi) obtained by extrapolatio n from the linear pulmonary arterial pressure (Ppa) - flow (Q-degrees) plot. Six dogs (group E) were infused with Escherichia coli endotoxin (0.25 mug/kg/min) for 2 hr, whereas six additional dogs (group C) ser ved as control. During baseline conditions, Pi approximated LAP in bot h groups. In group C dogs, increasing LAP at constant Q-degrees led to a proportional augmentation ot Ppa. In group E dogs, endotoxin result ed in a shift of the Ppa-Q relationships to higher pressures due to bo th increases in Pi and slope. In addition, changes in Pla over the sam e range as in control dogs affected Ppa only at the highest levels of Pla. We conclude that endotoxin insult increases the critical closing pressure that exceeds Pla and induces the occurrence of a Starling res istor responsible for the production of an effective vascular waterfal l.