PEEP INHIBITS HYPOXIC PULMONARY VASOCONSTRICTION IN DOGS

The effects of an increase in alveolar pressure on hypoxic pulmonary vasoconstriction (HPV) have been reported variably. We therefore studied the effects of positive end-expiratory pressure (PEEP) on pulmonary hemodynamics in 13 pentobarbital-anesthetized dogs ventilated alternately in hyperoxia [inspired O2 fraction (FI(O2) 0.4] and in hypoxia (FI(O2) 0.1). In this intact animal model, HPV was defined as the gradient between hypoxic and hyperoxic transmural (tm) mean pulmonary arterial pressure [PBARpa(tm)] at any level of cardiac index (Q). PBARpa(tm)/Q plots were constructed with mean transmural left atrial pressure [PBARla(tm)] kept constant at approximately 6 mmHg (n = 5 dogs), and PBARpa(tm)/PEEP plots were constructed with Q kept constant approximately 2.81.min-1.m-2 and PBARla(tm) kept constant approximately 8 mmHg (n = 8 dogs). Q was manipulated using a femoral arteriovenous bypass and a balloon catheter in the inferior vena cava. Pla(tm) was held constant by a balloon catheter placed by left thoracotomy in the left atrium. Increasing PEEP, from 0 to 12 Torr by 2-Torr increments, at constant Q and PBARla(tm), increased PBARpa(tm) from 14 +/- 1 (SE) to 19 +/- 1 mmHg in hyperoxia but did not affect PBARpa(tm) (from 22 +/- 2 to 23 +/- 1 mmHg) in hypoxia. Both hypoxia and PEEP, at constant PBARla(tm), increased PBARpa(tm) over the whole range of Q studied, from 1 to 5 l/min, but more at the highest than at the lowest Q and without change in extrapolated pressure intercepts. Adding PEEP to hypoxia did not affect PBARpa(tm) at all levels of Q. We conclude that in intact anesthetized dogs 1) neither PEEP nor hypoxia appear to generate a pulmonary vascular closing pressure higher than the imposed levels of Pla in the present experiments, 2) the site of HPV is extra-alveolar, and 3) PEEP inhibits HPV.