Partial liquid ventilation (PLV) and lung injury: is PLV able to modify pulmonary vascular resistance?

Introduction: Partial liquid ventilation (PLV) with perfluorocarbons can be advantageous in treating lung injury. We studied this phenomenon in isolated piglet lungs devoid of systemic detractors by studying the changes in pulmonary vascular resistance (PVR) after lung injury with and without PLV. The following questions were asked. (1) Does PLV alone affect PVR in the uninjured lung? (2) Does PLV prevent the increase in PVR associated with oleic acid-induced lung injury? (3) Does PLV modify the increase in PVR associated with oleic acid lung injury? (4) Are the prophylactic and therapeutic effects of PLV on the increased PVR associated with oleic acid-induced lung injury different?

Methods: Neonatal piglet (3 to 4 kg) lungs were prepared without pulmonary ischemia, hypoxia, or reperfusion injury for in situ study. Before pulmonary vascular isolation (eg, aortic and ductus arteriosus ligation) the pulmonary artery (PA) and left atrium (LA) were cannulated and attached to a blood-primed perfusion circuit (flow; 80 mL/kg/min). Pressure-limited volume-cycled ventilation (FiO2, 0.21; TV, 15 mL/kg; PIP, 25 cm H2O) was accomplished via occlusive tracheostomy. Blood gas parameters were monitored continuously and maintained within normal range (SpaO2, 75%; pH, 7.35 to 7.45; pCO2, 35 to 45 torr). Pulmonary artery pressure (Ppa), left atrial pressure (PLa) and pulmonary blood flow (Qpa) were recorded and PVR calculated (PVR = Ppa - Pla/Qpa). After achieving a stable baseline with gas ventilation only, the animal preparations were assigned to one of the following four groups. In group 1 (n = 7) PLV was given alone, using endotracheally administered perfluorodecalin (15 mL/kg). In group 2 (Prophylactic, n = 7) PLV was given prophylactically 60 minutes before lung injury induced by injecting oleic acid (OA) at 0.08 mL/kg into the pulmonary artery. In group 3 (Therapeutic, n = 8) PLV was given 60 minutes after OA-induced lung injury. PPA, PLA, and QPA were measured and PVR was calculated. In group 4 (n = 7) OA was given alone. Significance of differences between groups was obtained by repeated measures analysis of variance (ANOVA). Results were expressed as mean +/- SEM (mm Hg/L/Kg).

Results: Group I showed baseline PVR of the normoxic gas ventilated animals was 127 +/- 19 mm Hg/L/kg. PVR 180 minutes after PLV administration was 160 +/- 15 mm Hg/L/kg (P = ns v baseline). In group 2 after OA infusion, PVR increased from 109 +/- 13 to 281 +/- 26 mm Hg/L/kg (P < .01 v baseline), and 60 minutes later, PVR decreased to 193 +/- 22 mm Hg/L/kg (P < .05 v OA). In group 3 PVR on gas ventilation, before lung injury, was 137 +/- 28 mm Hg/L/kg. Sixty minutes after OA infusion, PVR increased to 314 +/- 23 mm Hg/L/kg (P < .01 v baseline). After 60 additional minutes of PLV, PVR decreased to 201 +/- 31 mm Hg/L/kg, (P < .05 v maximum). In group 4 baseline PVR was 96 +/- 16 mm Hg/L/kg. After 120 minutes of OA injection, PVR increased to 414 +/- 20 mm Hg/L/kg (P < .01 v baseline). Endpoint analysis of PVR at the conclusion of the recording interval showed no difference between group 2 and group 3 (P = not significant [ns]).

Conclusions: (1) PLV does not significantly after PVR in the uninjured lung when given for 2 hours; (2) prophylactic administration of PLV prevents the sustained increase in PVR known to be induced by OA injury; (3) PLV abates OA-induced elevation in PVR when given therapeutically after injury; and (4) Prophylactic and therapeutic PLV have similar effects on PVR in the OA-injured lung.