Nitric oxide during perfusion improves posttransplantation function of non- heart-beating donor lungs

We attempted to determine in a pig model whether 20 ppm of nitric oxide (NO) during perfusion ameliorates warm ischemic lung injury in the non-heart-beating donor (NHBD), thereby improving function with longer warm ischemia.

Lungs were retrieved from three groups (n=6): 1 hr (NHBD(1)) and 2 hr with and without NO (NHBD(2)NO, NHBD(2)) after hypoxic death. For assessment and preservation, left lungs were ventilated with 100% oxygen (NHBD(2)NO with added NO) and perfused for 20 min with neutrophil-depleted, deoxygenated blood in Perfadex solution. Pulmonary vascular and airway pressures and blood flow were measured with pulmonary venous blood gases. Perfusion temperature was reduced to 18 degrees C prior to storage at 4 degrees C before transplantation.

NO during perfusion significantly improved posttransplantation pulmonary venous oxygenation (NHBD(1) [mean +/- SD] 51+/-14 kPa, NHBD(2) 54+/-16 kPa, and NHBD(2)NO 61+/-6 kPa; P=0.01) and airway pressures (NHBD(1) 30.8+/-3.5, NHBD(2) 32.5+/-5.6, NHDB(2)NO 29.4+/-5.3; P=0.0001). NO significantly improved pulmonary vascular resistance (excluding the initial cold-induced vasoconstricted reperfusion period): NHBD(1) 19+/-9 Wood units, NHBD(2) 28+/-25 Wood units, NHDB(2)NO 16+/-10 Wood units, P=0.029. Neutrophil uptake was significantly lowered by NO: NHBD(1) 0.6+/-1.4*10(9) minute-1, NHBD(2) 1.2+/-1.0*10(9) minute-1, NHBD(2)NO 0.4+/-0.9*10(9) minute-1 (P=0.029).

This technique satisfactorily assesses and preserves the non-heart-beating lung. NO during preservation reverses the slight deterioration seen when increasing warm ischemia from 1 to 2 hr, significantly improving transplant oxygenation, vascular resistance, and airway pressures. This may be a result of the observed significant reduction in neutrophil sequestration.