EFFECTS OF VARIOUS TIMINGS AND CONCENTRATIONS OF INHALED NITRIC-OXIDEIN LUNG ISCHEMIA-REPERFUSION

Experimental studies reveal that inhaled nitric oxide (NO) can prevent , worsen, or have no effect on lung injury in the setting of ischemia- reperfusion (I-R). We tested the hypothesis that these disparate effec ts could be related to differences in the timing of administration and /or concentration of inhaled NO during I-R. Isolated rat lungs were su bjected to 1-h periods of ischemia followed by 1-h periods of blood re perfusion. We investigated the effects of NO (30 ppm) given during isc hemia, NO (30 or 80 ppm) begun immediately at reperfusion, or NO (30 p pm) given 15 min after the beginning of reperfusion, on total pulmonar y vascular resistance (PVR), the coefficient of filtration (K-fc), the lung wet/dry weight ratio (W/D) of lung tissue, and lung myeloperoxid ase activity (MPO). A control group did not receive NO. NO given durin g ischemia had no effect on K-fc or MPO, but decreased PVR. NO (30 ppm ) during reperfusion (early or delayed) decreased PVR, W/D, K-fc and M PO. NO at 80 ppm decreased PVR and MPO but not W/D or K-fc. In conclus ion, NO at 30 ppm, given immediately or in a delayed fashion during re perfusion, attenuates I-R-induced lung injury. NO at 30 ppm given duri ng ischemia or at 80 ppm during reperfusion is not protective.