953-38 Role of Nitric Oxide (EDRF/NO) in the Control of Pulmonary Vascular Resistance in Conscious Dogs with a Blalock-Taussig Shunt

The mechanism for preservation of normal pulmonary artery pressure in the presence of increased pulmonary blood flow is unknown. We hypothesized that NO/EDRF (through an increase in blood flow) is responsible for the low pulmonary vascular resistance seen after opening a Blalock-Taussig shunt. Six dogs were instrumented for the measurement of pulmonary and left atrial pressures and other parameters. A subclavian-pulmonary artery graft was created. A flow transducer and occluder were placed on the graft to record flow and temporarily occlude the shunt. The dogs were allowed to fully recover and all experiments were performed with the dogs awake. Two to four weeks after surgery, hemodynamics were recorded with the shunt open and repeated with the shunt closed. After infusion of nitro-L-arginine (NLA, 30mg/kg) which is an inhibitor of NO synthesis, measurements were repeated with the shunt closed and again after re-opening it. With the shunt closed, mean (M) pulmonary artery pressure (PAP) rose from 13±1.5 to 16±0.9 mmHg after NLA (ns). With the shunt open, MPAP rose from 14±2.4 to 23±1.9mmHg after NLA (P<0.05). Changes with the shunt open were statistically different from shunt closed. The calculated increase in pulmonary vascular resistance mirrored these findings (p<0.05). We conclude that EDRF is important in maintaining normal PAP in the presence of increased pulmonary blood flow. This mechanism may account for the physiologic pulmonary vascular accommodation which occurs in the presence of a surgical shunt or congenital left-right shunt lesions