Selective reduction of PVR by inhalation of a cGMP analogue in a porcine model of pulmonary hypertension

inhalation of a cGMP analogue in a porcine model of pulmo-nary hypertension. Am. J. Physiol. 268 (Heart Circ. Physiol. 37): H2056-H2062, 1995.-Selective reduction of pulmonary vascular resistance (PVR) remains a therapeutic goal for the treatment of pulmonary hypertension, but current therapeu-tic options remain limited. Although the gas nitric oxide (NO) selectively dilates the pulmonary vascular bed, it requires special equipment for administration, has a short biologic half-life, and is potentially toxic. We hypothesized that stimu-lation of the NO pathway at the level of its second messenger, guanosine 3’5’~cyclic monophosphate (cGMP), by targeted pulmonary delivery of a membrane-permeable nonhydrolyz-able cGMP analogue would cause selective pulmonary vasodi-lation. Pulmonary hypertension was induced in 21 pigs by the intravenous infusion of a thromboxane AZ analogue (9,11