Levcromakalim (LKM; a K-ATP channel opener) reverses hypoxic pulmonary vaso
constriction in isolated pulmonary arteries and perfused lungs. This vasore
laxation is blocked by glibenclamide (GLB; a K-ATP channel blocker). We eva
luated the hemodynamic effect of LKM followed by GLB in a chronically instr
umented neonatal porcine model of pulmonary hypertension, created by exposi
ng piglets to hypoxia (n = 7) or heat-killed group B streptococci (GBS) (n
= 6). Hypoxia increased pulmonary arterial pressure (PAP), which LKM decrea
sed, and GLB subsequently increased in a dose-dependent manner. Systemic ar
terial pressure (SAP) did not change with hypoxia but was also decreased by
LKM and increased by GLB. GBS also led to increased PAP, but LKM significa
ntly reduced only SAP, which was then increased by GLB. We conclude LKM is
capable of reversing hypoxic, but not GBS-induced, pulmonary hypertension b
ut lacks specificity for the neonatal pulmonary vasculature. Copyright (C)
2001 S. Karger AG, Basel.