Effect of inhaled nitric oxide during group B streptococcal sepsis in piglets

Group B streptococcus (GBS), a common gram-positive pathogen, causes similar pathophysiologic changes in newborn humans and animals. Infusion of GBS into neonatal animals produces pulmonary hypertension and ventilation/perfusion (Va/Q) mismatch in both early-phase (< 1 h) and late-phase (2 to 6 h) responses. Contrary to early phase, late phase causes pulmonary vascular injury. Nitric oxide (NO) is an inhaled vasodilator whose effect on pulmonary hypertension and Va/Q matching during early and late phases of GBS sepsis is unclear. We hypothesized that inhaled NO (150 ppm) would: (1) reverse early-phase GBS-induced pulmonary hypertension; (2) demonstrate less effectiveness in reversing late-phase GBS-induced pulmonary hypertension because of vascular injury; (3) improve late-phase GBS-induced Va/Q mismatching. Anesthetized, mechanically ventilated piglets (n = 10; 14 +/- 4 days of age) received a 240-min infusion of GBS (1.5 x 10(9) CFU/kg/h). Piglets received 30 min of NO (Study) or N2 (Control) at 30 and 210 min of GBS infusion. We found that inhaled NO selectively reversed early- and late-phase GBS-induced pulmonary hypertension and that NO was equally as effective in each phase. Inhaled NO did not reverse Va/Q mismatching during late-phase GBS. We conclude that 4 h of GBS sepsis does not injure neonatal pulmonary vascular smooth muscle sufficiently to impair its response to inhaled NO.