EFFECT OF INHALED NITRIC-OXIDE DURING GROUP-B STREPTOCOCCAL SEPSIS INPIGLETS

Group B streptococcus (GBS), a common gram-positive pathogen, causes s imilar pathophysiologic changes in newborn humans and animals. Infusio n of GBS into neonatal animals produces pulmonary hypertension and ven tilation/perfusion (VA/Q) mismatch in both early-phase (< 1 h) and lat e-phase (2 to 6 h) responses. Contrary to early phase, late phase caus es pulmonary vascular injury. Nitric oxide (NO) is an inhaled vasodila tor whose effect on pulmonary hypertension and VA/Q matching during ea rly and late phases of GBS sepsis is unclear. We hypothesized that inh aled NO (150 ppm) would: (1) reverse early-phase GBS-induced pulmonary hypertension; (2) demonstrate less effectiveness in reversing late-ph ase GBS-induced pulmonary hypertension because of vascular injury; (3) improve late-phase GBS-induced VA/Q mismatching. Anesthetized, mechan ically ventilated piglets (n = 10; 14 +/- 4 days of age) received a 24 0-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 fo und that inhaled NO selectively reversed early- and late-phase GBS-ind uced pulmonary hypertension and that NO was equally as effective in ea ch phase. Inhaled NO did not reverse VA/Q mismatching during late-phas e GBS. We conclude that 4 h of GBS sepsis does not injure neonatal pul monary vascular smooth muscle sufficiently to impair its response to i nhaled NO.