Abstract

Hypoxic pulmonary vasoconstriction (HPV) is attenuated after endotoxin infusion into adult dogs and sheep. High dose infusions of Group B Streptococcus (GBS), a neonatal pathogen, into newborn animals produce pulmonary hypertension, hypoxemia, and reduced cardiac output similar to high dose endotoxin infusions in adult animals. To avoid the compounding effects of reduced arterial and mixed venous PO2, HPV was studied after low dose endotoxin in adult animals. We hypothesized that HPV would be attenuated in piglets after a low dose GBS infusion. Both PVR and pressure-flow (P/Q) relationships were measured in piglets to characterize the neonatal pulmonary vascular response to alveolar hypoxia before and after GBS infusion. Hemodynamic measurements were made under Zone 3 conditions in 5 piglets breathing room air and 13% FIO2: (1) prior to GBS, (2) 20 min into a 1-h infusion of 3 +/- 1 x 10(8) cfu/kg/h live GBS, (3) 1 h, and (4) 3 h after completion of the GBS infusion. Prior to GBS, alveolar hypoxia increased PVR (14 +/- 1.3 to 33 +/- 3.6 mm Hg/L/min) and P/Q slope (12 +/- 2.3 to 41 +/- 6.8 mm Hg/L/min). During all subsequent exposures to 13% FIO2, the PVR and P/Q slopes were similar to pre-GBS values. When animals breathed room air, the PVR and P/Q slopes were greater than pre-GBS values during but not after the GBS infusion. We conclude that HPV is not altered 1 and 3 h after a 1-h low dose GBS infusion in neonatal piglets. Infusion of GBS and alveolar hypoxia independently increase pulmonary vascular resistance.

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