Comparative disposition kinetics of 111In-labeled group B streptococcus and neutrophils during onset of sepsis-induced pulmonary hypertension.

Little is known of the time course by which intravascular group B streptococcus (GBS) distributes into the infant lung, though the prompt onset of pulmonary hypertension in GBS-infected animals suggests that bacteria interact initially with a resident lung cell or that they promote rapid pulmonary influx of circulating effector cells. Using external gamma scintigraphy to monitor the organ-specific disposition kinetics of 111In-oxine-labeled GBS in anesthetized piglets, we found that 80% of the infused bacteria rapidly distributed into the lung and that pulmonary bacterial uptake exhibited a close temporal relationship with the onset of pulmonary hypertension. Companion studies demonstrated that the extent of pulmonary 111In-neutrophil sequestration was unaffected by GBS, although a neutrophil secretagogue, phorbol myristate acetate, caused rapid pulmonary neutrophil uptake. These observations support the hypothesis that the onset of pulmonary hypertension in GBS sepsis can be attributed to interactions between the bacteria and resident lung cells.