Abstract
We have previously shown that a toxin isolated from GBS causes pulmonary hypertension, hypoxemia and fever in adult unanesthetized sheep. (Fed.Proc.37:854,1978) We have subsequently studied its effects on pulmonary vascular permeability and circulating granulocytes.
Seven young adult sheep were instrumented to measure pulmonary artery and left atrial pressures, lung lymph flow and white blood cell and differential counts. Two mg of toxin caused an early phase of pulmonary hypertension and a late phase of increased lung vascular permeability. The granulocyte count fell to less than 10% of baseline values by 60 min and returned to near baseline by 5 hrs. The immature to total granulocyte ratio increased six fold by 5 hours. Granulocyte trapping and fragmentation in the pulmonary capillaries was demonstrated by electron microscopy in four sheep sacrificed during the second phase.
To explore the role of prostaglandins we compared the response to GBS toxin alone with the response to the same dose of toxin during the infusion of indomethacin (IN) or methylprednisolone (MP). IN prevented the initial pulmonary hypertensive phase but did not modify the granulocytopenic response. In contrast, MP blocked the granulocytopenia but had little effect on the pulmonary hemodynamic changes.
We concluded that the two components of the response seem to be independent. Biosynthesis of prostaglandin endoperoxides appears necessary for the acute pulmonary hypertensive response but not for the granulocytopenia. Sequestration of granulocytes may play an important role in the pathogenesis of the pulmonary vascular changes.
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Rojas, J., Larsson, L., Brigham, K. et al. 1061 PULMONARY VASCULAR AND GRANULOCYTE RESPONSE TO GROUP B STREPTOCOCCAL (GBS) TOXIN. Pediatr Res 15 (Suppl 4), 619 (1981). https://doi.org/10.1203/00006450-198104001-01087
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DOI: https://doi.org/10.1203/00006450-198104001-01087