Thromboxane synthesis inhibition reverses group B Streptococcus-induced pulmonary hypertension.

Academic Article

Abstract

  • Group B Streptococcus (GBS) sepsis in humans may cause the persistent pulmonary hypertension syndrome. Infusions of GBS in animals elevate pulmonary artery pressure (PAP) and resistance and are associated with elevated thromboxane levels. We investigated the hemodynamic effects of the specific thromboxane synthesis inhibitor, dazmegrel, in a piglet model of GBS-induced pulmonary hypertension. PAP rose from 22 +/- 6 to 42 +/- 11 (SD) mm Hg during infusion of heat-killed GBS; pulmonary vascular resistance increased from 1440 +/- 400 to 4000 +/- 1040 dyne X sec/cm5. No significant changes in cardiac output, mean arterial pressure, or left atrial pressure were noted. Treatment with 1 mg/kg of dazmegrel resulted in a rapid return of PAP and resistance to control values. No other hemodynamic effects of either bacteria or drug were observed despite continued infusion of GBS.
  • Published In

    Keywords

  • Animals, Blood Pressure, Cardiac Output, Female, Hypertension, Pulmonary, Imidazoles, Pulmonary Artery, Sepsis, Streptococcal Infections, Streptococcus agalactiae, Swine, Thromboxane-A Synthase
  • Author List

  • Tarpey MN; Graybar GB; Lyrene RK; Godoy G; Oliver J; Gray BM; Philips JB
  • Start Page

  • 644
  • End Page

  • 647
  • Volume

  • 15
  • Issue

  • 7