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OBJECTIVE To clarify the mechanism of the development of a severe pulmonary hypertensive response to group B streptococcus. METHODS Prospective, randomized controlled trial. METHODS Twelve chronically instrumented and six age-matched uninstrumented newborn piglets. METHODS Six animals received eight injections of group B streptococcus over an 11-day period (control group). Six additional animals (pretreatment group) were given 3 mg/kg of dazmegrel, a thromboxane synthase blocking agent, before each dose of group B streptococcus to prevent the pulmonary hypertensive response and to control for any secondary arterial remodeling. RESULTS Hemodynamic measurements, pulmonary arterial morphometry, and thromboxane concentrations were examined in the instrumented animals. Lungs from the uninstrumented piglets were examined to determine morphometric norms for this population. The animals given only group B streptococcus developed a significant pulmonary hypertensive response after five daily doses (+6.8 +/- 2.0 [SEM] mm Hg, p < .05) which became pronounced after eight doses (+13.2 +/- 1.0 mm Hg). Pulmonary hypertension was not observed in the pretreatment group when dazmegrel was given; however, on the final day in this group, dazmegrel was withheld before group B streptococcus dosing and a significant pulmonary hypertensive response was observed (+20 +/- 1.6 mm Hg). The medial thickness of pulmonary arteries was not different between the two groups nor when compared with that of six normal, uninstrumented animals. Plasma thromboxane B2 concentrations were determined from blood samples taken before and after group B streptococcus infusion at the first, seventh and eighth (final) dosing. Thromboxane concentrations increased significantly on days 7 and 8 in the control group (578 +/- 312 to 752 +/- 372 pg/mL, 638 +/- 201 to 1462 +/- 295 pg/mL, respectively) and on day 8 in the pretreatment group (545 +/- 160 to 705 +/- 187 pg/mL). CONCLUSIONS We conclude that the development of potentiated pulmonary hypertension is not due to pulmonary arterial remodeling, but is associated with increased thromboxane production.
E S Barefield, and
T P Hicks, and
J B Philips
July 1987,
Critical care medicine,
E S Barefield, and
T P Hicks, and
J B Philips
February 2001,
Pediatric research,
E S Barefield, and
T P Hicks, and
J B Philips
November 1989,
Pediatric research,
E S Barefield, and
T P Hicks, and
J B Philips
April 1993,
The American review of respiratory disease,
E S Barefield, and
T P Hicks, and
J B Philips
January 1992,
Developmental pharmacology and therapeutics,
E S Barefield, and
T P Hicks, and
J B Philips
April 2011,
Journal of perinatology : official journal of the California Perinatal Association,
E S Barefield, and
T P Hicks, and
J B Philips
April 1998,
Scandinavian journal of immunology,
E S Barefield, and
T P Hicks, and
J B Philips
April 1990,
Pediatric research,
E S Barefield, and
T P Hicks, and
J B Philips
May 2005,
Journal of immunology (Baltimore, Md. : 1950),
E S Barefield, and
T P Hicks, and
J B Philips
May 1983,
Chest,
