Cardiovascular Changes in Group B Streptococcal Sepsis in the Piglet: Response to Indomethacin and Relationship to Prostacyclin and Thromboxane A2

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Abstract
Summary: Seventeen piglets were infected with a continuous intravenous infusion of live group B β-hemolytic streptococci (GBS). Hemodynamic changes were recorded, and blood samples were drawn for measurement of thromboxane B2 (TxB2) (stable metabolite of thromboxane A2) and 6-keto-PGF1α (stable metabolite of prostacyclin). Control animals (n =9) received only bacteria, while treatment animals (n =8) received indomethacin, 3 mg/kg IV, 15 min after the start of the bacterial infusion. Control animals responded to the bacteria within 15 min with marked elevation in mean pulmonary artery pressure (Ppa) from 15 ± 8 to 39 ± 6 mm Hg and decline in Pao2 from 80 ± 11 to 51 ± 6 mm Hg and cardiac output (CO) from 0.24 ± 0.07 to 0.13 ± 0.07 liters/min/ kg. Mean arterial blood pressure (AoP) significantly decreased from baseline value of 95 ± 13 to 51 ± 32 mm Hg by 180 min. In animals treated with indomethacin, these changes were reversed or significantly attenuated. The hemodynamic changes were associated temporally with elevations in plasma concentrations of TxB2 or 6-keto-PGF1α. In he first 60 min, TxB2 levels in both groups correlated with Ppa (r =0.72, p < 0.001) and Pao2 (r =-0.60, p < 0.001). A strong negative correlation between TxB2 and CO was observed over the first 180 min (r =-0.73, p < 0.001). There was a statistically significant correlation between AoP and 6-keto-PGF1α concentration between 60 and 180 min (r =-0.54, p < 0.002). Indomethacin improved the hemodynamic function in this model of GBS sepsis. This improvement was related in part to inhibition of synthesis of thromboxane A2 and prostacyclin.

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