Abstract
We have shown that heat-killed Group B Streptococci (GBS) cause dose-related pulmonary artery hypertension in chronically instrumented piglets. These responses are similar to those seen with gram negative bacterial endotoxins. Prostanoids and endorphins have been implicated as mediators of these responses. We tested the effect of a cycloxygenase inhibitor, indomethacin; a thromboxane synthesis inhibitor, dazmegrel (UK-38,185); a leukotreine synthesis inhibitor, BW 540C; and an endorphin antagonist, naloxone on the response to a bolus of 5 × 107 heat-killed GBS Type III (M 732) /kg. We also tested the effect of pre-incubating the GBS with high-titer, type-specific rabbit antibody.Neither leukotriene nor endorphin blockade affected the response. In contrast, both cyolooxygenase and specific thromboxane synthesis inhibition markedly blunted the GBS-induced pulmonary hypertension. This suggests that thromboxane A2 mediates this response. Antibody coated organisms increased the response, suggesting antibody participation in this reaction. Further work will increase our understanding of the response to sepsis.
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