Endothelial Function in Coronary Arteries from Pneumonia-Infected Pigs

Abstract

This study investigated whether pneumonia is accompanied with endothelial dysfunction in coronary arteries. The lungs and hearts of normal and Mycoplasma hyopneumoniae-infected pigs (6-month-old females and castrated males) were obtained from a local abattoir, and left anterior descending coronary arteries were isolated from the hearts. Lymphocyte infiltration was observed in the lung tissue of pneumonia-infected pigs (PP). However, the histopathological images of coronary arteries in PP were not different from the images in normal pigs (NP). In organ chamber experiments, endothelium-dependent relaxation of coronary arteries by bradykinin (0.1 nM–0.1 μM) and A23187 (1 nM–1 μM) were identical between PP and NP; the relaxant responses were not different even in the presence of L-NAME (100 μM, nitric oxide synthase inhibitor) alone or in combination with indomethacin (10 μM, cyclooxygenase inhibitor). In addition, the relaxant responses to nitric oxide [sodium nitroprusside (1 nM–10 μM)], hydrogen peroxide (10 μM–1 mM), and 11, 12-epoxyeicosatrienoic acids (30 nM–3 μM), all of which function as endothelium-derived relaxing factors in pig coronary arteries, were also identical between PP and NP. These findings suggest that mycoplasma pneumonia in pigs is not a risk factor for endothelial dysfunction in coronary arteries.