It is routine practice for many cardiac surgeons to probe internal mammary arteries to dilate them before their use. The effects of such probing on endothelium integrity, prostacyclin production, and vasodilation resulting from endothelium-derived relaxing factor and from prostacyclin were investigated in vessels isolated from mongrel dogs. Dose-dependent relaxation responses of isolated segments of probed and unprobed mammary arteries to the endothelium-dependent vasodilators methacholine, calcium ionophore (A23187), and melittin were determined in both the presence and absence of indomethacin. Prostacyclin production by probed versus unprobed vascular segments was determined under basal and A23187-stimulated conditions by radioimmunoassay for 6-keto-prostaglandin F(1α), and endothelial integrity was determined by scanning electron microscopy. Scanning electron micrographs of segments revealed marked endothelial cell disruption in probed versus unprobed vessels. The dose-dependent relaxation responses to all drugs studied were significantly impaired (p < 0.05) in probed versus unprobed vessels in both the presence and absence of indomethacin. In addition, prostacyclin release as measured by production of 6-keto-prostaglandin F(1α) was significantly (p < 0.05) impaired in probed versus unprobed vessels under both basal and A23187-stimulated conditions. These results imply that routine probing of the internal mammary artery may damage endothelium, impair prostacyclin production, and impair endothelium-dependent vasodilation resulting from both prostacyclin and endothelium-derived relaxing factor.
|Original language||English (US)|
|Number of pages||7|
|Journal||Journal of Thoracic and Cardiovascular Surgery|
|Publication status||Published - Jan 1 1989|
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
- Cardiology and Cardiovascular Medicine