Probing of the canine mammary artery damages endothelium and impairs vasodilation resulting from prostacyclin and endothelium-derived relaxing factor

Roger A Johns, M. J. Peach, T. Flanagan, I. L. Kron

Research output: Contribution to journalArticle

Abstract

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 languageEnglish (US)
Pages (from-to)252-258
Number of pages7
JournalJournal of Thoracic and Cardiovascular Surgery
Volume97
Issue number2
StatePublished - 1989
Externally publishedYes

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Endothelium-Dependent Relaxing Factors
Mammary Arteries
Epoprostenol
Vasodilation
Endothelium
Canidae
Calcimycin
Prostaglandins F
Indomethacin
Melitten
Methacholine Chloride
Calcium Ionophores
Electron Scanning Microscopy
Radioimmunoassay
Blood Vessels
Endothelial Cells
Dogs
Electrons
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

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title = "Probing of the canine mammary artery damages endothelium and impairs vasodilation resulting from prostacyclin and endothelium-derived relaxing factor",
abstract = "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.",
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T1 - Probing of the canine mammary artery damages endothelium and impairs vasodilation resulting from prostacyclin and endothelium-derived relaxing factor

AU - Johns, Roger A

AU - Peach, M. J.

AU - Flanagan, T.

AU - Kron, I. L.

PY - 1989

Y1 - 1989

N2 - 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.

AB - 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.

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