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Rebecca J. Dignan
Cornelius M. Dyke
Anwar S. Abd-Elfattah
Harry A. Lutz
Thomas Yeh, Jr
Jitendra Parmar
Andrew S. Wechsler
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Ann Thorac Surg 1992;53:311-317
© 1992 The Society of Thoracic Surgeons

Articles

Coronary artery endothelial cell and smooth muscle dysfunction after global myocardial ischemia

Rebecca J. Dignan, MD, Cornelius M. Dyke, MD, Anwar S. Abd-Elfattah, PhD, Harry A. Lutz, PhD, Thomas Yeh, Jr, MD, K.Francis Lee, MD, Jitendra Parmar, MD, Andrew S. Wechsler, MD*

Department of Surgery, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia, USA

Accepted for publication August 21, 1991.

* Address reprint requests to Dr Wechsler, Medical College of Virginia, PO Box 645, MCV Station. Richmond, VA 23298.

We hypothesized that coronary artery endothelial cell function and smooth muscle function are modified by global myocardial ischemia and used bradykinin-induced secretion of endothelium-derived relaxing factor as a marker of endothelial cell function. Bradykinin and sodium nitroprusside together determined maximum smooth muscle relaxation. Potassium chloride-induced contraction determined smooth muscle contractility. Endothelium-mediated smooth muscle relaxation expressed as a ratio of total coronary smooth muscle relaxation before and after ischemia quantified endothelial cell function. The effect of global normothermic ischemia on in situ coronary arteries from 7 swine hearts was studied. Coronary arterial rings taken from 0 to 220 minutes of ischemia at 20-minute intervals were studied in vitro. The data revealed unexpected tolerance of endothelium-mediated relaxation to ischemia. Endothelium-derived relaxing factor function was maintained to 160 minutes and smooth muscle function, to 120 minutes of ischemia. Coronary artery dysfunction seen in other studies after less ischemia may be the result of injury introduced during reperfusion, may be the consequence of myocardial injury, or may be due to events operative at the level of small arterioles.




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