Faculty Collaboration Database

Endothelial cell dysfunction after ischemic arrest and reperfusion: a possible mechanism of myocardial injury during reflow. J Thorac Cardiovasc Surg 1991 Nov;102(5):688-94

Date

11/01/1991

Pubmed ID

1943187

DOI

10.1016/s0022-5223(19)36858-8

Scopus ID

2-s2.0-0026353451 (requires institutional sign-in at Scopus site)   78 Citations

Abstract

To determine the mechanism(s) responsible for decreased coronary flow after global cardiac ischemia and reperfusion, we studied 40 isolated rabbit hearts before and after 30 minutes of normothermic ischemic arrest and reperfusion. In the control group (n = 10) we evaluated the time course of recovery of coronary flow, vascular reactivity, and myocardial function. In experimental groups A (n = 10) and B (n = 10), metabolic control of autoregulation was assessed by plots of myocardial oxygen consumption versus coronary flow generated by incremental increases in heart rate. The slope and intercept of these plots suggested that autoregulation of coronary flow was maintained after ischemia. In group B hearts (n = 10) hyperosmolar reperfusion with mannitol decreased myocardial water by 2% (p less than 0.01) but did not increase coronary flow. Endothelium-dependent function was assessed in group C (n = 10) by the administration of an endothelium-dependent vasodilator (serotonin) and a smooth muscle vasodilator (adenosine). Coronary artery smooth muscle function was comparable in hearts before and after ischemia. However, endothelium-dependent increases in coronary flow to serotonin were significantly impaired after ischemia (p less than 0.01), and this was accompanied by a significant decrease in prostacyclin synthesis by the endothelium (p less than 0.001). Global cardiac ischemia and reperfusion damages coronary artery endothelium, causing increased coronary vasomotor tone; this may be an important mechanism of decreased coronary perfusion and subsequent myocardial injury during reflow.

Author List

Hashimoto K, Pearson PJ, Schaff HV, Cartier R

Author

Paul Joseph Pearson MD, PhD Chief, Professor in the Surgery department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Animals
Coronary Circulation
Coronary Vessels
Endothelium, Vascular
Epoprostenol
Heart Arrest, Induced
In Vitro Techniques
Lactates
Male
Muscle, Smooth, Vascular
Myocardium
Oxygen Consumption
Rabbits
Reperfusion Injury
Serotonin