Endothelial cell dysfunction after ischemic arrest and reperfusion: A possible mechanism of myocardial injury during reflow

K. Hashimoto, P. J. Pearson, Hartzell V Schaff, R. Cartier

Research output: Contribution to journalArticle

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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 < 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 < 0.01), and this was accompanied by a significant decrease in prostacyclin synthesis by the endothelium (p < 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.

Original languageEnglish (US)
Pages (from-to)688-694
Number of pages7
JournalJournal of Thoracic and Cardiovascular Surgery
Volume102
Issue number5
StatePublished - 1991

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Reperfusion
Ischemia
Endothelial Cells
Endothelium
Wounds and Injuries
Smooth Muscle
Serotonin
Coronary Vessels
Homeostasis
Endothelium-Dependent Relaxing Factors
Mannitol
Epoprostenol
Reperfusion Injury
Vasodilator Agents
Oxygen Consumption
Adenosine
Blood Vessels
Perfusion
Heart Rate
Rabbits

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Endothelial cell dysfunction after ischemic arrest and reperfusion : A possible mechanism of myocardial injury during reflow. / Hashimoto, K.; Pearson, P. J.; Schaff, Hartzell V; Cartier, R.

In: Journal of Thoracic and Cardiovascular Surgery, Vol. 102, No. 5, 1991, p. 688-694.

Research output: Contribution to journalArticle

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