Loss of endothelium-dependent vasodilatation and nitric oxide release after myocardial protection with University of Wisconsin solution Jeffrey M. Pearl,

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Presentation transcript:

Loss of endothelium-dependent vasodilatation and nitric oxide release after myocardial protection with University of Wisconsin solution Jeffrey M. Pearl, MD, Hillel Laks, MD, Davis C. Drinkwater, MD, Thomas J. Sorensen, BS, Paul Chang, BS, Alon S. Aharon, MD, Russell E. Byrns, MS, Louis J. Ignarro, PhD The Journal of Thoracic and Cardiovascular Surgery Volume 107, Issue 1, Pages 257-264 (January 1994) DOI: 10.5555/uri:pii:S0022522394704791 Copyright © 1994 Mosby, Inc. Terms and Conditions

Fig. 1 Endothelium-dependent coronary blood flow. Before cardioplegic arrest, there was a significant increase in coronary blood flow with bradykinin stimulation in both group 1 and group 2, 245% and 265% of baseline, respectively. After UW solution arrest, there was a loss of vasodilatation in response to bradykinin, reaching only 117% of baseline (p = 0.0011). Vasodilatory response was preserved in hearts protected with low-potassium blood cardioplegia (group 2). NS, Not significant; Blood CP, blood cardioplegia. The Journal of Thoracic and Cardiovascular Surgery 1994 107, 257-264DOI: (10.5555/uri:pii:S0022522394704791) Copyright © 1994 Mosby, Inc. Terms and Conditions

Fig. 2 Endothelium-independent coronary blood flow. There was no significant difference in vasodilatory response to nitroprusside before and after arrest in hearts protected with UW solution (group 1). There was a small but significant decrease in vasodilatation in hearts protected with blood cardioplegia (group 2). NS, Not significant; Blood CP, blood cardioplegia. The Journal of Thoracic and Cardiovascular Surgery 1994 107, 257-264DOI: (10.5555/uri:pii:S0022522394704791) Copyright © 1994 Mosby, Inc. Terms and Conditions

Fig. 3 Nitric oxide release before and after cardioplegic arrest with UW solution. There was a significant increase in nitric oxide release in response to bradykinin infusion before arrest in group 1. After arrest with UW solution, there was complete loss of nitric oxide release (p = 0.0039), which correlated with observed lack of vasodilatation. The Journal of Thoracic and Cardiovascular Surgery 1994 107, 257-264DOI: (10.5555/uri:pii:S0022522394704791) Copyright © 1994 Mosby, Inc. Terms and Conditions