Effect of Sialyl Lewisx Selectin Blockade on Myocardial Protection During Cardioplegic Arrest and Reperfusion
(#2001-87347 ... August 9, 2001)
H. Henning Sauer, MD,1 Steven J. Allen, MD, 1 Charles S. Cox Jr., MD, 2 Glen A. Laine, PhD1,3
Departments of Anesthesiology1 and Surgery, 2 and the Center for Microvascular and Lymphatic Studies, University of Texas-Houston Medical School, and Department of Veterinary Physiology and Pharmacology, 3 Texas A&M University, College Station, Texas
ABSTRACT
Purpose: Selectins play a crucial role in the neutrophil-mediated myocardial injury associated with ischemia/reperfusion. We investigated the effect of selectin inhibition on neutrophil-endothelial cell adhesion, myocardial water content, and left ventricular (LV) recovery after cardiopulmonary bypass (CPB) and cardioplegia.
Methods: Dogs were subjected to CPB and 60 minutes of hypothermic cardioplegia. A selectin inhibitor (SI) (25 mg/kg) was given five minutes prior to CPB and as a continuous infusion (5 mg/kg/h) throughout CPB (n = 6). Saline-treated controls (n = 6) received identical volumes. Preload recruitable stroke work (PRSW) was calculated by sonomicrometry and micromanometry. Myocardial water content was determined by microgravimetry. Myeloperoxidase (MPO) activity was measured to quantify polymorphonuclear neutrophil (PMN) infiltration.
Results: SI did not attenuate PRSW as well as post-CPB MPO tissue activity. While we found no difference in myocardial water gain between groups 120 minutes post-CPB, there was better edema resolution with SI.
Conclusions: Selectin antagonism does not reduce CPB-associated myocardial injury, and contractile recovery is not enhanced.
AUTHOR/ARTICLE INFORMATION
Submitted August 2, 2001; accepted August 9, 2001.
Address correspondence and reprint requests to: H. Henning Sauer, MD, Klinik für Herzchirurgie, Städt. Kliniken Oldenburg, Dr.-Eden-Str. 10, 26133 Oldenburg, Germany, Phone: +49 (441) 998-9145, Fax: +49 (441) 403-2830, E-mail: Henning.Sauer@ewetel.net
Acknowledgments
The authors thank John R. Frederick for excellent technical assistance. We gratefully acknowledge the generous supply of TBC-1269 received from Texas Biotechnology Corp., Houston, TX. We kindly appreciate support of Cobe Cardiovascular Division Inc. Dr Sauer is the recipient of a fellowship granted by Dr F. Köhler Chemie Corp., Germany.
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