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1 Department of Anesthesiology, The University of Texas Medical Branch, Galveston, Texas, USA; Department of Anesthesiology and Pain Management, The University of Texas Southwestern Medical Center, Dallas, Texas, USA
2 Department of Anesthesiology, The University of Texas Medical Branch, Galveston, Texas, USA; The Shriners Hospital for Children, Galveston, Texas, USA
* To whom correspondence should be addressed. E-mail: ersherwo{at}utmb.edu.
We previously showed that 
2 microglobulin knockout mice treated with anti-asialoGM1 (2M/
AsGM1 mice) exhibit less hypothermia, reduced production of pro-inflammatory cytokines, less metabolic acidosis and improved survival following cecal ligation and puncture (CLP) compared to wild type mice. The present study was designed to assess hemodynamics and left ventricular contractility at 18 hours after CLP. Arterial pressure was measured by carotid artery cannulation and left ventricular pressure-volume loops were obtained by insertion of a 1.4F conductance catheter into the left ventricle. Heart rate, stroke volume and cardiac output were not significantly different between wild type and 2M/AsGM1 mice following CLP. However, 2M/AsGM1 mice exhibited improved mean arterial pressure and systemic vascular resistance compared to wild type mice. Myocardial function was also better preserved in 2M/AsGM1 mice as indicated by improved left ventricular pressure development over time, time varying maximum elastance, end systolic pressure volume relationship and preload recruitable stroke work. Overall, this study shows that cardiovascular collapse characterized by hypotension, myocardial depression and low systemic vascular resistance occurs after CLP in wild type mice. However, 2M/AsGM1 mice exhibit improved hemodynamics and cardiac contractile function following CLP that may account, in part, for our previously observed survival benefit.
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