The Journal of thoracic and cardiovascular surgery
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J. Thorac. Cardiovasc. Surg. · Jun 2013
Adenosine A1 receptor activation attenuates lung ischemia-reperfusion injury.
Ischemia-reperfusion injury contributes significantly to morbidity and mortality in lung transplant patients. Currently, no therapeutic agents are clinically available to prevent ischemia-reperfusion injury, and treatment strategies are limited to maintaining oxygenation and lung function. Adenosine can modulate inflammatory activity and injury by binding to various adenosine receptors; however, the role of the adenosine A1 receptor in ischemia-reperfusion injury and inflammation is not well understood. The present study tested the hypothesis that selective, exogenous activation of the A1 receptor would be anti-inflammatory and attenuate lung ischemia-reperfusion injury. ⋯ Exogenous A1 receptor activation improves lung function and decreases inflammation, edema, and neutrophil chemotaxis after ischemia and reperfusion. These results suggest a potential therapeutic application for A1 receptor agonists for the prevention of lung ischemia-reperfusion injury after transplantation.
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J. Thorac. Cardiovasc. Surg. · Jun 2013
Patterns of recurrent and persistent intestinal metaplasia after successful radiofrequency ablation of Barrett's esophagus.
Radiofrequency ablation can eradicate Barrett's esophagus successfully in the majority of cases. We sought to determine (1) how often intestinal metaplasia is detected during follow-up endoscopy after successful ablation and (2) patterns of persistent/recurrent intestinal metaplasia. ⋯ Recurrent/persistent intestinal metaplasia after successful radiofrequency ablation of Barrett's esophagus is relatively common. This finding has implications for the continued surveillance of patients who are ablated successfully.
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J. Thorac. Cardiovasc. Surg. · Jun 2013
Significance of force transfer in mitral valve-left ventricular interaction: in vivo assessment.
The objective of this study was to assess the combined force transfer from the papillary muscle tips to the mitral valve through the chordae tendineae in vivo, and thereby quantify the force transmitted through the papillary-chordal complex to augment left ventricular ejection. ⋯ This study is the first to assess the magnitude and time course of the longitudinal force transmitted through the papillary-chordal complex to the left ventricular wall during ejection. The study also demonstrates a significant force transfer to the closing force acting on the mitral valve leaflets that constitutes an essential component of valvular-ventricular interaction to enhance left ventricular systolic pump performance. The magnitude of the combined papillary muscle force component emphasizes the crucial role of preserving mitral valve-left ventricular continuity in mitral valve surgery.