Among them, 44 patients underwent nonretransplant cardiac surgery, 4 of them repeatedly. The procedures included 19 coronary artery revascularizations, 20 tricuspid valve procedures, 4 other valvular procedures, 4 aortic operations, and 1 right atrial thrombectomy. Long-term results of these patients were compared with those of 20 patients after late cardiac retransplantation.
Results: Indications for nonretransplant surgery included cardiac allograft vasculopathy, tricuspid regurgitation, aortic and mitral valve insufficiency, as well as acute aortic dissection type A. Mean interval between heart transplantation and reoperation was 8.4 years. Mean follow-up was 5.8 years. Early
mortality was 4.5% (2/44). The early deaths were caused by intracerebral bleeding and acute LCL161 price rejection. Actuarial survivals at 1, 5, and 7 years were 84%, 64%, and 58%, respectively. In BI-D1870 in vivo comparison, early mortality in the retransplant group was 20% (4/20) and survivals at the same time points were 70%, 70%, and 47%,
Conclusions: According to these results, we consider nonretransplant surgical options for cardiac allograft vasculopathy and valvular disease a safe and effective therapeutic approach with low early mortality and acceptable long-term results. (J Thorac Cardiovasc Surg 2010; 140: 433-9)”
“Increasing evidence implicates mitochondrial failure as a crucial factor in the pathogenesis of mental disorders, such as depression. The aim of the present study was to investigate the effects of exposure to chronic mild stress (CMS), a paradigm developed in the late 1980s as an animal model of depression, on the mitochondrial function and mitochondrial ultrastructure in the mouse brain. The results showed that the CMS regime induced depressive-like symptoms
in mice characterized by reduced sucrose preference and body weight. Moreover, CMS exposure was associated with a significant increase in immobility time in the tail suspension test. Exposure to the CMS paradigm inhibited mitochondrial respiration rates and dissipated mitochondrial membrane potential in hippocampus, cortex and hypothalamus of mice. In addition, we found a damaged mitochondrial ultrastructure in brains of mice exposed to CMS. These findings provide evidence for brain mitochondrial dysfunction found and ultrastructural damage in a mouse model of depression. Moreover, these findings suggest that mitochondrial malfunction-induced oxidative injury could play a role in stress-related disorders such as depression. (C) 2010 Elsevier Ireland Ltd. All rights reserved.”
“Objective: Adenosine and the activation of specific adenosine receptors are implicated in the attenuation of inflammation and organ ischemia-reperfusion injury. We hypothesized that activation of A(1), A(2A), or A(3) adenosine receptors would provide protection against lung ischemia-reperfusion injury.