Transient cardiac ischemia activates cell survival signaling, conferring subsequent ischemia tolerance to the heart. This biological phenomenon, termed ischemic preconditioning, results in improved clinical outcome and attenuated infarct size following myocardial infarction. To explore genomic modifications underpinning this ischemia tolerance, we delineated the regulation and function of the cardiac enriched mitochondrial uncoupling proteins 2 and 3 during delayed ischemic preconditioning in the rat. Cardiac transcripts of genes encoding uncoupling proteins 2 and 3 are upregulated in parallel with infarct size reduction in preconditioned hearts. Mitochondria isolated from preconditioned hearts exhibit an augmented inducible proton leak. In parallel, following anoxiareoxygenation these mitochondria generate less hydrogen peroxide compared with non-preconditioned mitochondria. Preconditioning in rat cardiac derived myoblasts is abolished following uncoupling protein-2 depletion by RNA-interference. RNAi of uncoupling protein-3 partially attenuates the capacity to precondition these cells. Functional characterization of anoxia and reoxygenation tolerance following uncoupling protein 2 or 3 and combined 2 and 3 RNAi shows the largest reduction in viability follows depletion of both homologues. Uncoupling protein-2 depletion alone significantly attenuates anoxia-reoxygenation tolerance but uncoupling protein-3 depletion does not reduce anoxia tolerance. In parallel combined uncoupling protein depletion and isolated uncoupling protein-2 depletion augments ROS production in viable cardiomyocytes following anoxia-reoxygenation. Concurrent antioxidant administration ameliorates the uncoupling protein-depleted anoxia-susceptible phenotype. In conclusion, mitochondrial uncoupling proteins are necessary components of ischemia tolerance and function as components of the cellular antioxidant defense program. In the cytoprotective hierarchy, uncoupling protein-2 appears to play a greater role than uncoupling protein-3 in modulating ischemia/anoxia tolerance in heart-derived cells.The cell survival program, termed ischemic preconditioning, evoked by transient nonlethal tissue ischemia, is evolutionarily conserved and is evident across multiple organs/tissues. The signal transduction networks engendering this phenomenon are well described (1); however, functional cellular modifications conferring ischemia tolerance are less tangible. Interestingly, the invariable metabolic signature of preconditioned tissue is enhanced capacity to restore mitochondrial function and ATP production following an ischemic insult (2). The mechanistic links between the molecular adaptations of the mitochondrion and the preconditioning cell survival program require further characterization. Further credence to the importance of mitochondrial adaptation to preconditioning-induced cell survival has been shown by improved mitochondrial respiratory and bioenergetic recovery following anoxia and reoxygenation in mitochondria extracted from ischemic, genomi...

In this series, percutaneous endovascular intervention for type II endoleak with aneurysm sac growth does not appear to alter the rate of aneurysm sac growth, and the majority of patients display persistent/recurrent endoleak. However, diagnostic angiographic evaluation may reveal unexpected type I and III endoleaks and is therefore recommended for all patients with T2EL and sac growth. While coil and glue embolization of aneurysm sac and selected branch vessels does not appear to yield benefit in our series, the diagnosis and subsequent definitive treatment of previously occult type I and III endoleaks may explain the absence of delayed rupture and ARM in our series.

Objectives Surgical ablation of ganglionated plexi (GP) has been proposed to increase the efficacy of the surgical treatment of atrial fibrillation (AF). This experimental canine study examined the electrophysiological attenuation and recovery of atrial vagal effects following GP ablation alone and combined with standard surgical lesion sets used to treat AF. Methods Dogs were divided into 3 groups: Group 1 (N=6) had focal ablation of the 4 major epicardial GP fat pads; Group 2 (N=6) had pulmonary vein isolation with GP ablation; and Group 3 (N=6) had posterior left atrial isolation with GP ablation. All fat pads were ablated. Sinus and atrioventricular (AV) interval changes during bilateral vagosympathetic trunk stimulation were examined before, after, and at four weeks post-ablation. Vagally induced effective refractory period (ERP) changes and mean QRST area changes (index of local innervation) were examined in 5 atrial regions. Results Sinus and AV interval changes and heart rate variability decreased immediately following ablation, but only sinus interval changes were restored significantly after 4 weeks in all groups. Ablation modified vagal effects on ERP or QRST area changed heterogeneously in Groups 1 and 2. In Group 3, regional vagal effects were attenuated extensively post-ablation in both atria. Posterior left atrial isolation with GP ablation incrementally denervated the atria. Chronically, vagal stimulation increased QRST area changes over control values in all groups. Heart rate variability was also assessed. Conclusions GP ablation significantly reduced vagal innervation to the atria. Restoration of vagal effects at 4 weeks suggested early atrial reinnervation.

Patients treated by primary VATS had a shorter stay and lower hospital charges than patients treated by chest tube and antibiotic therapy alone. There were no demographic, physiologic, laboratory, or chest radiographic data that predicted the selection of VATS as an initial treatment. These data suggest a strategy of primary VATS as first-line treatment in the management of empyema or parapneumonic effusion as a complication of pneumonia in pediatric patients.