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Obtaining endolumenal closure of hollow visceral defects may complement conventional, incision-based, surgical alternatives and benefit the experimental field of natural orifice translumenal endoscopic surgery (NOTES). Endoscopic tissue plicating devices (TPD) represent a promising closure technology; however, the long-term integrity of resultant closures is uncertain. Swine (n=10) underwent survival transgastric NOTES peritoneoscopy procedures with TPD gastrotomy closure while device performance and closure integrity were evaluated. Following uncomplicated procedures, no animals revealed leakage on upper gastrointestinal contrast fluoroscopy immediately following closure and on postoperative days 2 and 7. Necropsy performed on the 14th postoperative day revealed a subclinical colonic injury for one animal; the remaining nine animals had no complications. Gastric burst testing revealed the strength of closure was comparable to that of nonsurgical control stomachs (85.1 vs. 85.3 mm Hg, p=0.98). For six of nine (66%) TPD animals, bursting occurred remote to the closure site in nonsurgical tissue, indicating that closure strength equaled that of native tissue. Endoscopic TPD closure of standardized NOTES gastric defects results in strong, leak-proof closure; however, injuries can occur. These findings support evaluation of TPD closure in human trials involving noncontrolled gastric defects.

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Background The purpose of this study investigation was to characterize differential right atrial (RA) and ventricular (RV) molecular changes in Ca2+-handling proteins consequent to RV pressure overload and hypertrophy in two common, yet distinct models of pulmonary hypertension, dehydromonocrotaline (DMCT) toxicity and pulmonary artery (PA) banding. Materials and methods Eighteen dogs underwent sternotomy with four groups: 1.) DMCT toxicity (n=5), 2.) mild PA banding over 10 weeks to match the RV pressure rise with DMCT (n=5), 3.) progressive PA banding to generate severe RV overload (n=4), and 4.) sternotomy only (n=4). Results Right Ventricle: With DMCT, there was no change in sarcoplasmic reticulum Ca2+-ATPase (SERCA) or phospholamban (PLB), but a trend to downregulation of phosphorylated PLB at serine-16 (p(Ser-16)PLB) (P = 0.07). Similarly, with mild PA banding, there was no change in SERCA or PLB, but p(Ser-16)PLB was downregulated by 74% (P < 0.001). With severe PA banding, there was no change in PLB, but SERCA fell by 57% and p(Ser-16)PLB fell by 67% (P < 0.001). Right Atrium: With DMCT, there were no significant changes. With both mild and severe PA banding, p(Ser-16)PLB fell (P < 0.001), but SERCA and PLB did not change. Conclusions Perturbations in Ca2+-handling proteins depend on the degree of RV pressure overload and the model used to mimic the RV effects of pulmonary hypertension and are similar, but blunted, in the atrium compared to the ventricle.