Background Diagnostic natural-orifice transluminal endoscopic surgery (NOTES) peritoneoscopy can easily be performed with standard endoscopic equipment in animal studies. The efficacy and optimal ...transgastric site for NOTES access in humans, however, has not been determined. Objective To characterize the efficacy of various anterior gastric access locations for diagnostic transgastric NOTES peritoneoscopy in humans. Design Prospective clinical study. Setting Tertiary-care center with experience in NOTES peritoneoscopy. Patients Patients undergoing planned laparoscopic gastrectomy or gastrotomy involving the anterior aspect of the stomach were eligible. Interventions An anterior gastric site for NOTES gastrotomy was chosen and transgastric NOTES access was independently established after laparoscopic abdominal exploration. Peritoneoscopy was then performed. The site of gastrotomy was closed as part of the intended laparoscopic procedure. Main Outcome Measures The ability to visualize the abdominal and pelvic organs in all four quadrants was determined. Patients were evaluated postoperatively for complications. Results Eight patients requiring 9 procedures were studied. Gastrotomy sites were classified as body (n = 3), lesser curvature (n = 3), greater curvature (n = 1), fundus (n = 1), and antrum (n = 1). Satisfactory navigation could only be performed to the right upper and both lower quadrants. The left upper quadrant, specifically the spleen, was adequately visualized in only 1 case (11%), where the gastrotomy site was at the greater curvature. One patient developed a surgical site infection requiring oral antibiotic therapy. The median postoperative stay was 2 days (range, 0-3 days). Limitations Small number of patients. Conclusion NOTES peritoneoscopy with a gastrotomy on the anterior stomach permits adequate visualization of organs in the right upper and both lower quadrants. Visualization of the left upper quadrant and spleen is, however, limited unless access is gained on the greater curvature of the stomach. The accuracy of NOTES in identifying intra-abdominal pathology compared with laparoscopy remains to be determined.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UL, UM, UPCLJ, UPUK
Hybrid procedures combine laparoscopy and natural orifice surgery techniques. Some groups are currently using hybrid procedures to investigate the concepts of pure natural orifice surgery. Thus far, ...hybrid procedures have validated the safety of transgastric peritoneoscopy, although improved instrumentation is imperative before widespread clinical applications. As technical improvements develop from hybrid surgery, gastrointestinal endoscopy and abdominal surgery could be revolutionized.
Background The purpose of this study was to identify factors predicting risk of aortic arch recoarctation after the Norwood procedure. Methods Patient records were reviewed retrospectively for ...consecutive patients who underwent the Norwood procedure from 1996 to 2005. Preoperative and intraoperative parameters were identified for analysis. Aortic arch recoarctation was defined by the need for catheter or surgical reintervention. Data were analyzed using survival analysis, with freedom from intervention as the outcome. Factors predicting need for reintervention were analyzed using Cox proportional hazards regression. Results Thirty-five recoarctations were observed in 117 patients (30%). Freedom from aortic arch reintervention at six months, one, three, and five years were 72%, 63%, 56%, and 52%, respectively. The majority of arch reinterventions occurred in the first six months (63%), involving either surgical (43%) or catheter (57%) techniques. The use of bovine pericardium showed the greatest risk for potential recoarctation (hazard ratio = 1.81 0.90–3.64, p = 0.09). Age, gender, weight, ascending aortic diameter, ventricular morphology, primary anatomic diagnosis, and coarctation shelf resection were not found to be predictors of recoarctation. Conclusions Most interventions for aortic arch recoarctation after the Norwood procedure occur within the first six months of life. The type of patch material used for arch reconstruction appears to influence, most strongly, the long-term risk of aortic arch recoarctation.
Cardiac dysfunction after brain death (BD) limits donors for cardiac transplantation. Glucocorticoids ameliorate brain death-induced donor heart dysfunction. We hypothesized that glucocorticoid ...therapy alleviates myocardial depression through altering the balance between pro- and anti-inflammatory mediators via the nuclear factor-kappaB (NF-kappaB)/inhibitor of kappaB-alpha (IkappaBalpha) pathway and/or by preserving beta-adrenergic receptor (betaAR) signaling in the heart.
Crossbred pigs (25 to 35 kg) were randomly assigned to the following groups (n = 5/treatment): sham (Group 1); BD (Group 2); and BD with glucocorticoids (30 mg/kg methylprednisolone), either 2 hours before (Group 3) or 1 hour after BD (Group 4). Tumor necrosis factor-alpha (TNF-alpha) levels were measured in plasma at baseline and 1 hour and 6 hours after BD. Protein levels were measured in left ventricular homogenates procured 6 hours after BD.
Pro-inflammatory proteins (TNF-alpha) and interleukin-6 were lower in Group 3 and Group 4 compared with Group 2 at 6 hours after BD (p < 0.01). Intracellular adhesion molecule-1 was also lower in Group 4 compared with Group 2 (p = 0.001). Interleukin-10, an anti-inflammatory mediator, was lower in Group 4 than in Group 2 (p < 0.001), but not different between Groups 2 and 3. At 6 hours after BD, neither NF-kappaB activity nor basal adenylate cyclase activity differed between Groups 3 and 4 compared with Group 2.
Glucocorticoids maintained myocardial function and shifted the balance of pro- and anti-inflammatory mediators after BD. The mechanisms by which glucocorticoids preserve myocardial function, however, do not appear to involve the NF-kappaB pathway or betaAR signaling.
Objective β-Adrenergic receptor desensitization through activation of the G protein–coupled receptor kinase 2 is an important mechanism of early cardiac dysfunction after brain death. We hypothesized ...that acute β-blockade can prevent myocardial β-adrenergic receptor desensitization after brain death through attenuation of G protein–coupled receptor kinase 2 activity, resulting in improved cardiac function. Methods Adult pigs underwent either sham operation, induction of brain death, or treatment with esmolol (β-blockade) for 30 minutes before and 45 minutes after brain death (n = 8 per group). Cardiac function was assessed at baseline and for 6 hours after the operation. Myocardial β-adrenergic receptor signaling was assessed 6 hours after operation by measuring sarcolemmal membrane adenylate cyclase activity, β-adrenergic receptor density, and G protein–coupled receptor kinase 2 expression and activity. Results Baseline left ventricular preload recruitable stroke work was similar among sham, brain death, and β-blockade groups. Preload recruitable stroke work was significantly decreased 6 hours after brain death versus sham, and β-blockade resulted in maintenance of baseline preload recruitable stroke work relative to brain death and not different from sham. Basal and isoproterenol-stimulated adenylate cyclase activities were preserved in the β-blockade group relative to the brain death group and were not different from the sham group. Left ventricular G protein–coupled receptor kinase 2 expression and activity in the β-blockade group were markedly decreased relative to the brain death group and similar to the sham group. β-Adrenergic receptor density was not different among groups. Conclusion Acute β-blockade before brain death attenuates β-adrenergic receptor desensitization mediated by G protein–coupled receptor kinase 2 and preserves early cardiac function after brain death. These data support the hypothesis that acute β-adrenergic receptor desensitization is an important mechanism in early ventricular dysfunction after brain death. Future studies with β-blocker therapy immediately after brain death appear warranted.
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GEOZS, IJS, IMTLJ, KILJ, KISLJ, NLZOH, NUK, OILJ, PNG, SAZU, SBCE, SBJE, UILJ, UL, UM, UPCLJ, UPUK, ZAGLJ, ZRSKP
Cardiac dysfunction after brain death decreases the already limited number of potential donors for cardiac transplantation. Acute beta-adrenergic receptor (betaAR) desensitization after the brain ...death-associated catecholamine surge is an important mechanism. We hypothesized that acute betaAR antagonism could improve myocardial function after brain death by preserving betaAR signaling.
Pigs were randomly assigned to three study groups (n = 5): sham; brain death; and brain death with betaAR antagonist (200 microg/kg/min esmolol), 30 minutes before brain death until 45 minutes after brain death. Functional data were collected for 6 hours after brain death and tissues procured.
Compared with baseline, pre-load recruitable stroke work (PRSW), a pre-load-independent measure of systolic function (21.4 +/- 7.5 vs 43.3 +/- 6.8, slope of regression line during vena caval occlusion, p < 0.001), diastolic function (Tau, 101 +/- 54.7 vs 36.4 +/- 5.4 ms, p = 0.03) and systemic oxygen delivery (151 +/- 79.7 vs 298 +/- 78.7 ml/min, p < 0.001) deteriorated in untreated animals at 6 hours after brain death. In contrast, betaAR antagonist maintained baseline systolic function (PRSW, 37.8 +/- 5.6 vs 38.2 +/- 4.7, slope of regression line during vena caval occlusion, p = 0.92), diastolic function (Tau, 32.6 +/- 5.1 vs 48.5 +/- 28.3 ms, p = 0.57) and oxygen delivery (427 +/- 116 vs 397 +/- 98.8 ml/min, p = 0.36) at 6 hours after brain death. betaAR antagonist preserved betaAR signaling, as demonstrated by similar left ventricular (LV) basal (55.4 +/- 32.8 vs 58.8 +/- 10.9 pmol/mg/min, p = 0.40) and isoproterenol-stimulated (125 +/- 70.5 vs 124 +/- 52.0 pmol/mg/min, p = 0.49) adenylate cyclase activity at 6 hours after brain death, upon comparing betaAR antagonist and sham treatment groups. Both LV basal and isoproterenol-stimulated adenyl cyclase activity were higher with betaAR antagonist (25.9 +/- 4.8 pmol/mg/min, p = 0.03) than with untreated brain death (55.6 +/- 17.3 pmol/mg/min, p = 0.02).
Beta-adrenergic receptor antagonism before brain death preserves cardiac function by preventing betaAR desensitization. This therapy in potential donors might increase the number of organs available for transplantation.
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