Nitric oxide appears to play an important role in maintaining gastric mucosal integrity. This study aimed to investigate whether a nitric oxide donor (sodium nitroprusside) or stimulation of endogenous nitric oxide synthesis (with acetylcholine) protects against gastric ischemia-reperfusion injury. Rats were subjected to 30 min of ischemia followed by 15 min of reperfusion. Injury was assessed by quantitative histology. Intravenous sodium nitroprusside (50-75 micrograms/kg) or acetylcholine (10-25 micrograms/kg), immediately before reperfusion, significantly reduced the percentage of mucosal injury compared with controls. Inhibition of nitric oxide synthesis by topical application of 12.5 mg/kg NG-methyl-L-arginine before acetylcholine treatment, abolished the effects of acetylcholine. The protective effects of acetylcholine and sodium nitroprusside did not appear to be related to local vasodilation since neither drug improved gastric blood flow and infusion of a non-nitric oxide vasodilator (papaverine, 1 mg/kg), had no protective effect on reperfusion injury. Sodium nitroprusside (50 micrograms/kg) and acetylcholine (25 micrograms/kg) significantly reduced polymorphonuclear leukocyte infiltration and extravasation into the mucosa compared with controls. NG-Methyl-L-arginine pretreatment before acetylcholine abolished these effects. We conclude that nitric oxide generators significantly reduce mucosal injury following ischemia-reperfusion and that this may occur via a reduction in polymorphonuclear leukocyte infiltration into the mucosa.

IFN-γ released from inflamed omental adipose tissue may contribute to the metabolic abnormalities seen in human obesity.

The mechanisms of gastric mucosal injury following a period of ischemia remain unclear. The aim of this study was to determine the relative contributions of ischemia, reperfusion, and reactive oxygen metabolites to mucosal injury induced by temporary occlusion of the celiac artery. Rats were subjected to 30 min of gastric ischemia in the presence of 100 mM HCl. Reperfusion periods ranged from 1 min to 24 hr. Drug treatments included allopurinol (100 mg/kg) or a combination of superoxide dismutase (15,000 units/kg), catalase (90,000 units/kg), and desferrioxamine (50 mg/kg). Mucosal injury was assessed by quantitative histology and the extent of macroscopic hemorrhage. Approximately one third of the total injury to the volume of the mucosa (11.8 +/- 9.1%) was due to ischemia alone. Another third was blocked by allopurinol or superoxide dismutase, catalase, and desferrioxamine (22.1 +/- 6.9%, P less than 0.001; and 25.9 +/- 4.6%, P less than 0.01), respectively, compared with control (32.5 +/- 5.1%). In contrast, extensive surface mucosal injury (62.2 +/- 27.6%) occurred primarily during ischemia and was not affected by antioxidants. Macroscopic hemorrhage was halved by treatment with allopurinol (17.5 +/- 12.6%, P less than 0.01) or superoxide dismutase, catalase, and desferrioxamine (15.9 +/- 14.5%, P less than 0.01). We conclude that temporary celiac occlusion results in gastric mucosal damage that consists of both ischemic and reperfusion components. The majority of surface mucosal injury occurred during ischemia, whereas injury to the volume of the mucosa and the vasculature occurred equally during reperfusion and was associated with reactive oxygen metabolites.

Introduction/Background Adults with chest pain presenting to an emergency department are high-risk and high-volume. A methodology which gathers practicing physicians together to review evidence and share practice experience to formulate a written algorithm with key decision points and measures is discussed with implementation, based on change management principles, and results. Methods A methodology was followed to “establish the standard-of-care”. Literature and data were reviewed, a written consensus algorithm was designed with ability to track adherence and deviations. We performed a before and after analysis of a performance improvement intervention in adult patients with undifferentiated chest pain in our nine-campus hospital system in Florida between January 1st, 2014 and December 31st, 2018. Results A total of 200,691 patients were identified as adults with chest pain and the algorithm was used. A dramatic change in the disposition decision rate was noted. When the ‘Baseline-Year’ was compared with the ‘Performance-Year’, chest pain patients discharged from the ED increased by 99%, those going to the ‘Observation’ status decreased by 20%, and inpatient admissions decreased by 63% ( p < 0.0001) All patients were tracked for 30-days for major adverse cardiac event (MACE) or return to the ED within the same system. If the s emergency physicians had not changed their practice/behavior and the Baseline-Year decision rate during the entire Performance-Year was unchanged, then 4563 more patients would have gone to Observation and 7986 patients to Inpatient. The opportunity costs avoided would be approximately $31million (US$. Conclusions For successful clinical transformation through change management, we learned: select strategic topics, get active physicians together, write a consensus algorithm with freedom to deviate, identify and remove barriers, communicate vision, pilot with feedback, implement, sustain by “hard wiring” into the electronic medical record and measure outputs.

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