BACKGROUND Using rat stomach perforation as a prototypic direct lesion applied in cytoprotection research,we focused on the first demonstration of the severe occlusion/occlusion-like syndrome induced by stomach perfor...BACKGROUND Using rat stomach perforation as a prototypic direct lesion applied in cytoprotection research,we focused on the first demonstration of the severe occlusion/occlusion-like syndrome induced by stomach perforation.The revealed stomachinduced occlusion/occlusion-like syndrome corresponds to the previously described occlusion/occlusion-like syndromes in rats suffering multicausal pathology and shared severe vascular and multiorgan failure.This general point was particularly reviewed.As in all the described occlusion/occlusion-like syndromes with permanent occlusion of major vessels,peripheral and central,and other similar noxious procedures that severely affect endothelium function,the stable gastric pentadecapeptide BPC 157 was resolving therapy.AIM To reveal the stomach perforation-induced general occlusion/occlusion-like syndrome and BPC 157 therapy effect.METHODS The procedure included deeply anesthetized rats,complete calvariectomy,laparotomy at 15 min thereafter,and stomach perforation to rapidly induce vascular and multiorgan failure occlusion/occlusion-like syndrome.At 5 min post-perforation time,rats received therapy[BPC 157(10μg or 10 ng/kg)or saline(5 mL/kg,1 mL/rat)(controls)]into the perforated defect in the stomach).Sacrifice was at 15 min or 60 min post-perforation time.Assessment(gross and microscopy;volume)included:Brain swelling,peripheral vessels(azygos vein,superior mesenteric vein,portal vein,inferior caval vein)and heart,other organs lesions(i.e.,stomach,defect closing or widening);superior sagittal sinus,and peripherally the portal vein,inferior caval vein,and abdominal aorta blood pressures and clots;electrocardiograms;and bleeding time from the perforation(s).RESULTS BPC 157 beneficial effects accord with those noted before in the healing of the perforated defect(raised vessel presentation;less bleeding,defect contraction)and occlusion/occlusion-like syndromes counteraction.BPC 157 therapy(into the perforated defect),induced immediate shrinking and contraction of the whole stomach(unlike considerable enlargement by saline application).Accordingly,BPC 157 therapy induced direct blood delivery via the azygos vein,and attenuated/eliminated the intracranial(superior sagittal sinus),portal and caval hypertension,and aortal hypotension.Thrombosis,peripherally(inferior caval vein,portal vein,abdominal aorta)and centrally(superior sagittal sinus)BPC 157 therapy markedly reduced/annihilated.Severe lesions in the brain(swelling,hemorrhage),heart(congestion and arrhythmias),lung(hemorrhage and congestion),and marked congestion in the liver,kidney,and gastrointestinal tract were markedly reduced.CONCLUSION We revealed stomach perforation as a severe occlusion/occlusion-like syndrome,peripherally and centrally,and rapid counteraction by BPC 157 therapy.Thereby,further BPC 157 therapy may be warranted.展开更多
AIM To elucidate the epidemiological characteristics and associated risk factors of perforated peptic ulcer(PPU).METHODS We retrospectively reviewed medical records of patients who were diagnosed with benign PPU from ...AIM To elucidate the epidemiological characteristics and associated risk factors of perforated peptic ulcer(PPU).METHODS We retrospectively reviewed medical records of patients who were diagnosed with benign PPU from 2010 through 2015 at 6 Hallym university-affiliated hospitals.RESULTS A total of 396 patients were identified with postoperative complication rate of 9.1% and mortality rate of 0.8%. Among 174(43.9%) patients who were examined for Helicobacter pylori(H. pylori) infection, 78(44.8%) patients were positive for H. pylori infection, 21(12.1%) were on non-steroidal anti-inflammatory drugs(NSAIDs) therapy, and 80(46%) patients were neither infected of H. pylori nor treated by any kinds of NSAIDs. Multivariate analysis indicated that older age(OR = 1.09, 95%CI: 1.04-1.16) and comorbidity(OR = 4.11, 95%CI: 1.03-16.48) were risk factors for NSAID-associated PPU compared with non-H. pylori, non-NSAID associated PPU and older age(OR = 1.04, 95%CI: 1.02-1.07) and alcohol consumption(OR = 2.08, 95%CI: 1.05-4.13) were risk factors for non-H. pylori, non-NSAID associated PPU compared with solely H. pylori positive PPU.CONCLUSION Elderly patients with comorbidities are associated with NSAIDs-associated PPU. Non-H. pylori, non-NSAID peptic ulcer is important etiology of PPU and alcohol consumption is associated risk factor.展开更多
文摘BACKGROUND Using rat stomach perforation as a prototypic direct lesion applied in cytoprotection research,we focused on the first demonstration of the severe occlusion/occlusion-like syndrome induced by stomach perforation.The revealed stomachinduced occlusion/occlusion-like syndrome corresponds to the previously described occlusion/occlusion-like syndromes in rats suffering multicausal pathology and shared severe vascular and multiorgan failure.This general point was particularly reviewed.As in all the described occlusion/occlusion-like syndromes with permanent occlusion of major vessels,peripheral and central,and other similar noxious procedures that severely affect endothelium function,the stable gastric pentadecapeptide BPC 157 was resolving therapy.AIM To reveal the stomach perforation-induced general occlusion/occlusion-like syndrome and BPC 157 therapy effect.METHODS The procedure included deeply anesthetized rats,complete calvariectomy,laparotomy at 15 min thereafter,and stomach perforation to rapidly induce vascular and multiorgan failure occlusion/occlusion-like syndrome.At 5 min post-perforation time,rats received therapy[BPC 157(10μg or 10 ng/kg)or saline(5 mL/kg,1 mL/rat)(controls)]into the perforated defect in the stomach).Sacrifice was at 15 min or 60 min post-perforation time.Assessment(gross and microscopy;volume)included:Brain swelling,peripheral vessels(azygos vein,superior mesenteric vein,portal vein,inferior caval vein)and heart,other organs lesions(i.e.,stomach,defect closing or widening);superior sagittal sinus,and peripherally the portal vein,inferior caval vein,and abdominal aorta blood pressures and clots;electrocardiograms;and bleeding time from the perforation(s).RESULTS BPC 157 beneficial effects accord with those noted before in the healing of the perforated defect(raised vessel presentation;less bleeding,defect contraction)and occlusion/occlusion-like syndromes counteraction.BPC 157 therapy(into the perforated defect),induced immediate shrinking and contraction of the whole stomach(unlike considerable enlargement by saline application).Accordingly,BPC 157 therapy induced direct blood delivery via the azygos vein,and attenuated/eliminated the intracranial(superior sagittal sinus),portal and caval hypertension,and aortal hypotension.Thrombosis,peripherally(inferior caval vein,portal vein,abdominal aorta)and centrally(superior sagittal sinus)BPC 157 therapy markedly reduced/annihilated.Severe lesions in the brain(swelling,hemorrhage),heart(congestion and arrhythmias),lung(hemorrhage and congestion),and marked congestion in the liver,kidney,and gastrointestinal tract were markedly reduced.CONCLUSION We revealed stomach perforation as a severe occlusion/occlusion-like syndrome,peripherally and centrally,and rapid counteraction by BPC 157 therapy.Thereby,further BPC 157 therapy may be warranted.
文摘AIM To elucidate the epidemiological characteristics and associated risk factors of perforated peptic ulcer(PPU).METHODS We retrospectively reviewed medical records of patients who were diagnosed with benign PPU from 2010 through 2015 at 6 Hallym university-affiliated hospitals.RESULTS A total of 396 patients were identified with postoperative complication rate of 9.1% and mortality rate of 0.8%. Among 174(43.9%) patients who were examined for Helicobacter pylori(H. pylori) infection, 78(44.8%) patients were positive for H. pylori infection, 21(12.1%) were on non-steroidal anti-inflammatory drugs(NSAIDs) therapy, and 80(46%) patients were neither infected of H. pylori nor treated by any kinds of NSAIDs. Multivariate analysis indicated that older age(OR = 1.09, 95%CI: 1.04-1.16) and comorbidity(OR = 4.11, 95%CI: 1.03-16.48) were risk factors for NSAID-associated PPU compared with non-H. pylori, non-NSAID associated PPU and older age(OR = 1.04, 95%CI: 1.02-1.07) and alcohol consumption(OR = 2.08, 95%CI: 1.05-4.13) were risk factors for non-H. pylori, non-NSAID associated PPU compared with solely H. pylori positive PPU.CONCLUSION Elderly patients with comorbidities are associated with NSAIDs-associated PPU. Non-H. pylori, non-NSAID peptic ulcer is important etiology of PPU and alcohol consumption is associated risk factor.
