Published online Jul 21, 2023. doi: 10.3748/wjg.v29.i27.4289
Peer-review started: February 19, 2023
First decision: May 23, 2023
Revised: June 1, 2023
Accepted: June 19, 2023
Article in press: June 19, 2023
Published online: July 21, 2023
Taking stomach perforation as a prime direct injury regularly used in cytoprotection studies, as a new insight in resolving the full extent of the cytoprotection issue, there is the rapid progression of severe occlusion/occlusion-like syndrome considerably complicating the course following stomach perforation in rats. Otherwise, such occlusion/occlusion-like syndrome may suffer rats with permanent occlusion of the major vessel(s), veins and/or arteries, peripherally and centrally, and rats who underwent similar noxious procedures that all severely affect endothelium function. There were cause-consequence lesions in the brain (intracerebral and intraventricular hemorrhage), heart (congestion), lung (hemorrhage), congestion in the liver, kidney, and gastrointestinal tract, arrhythmias, vessel failure (congested inferior caval and superior mesenteric vein, collapsed azygos vein), and blood pressure disturbances (intracranial (superior sagittal sinus), portal and caval hypertension, and aortal hypotension), and widespread thrombosis, peripherally and centrally.
In occlusion/occlusion-like syndromes, stable gastric pentadecapeptide BPC 157 was recognized as counteracting therapy, and has already presented in recent reviews (Curr Med Chem 2023; 30: 1568-1573; World J Gastroenterol 2022; 28: 23-46). In the rats with perforated stomachs, and subsequent occlusion/occlusion-like syndrome, we emphasized the cytoprotection potential of the stable gastric BPC 157 as native and stable in gastric juice, thought to play the role of cytoprotection mediator maintaining stomach mucosa integrity. As a particular clue recognized also in the counteraction of stomach perforation-induced occlusion/occlusion-like syndromes, there was activation of collateral pathways depending on the injury, locally (raised vessel presentation; less bleeding, defect contraction) and systemically. Accordingly, BPC 157 therapy induced direct blood delivery from the inferior caval vein to the superior caval vein via the azygos vein. Application of the BPC 157 therapy (10 µg/kg and 10 ng/kg) into the perforated defect, induced immediate shrinking and contraction of the whole stomach. Simultaneously, there were attenuated/eliminated 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, and the severe lesions in the brain, heart (congestion and arrhythmias), lung (hemorrhage and congestion) and marked congestion in the liver, kidney and gastrointestinal tract markedly reduced. In conclusion, with stomach perforation severe occlusion/occlusion-like syndrome, and rapid progression peripherally and centrally, the rapid counteraction should be by BPC 157 therapy.
The first objective was stomach perforation presentation in rats as severe occlusion/occlusion-like syndrome, peripherally and centrally. The second objective was rapid counteraction by BPC 157 therapy.
In deeply anesthetized rats underwent calvariectomy, stomach perforation was performed and rats received BPC 157 therapy or saline into the defect in the stomach. Then, in addition to assessing shrinking and contraction/enlargement of the whole stomach, the assessment (gross and microscopy, volume) was as in the occlusion/occlusion-like studies and included all points regularly analyzed. Assessed were swollen brain, failed peripheral vessels (azygos vein, superior mesenteric vein, portal vein, inferior caval vein) and heart, other organs lesions (i.e., stomach, defect closing or widening); intracranial (superior sagittal sinus), portal and caval hypertension, aortal hypotension; clots peripherally and centrally; ECGs; and bleeding time from the perforation(s).
BPC 157 effects accord with the beneficial effect noted before in the healing of the perforated defect (raised vessel presentation; less bleeding, defect contraction) and in the occlusion/occlusion-like syndromes. In rats with perforated stomachs, BPC 157 therapy (10 µg/kg and 10 ng/kg) given into the perforated defect, induced immediate shrinking and contraction of the whole stomach (unlike saline-induced immediate stomach considerable enlargement). There were cause-consequence lesions all eliminated/attenuated by BPC 157 therapy (i.e., direct blood flow delivery via azygos vein). There were eliminated/attenuated lesions in the brain (i.e., swelling, hemorrhage), heart (congestion), lung (hemorrhage), congestion in the liver, kidney, and gastrointestinal tract, arrhythmias, and blood pressure disturbances (intracranial (superior sagittal sinus), portal and caval hypertension, and aortal hypotension). Counteracted was major vessel failure (i.e., reversal of congested inferior caval vein and superior mesenteric vein, collapsed azygos vein), and eliminated widespread thrombosis, peripherally and centrally.
Stomach perforation occurred as severe occlusion/occlusion-like syndrome, peripherally and centrally. Rapid counteraction was by BPC 157 therapy. Thereby, further BPC 157 therapy may be warranted.
Stomach perforation as severe occlusion/occlusion-like syndrome needs immediate additional medical attention. There, BPC 157, as a prototype cytoprotective agent, should be also considered as further therapy.