Published online Nov 8, 2020. doi: 10.4292/wjgpt.v11.i5.93
Peer-review started: February 13, 2020
First decision: March 26, 2020
Revised: August 13, 2020
Accepted: September 10, 2020
Article in press: September 10, 2020
Published online: November 8, 2020
The excise parietal peritoneum with the underlying superficial layer of muscle tissue, since the very early events to the huge bowel adhesion, may represent a model relevant to adhesion-related obstruction and a considerable number of emergency surgical presentation. The downhill course can be counteracted with the recovery by the stable gastric pentadecapeptide BPC 157 and NO-system involvement. This may be the rapid recovery of the failed blood vessels after the initial injury induction. The previous studies of vascular occlusion reveal its particular effect on the occluded vessels, and bypassing of the occlusion, in the therapy of the deep vein thrombosis and colitis ischemia/reperfusion, duodenal venous congestion and cecum perforation, bile duct ligation-induced liver cirrhosis and portal hypertension rat injuries, Pringle maneuver ischemia and reperfusion (portal triad temporary occlusion) as well as Budd-Chiari syndrome (induced by the suprahepatic occlusion of the inferior caval vein). Also, the BPC 157 cytoprotective endothelium impact can have special importance. Namely, the peritoneal lining of the cavity serves as a conduit for the blood vessels that should be markedly disturbed by parietal peritoneum injury. Thus, we considered that BPC 157 therapy is suited for the realization of the peritoneal defect healing with minimal or no adhesion formation.
Adhesion-related obstruction accounts for a considerable number of emergency surgical presentation, and thereby, whatever mechanisms, the continued research for preventing is more than desirable. Therefore, BPC 157 therapy, establishing vessels-adhesions-BPC 157-NO-system relation, can be suited for the realization of the peritoneal defect healing with minimal or no adhesion formation.
The focus was on the possible therapeutic effect of the application of the stable gastric pentadecapeptide BPC 157, and NO-agents, L-NAME, and L-arginine after the creation of a particular defect by excision of parietal peritoneum with an underlying superficial layer of muscle tissue in rats. The revealing focus was on the formation of the adhesion, which could extensively occupy and obstruct the abdominal wall and intestine and pelvic organs, with respect to the initial defect creation, and the early blood vessels presentation in and close to the peritoneal defect. The support was the presentation of the MDA- and NO-tissue level in adhesion tissues.
In the rats with the excised parietal peritoneum with the underlying superficial layer of muscle tissue, we suggest that this formation of adhesion would be an effect on the NO-system and that the BPC 157 beneficial effect would be an effect related to the NO-system.
The medication was BPC 157, L-NAME, L-arginine administered alone or in combinations. The medication was applied either once, at 1 min after defect creation as an abdominal bath (1 mL /rat) to perceive the initial post-injury course, blood vessel presentation (assessed by USB microscope camera, the blood vessels presentation augmentation/reduction to perceive subsequent course leading to the adhesion formation). Application was intraperitoneally once daily, first application at 30 min after surgery, last application 24 h before assessment. Alternatively, from day 7, BPC 157 was given intraperitoneally once daily as a postponed therapy to pre-existing adhesion. At these points in the injured tissue (gross and microscopy assessment), levels of MDA and NO were also assessed.
After parietal peritoneum excision with an underlying superficial layer of muscle tissue in rats, there is failed vasculature, and finally, increased adhesion formation. NO-agents, L-NAME and/or L-arginine have diverse effects, the initial weakening of blood vessel disappearance and finally, severe worsening of adhesions (L-NAME) vs the initial weakening of blood vessel disappearance and finally, attenuation of adhesions formation (L-arginine), which counteract each other response given together. The application of the stable gastric pentadecapeptide BPC 157 with its most recent described vascular effects (“vascular recruitment”) recovers abundant vascular vessel presentation in and close to the defect, which occurs rapidly. Finally, BPC 157 attenuated bowel adhesion formation and NO- and MDA-tissue values.
BPC 157 therapy can be suited for the realization of the peritoneal defect healing with minimal or no adhesion formation. In practical BPC 157 therapy realization, establishing vessels-adhesions-BPC 157-NO-system relation may be important. Finally, BPC 157, with LD1 not achieved, implemented in inflammatory bowel disease trials, with a particular effect on vessel presentation and counteracting effect on NO-agents harmful effect, free radical formation, and NO-values normalization, should be the practical hallmark of the further therapy to avoid adhesion formation.
This study of abdominal wall injury has basic relationships, such as more vascular failure (vessels, since empty “disappear”) at a very early post-injury period, as the more failed outcome (i.e., the huge adhesion formation). MDA values and NO-levels increased at the initial abdominal wall defect, and thus increase during subsequent adhesions. On the contrary, the possible recovering effect is that the filled vessels “reappear”; adhesion formation attenuated. Decreasing of the increased NO- and MDA- values match with the beneficial outcome (less adhesion formation). Only the BPC 157 therapy in the damaged abdominal wall healing fulfils this combined beneficial effect. The very rapid activation of the blood vessels in the initial defect likely circumvents subsequent negative chain of events and results in the resolution of the adhesion and obstruction, decreasing of the increased NO- and MDA values match with the beneficial outcome (less adhesion formation).