Rat inferior caval vein (ICV) ligature and particular new insights with the stable gastric pentadecapeptide BPC 157

BPC 157 Cytoprotection (cytoprotection concept in damaged stomach interpreted as endothelium recovery toward epithelium recovery [1]involves controlling functions of two defensive systems, prostaglandins (PGs)-system (BPC 157 counteracts large scale of toxicity induced by NSAIDs, both COX 1-blockers and COX -blockers [4])and NO-system ([5]; [6]; [7]) (in addition to preserve endothelium maintenance (a common point for all cytoprotective agents to induce stomach cytoprotection [1]), BPC 157 induces NO-release from stomach tissue homogenates [11]). With major vessel essential obstruction, such as ICV, this particular endothelium protection should be generalized toward particular activation of blood vessels, seen once obstructed, with particular collateral vessels recruitment to bypass obstruction. Rapidly activated bypassing loop (LOV and other collaterals) and ligation-stop effectively bypassed may be likely related to the BPC 157 ability to interact with NO-system in different models and species and modulate its function as seen in particular with the counteraction of L-NAME-hypertension as well as counteraction of L-arginine-hypotension ([5]; [6]; [7]; [11]). Likely along with the proposed involvement of the defensive systems, PGs-system and NO-system in BPC 157 endothelium protection in cytoprotection ([1]; [4]; [5]; [6]; [7]; [11]), should be the effects of the BPC 157 on bleeding disorders ([13]; [34]; [35]), providing prevention and reversal of thrombosis after abdominal aorta anastomosis [13] as well as counteraction of prolonged bleeding and thrombocytopenias after amputation and anticoagulants (heparin, warfarin, aspirin) application, thought to be NO-system related ([34]; [35]), and thereby, in ICV rats BPC 157 did not affect clotting parameters, thereby, attenuated thrombocytopenia and bleeding upon injury. Finally, further attention merits the evidence that with BPC 157 administration in rats which underwent ligation of ICV, these beneficial effects were combined with the altered EGR, NOS, SRF, VEGR and KRAS: increased (EGR, NOS, SRF, KRAS) or decreased (EGR, VEGFR, PLCÉ£), while AKT1 remained unchanged in the ICV, as well as in the ROV and LOV. Consequently, particular pathways with both local and systemic relevance could be suggested. Of note, in ischemic colitis model induced by two ligations on left colic artery and vein, upon BPC 157 administration ligation-stops were effectively bypassed, interconnected loop of intestinal arcade vessels presented particular collateral vessels recruitment to bypass obstruction [36].316