Occlusion of the Superior Mesenteric Artery in Rats Reversed by Collateral Pathways Activation: Gastric Pentadecapeptide BPC 157 Therapy Counteracts Multiple Organ Dysfunction Syndrome; Intracranial, Portal, and Caval Hypertension; and Aortal Hypotension.
Knezevic. Mario M; Gojkovic. Slaven S; Krezic. Ivan I; Zizek. Helena H; Malekinusic. Dominik D; Vrdoljak. Borna B; Vranes. Hrvoje H; Knezevic. Tamara T; Barisic. Ivan I; Horvat Pavlov. Katarina K; Drmic. Domagoj D; Staroveski. Miro M; Djuzel. Antonija A; Rajkovic. Zoran Z; Kolak. Toni T; Kocman. Ivica I; Lovric. Eva E; Milavic. Marija M; Sikiric. Suncana S; Tvrdeic. Ante A; Patrlj. Leonardo L; Strbe. Sanja S; Kokot. Antonio A; Boban Blagaic. Alenka A; Skrtic. Anita A; Seiwerth. Sven S; Sikiric. Predrag P
Key Findings
- BPC‑157 rapidly activates collateral vessels (pancreaticoduodenal and inferior mesenteric arteries) to bypass a blocked superior mesenteric artery.
- Treatment markedly reduces portal, caval, and central venous hypertension as well as aortal hypotension.
- The peptide almost eliminates arterial and venous thrombosis and lessens damage to multiple organs, including the brain.
Practical Outcomes
- For biohackers, the study hints that BPC‑157 may support vascular health and tissue repair after acute blood‑flow loss, but it was only tested in rats with a severe surgical model. While the dose used (10 µg or 10 ng in an abdominal bath) is not directly translatable, the findings encourage cautious exploration of BPC‑157 for circulatory support, especially in gut‑related injuries. More human data are needed before adopting it as a standard protocol.
Summary
In a rat study, a short burst of the peptide BPC‑157 was applied after the main gut artery was blocked. The peptide quickly opened up tiny backup blood vessels, lowered dangerous blood‑pressure spikes, reduced clot formation, and protected the heart, lungs, liver, gut and brain from damage. The results suggest BPC‑157 can help the body reroute blood flow and limit organ injury after a severe vascular blockage.
Abstract
Gastric pentadecapeptide BPC 157 therapy counteracts multiple organ dysfunction syndrome in rats, which have permanent occlusion of the superior mesenteric artery close to the abdominal aorta. Previously, when confronted with major vessel occlusion, its effect would rapidly activate collateral vessel pathways and resolve major venous occlusion syndromes (Pringle maneuver ischemia, reperfusion, Budd-Chiari syndrome) in rats. This would overwhelm superior mesenteric artery permanent occlusion, and result in local, peripheral, and central disturbances. <b>Methods:</b> Assessments, for 30 min (gross recording, angiography, ECG, pressure, microscopy, biochemistry, and oxidative stress), included the portal hypertension, caval hypertension, and aortal hypotension, and centrally, the superior sagittal sinus hypertension; systemic arterial and venous thrombosis; ECG disturbances; MDA-tissue increase; and multiple organ lesions and disturbances, including the heart, lung, liver, kidney, and gastrointestinal tract, in particular, as well as brain (cortex (cerebral, cerebellar), hypothalamus/thalamus, hippocampus). BPC 157 therapy (/kg, abdominal bath) (10 µg, 10 ng) was given for a 1-min ligation time. <b>Results:</b> BPC 157 rapidly recruits collateral vessels (inferior anterior pancreaticoduodenal artery and inferior mesenteric artery) that circumvent occlusion and ascertains blood flow distant from the occlusion in the superior mesenteric artery. Portal and caval hypertension, aortal hypotension, and, centrally, superior sagittal sinus hypertension were attenuated or eliminated, and ECG disturbances markedly mitigated. BPC 157 therapy almost annihilated venous and arterial thrombosis. Multiple organ lesions and disturbances (i.e., heart, lung, liver, and gastrointestinal tract, in particular, as well as brain) were largely attenuated. <b>Conclusions</b>: Rats with superior mesenteric artery occlusion may additionally undergo BPC 157 therapy as full counteraction of vascular occlusion-induced multiple organ dysfunction syndrome.
Study Information
pubmed
2021
2021-05-26T00:00:00.000Z
10.3390/biomedicines9060609
27
87