Stable Gastric Pentadecapeptide BPC 157 Therapy for Primary Abdominal Compartment Syndrome in Rats.
Tepes. Marijan M; Gojkovic. Slaven S; Krezic. Ivan I; Zizek. Helena H; Vranes. Hrvoje H; Madzar. Zrinko Z; Santak. Goran G; Batelja. Lovorka L; Milavic. Marija M; Sikiric. Suncana S; Kocman. Ivica I; Simonji. Karol K; Samara. Mariam M; Knezevic. Mario M; Barisic. Ivan I; Lovric. Eva E; Strbe. Sanja S; Kokot. Antonio A; Sjekavica. Ivica I; Kolak. Toni T; Skrtic. Anita A; Seiwerth. Sven S; Boban Blagaic. Alenka A; Sikiric. Predrag P
Key Findings
- BPC‑157 (10 µg or 10 ng/kg subcutaneously) quickly restored collapsed veins and improved venous collateral flow after severe intra‑abdominal hypertension.
- The peptide reduced dangerous blood‑pressure changes in the brain, portal, and caval systems and prevented severe ECG abnormalities.
- It prevented widespread organ damage—including gut lining loss, liver congestion, lung hemorrhage, heart infarction, kidney bleeding, and brain edema—seen in the untreated rats.
Practical Outcomes
- For biohackers, the data suggest BPC‑157 could be a powerful rescue agent in extreme abdominal pressure events, but the evidence is limited to rats. The study used a single low dose given shortly after injury, so any human protocol would be highly experimental and should await clinical trials.
Summary
In a rat study, giving the peptide BPC‑157 right after the abdomen was pressurized saved the animals from a cascade of life‑threatening problems. It reopened blocked veins, steadied blood pressure, stopped organ swelling, bleeding and heart rhythm issues, and protected the gut, liver, lungs, heart, kidneys and brain.
Abstract
Recently, the stable gastric pentadecapeptide BPC 157 was shown to counteract major vessel occlusion syndromes, i.e., peripheral and/or central occlusion, while activating particular collateral pathways. We induced abdominal compartment syndrome (intra-abdominal pressure in thiopental-anesthetized rats at 25 mmHg (60 min), 30 mmHg (30 min), 40 mmHg (30 min), and 50 mmHg (15 min) and in esketamine-anesthetized rats (25 mmHg for 120 min)) as a model of multiple occlusion syndrome. By improving the function of the venous system with BPC 157, we reversed the chain of harmful events. Rats with intra-abdominal hypertension (grade III, grade IV) received BPC 157 (10 µg or 10 ng/kg sc) or saline (5 ml) after 10 min. BPC 157 administration recovered the azygos vein via the inferior-superior caval vein rescue pathway. Additionally, intracranial (superior sagittal sinus), portal, and caval hypertension and aortal hypotension were reduced, as were the grossly congested stomach and major hemorrhagic lesions, brain swelling, venous and arterial thrombosis, congested inferior caval and superior mesenteric veins, and collapsed azygos vein; thus, the failed collateral pathway was fully recovered. Severe ECG disturbances (i.e., severe bradycardia and ST-elevation until asystole) were also reversed. Microscopically, transmural hyperemia of the gastrointestinal tract, intestinal mucosa villi reduction, crypt reduction with focal denudation of superficial epithelia, and large bowel dilatation were all inhibited. In the liver, BPC 157 reduced congestion and severe sinusoid enlargement. In the lung, a normal presentation was observed, with no alveolar membrane focal thickening and no lung congestion or edema, and severe intra-alveolar hemorrhage was absent. Moreover, severe heart congestion, subendocardial infarction, renal hemorrhage, brain edema, hemorrhage, and neural damage were prevented. In conclusion, BPC 157 cured primary abdominal compartment syndrome.
Study Information
pubmed
2021
2021-12-13T00:00:00.000Z
10.3389/fphar.2021.718147
24
111