9 research outputs found
Su1539 – Pentadecapeptide Bpc 157 Counteracts Portal Hypertension, Caval Hypertension and Aortal Hypotension in Rats with Suprahepatic Occlusion of Inferior Caval Vein (Budd-Chiari Syndrome) in Rats
Su1525 – Suprahepatic Inferior Caval Vein Occlusion and Reperfusion in Rats Induced Portal and Caval Hypertension, Aortic Hypotension, and Esophageal Bleeding. Therapy with Pentadecapeptide Bpc 157
Su1534 – Bpc 157 Given During Reperfusion Counteracts Portal Hypertension, Caval Hypertension and Aortal Hypotension in Rats Used to Have Portal Triad Obstruction (Pringle Maneuver)
Su1526 – Complications of Portal Triad Obstruction and Reperfusion in Rats. Pentadecapeptide Bpc 157 Counteracts Venous and Arterial Thrombosis and Arrhythmias
Su1529 – Portal Triad Obstruction and Reperfusion in Rats Induced the Hemorrhagic Congestion in the Stomach, Duodenum, Jejunum, Cecum, Colon, and Esophageal Bleeding. Pentadecapeptide Bpc 157 Counteracts These Complications Along with Portal Hypertension
Su1531 – Splenectomy in Rats Induced Portal and Caval Hypertension, Aortic Hypotension, Venous Thrombosis, Peaked P Waves and Tachycardia. Therapy with Pentadecapeptide Bpc 157
Mo1101 – Superior Mesenteric Vein Occlusion in Rats Induced Portal and Caval Hypertension, Aortic Hypotension, and Peaked P Waves, Tachycardia. Therapy with Pentadecapeptide Bpc 157. Bypassing Pathway to Circumvent Venous Occlusion
Therapy Effect of the Stable Gastric Pentadecapeptide BPC 157 on Acute Pancreatitis as Vascular Failure-Induced Severe Peripheral and Central Syndrome in Rats
We revealed the therapy effect of the stable gastric pentadecapeptide BPC 157 (10 μg/kg, 10 ng/kg ig or po) with specific activation of the collateral rescuing pathways, the azygos vein, on bile duct ligation in particular, and acute pancreatitis as local disturbances (i.e., improved gross and microscopy presentation, decreased amylase level). Additionally, we revealed the therapy’s effect on the acute pancreatitis as vascular failure and multiorgan failure, both peripherally and centrally following “occlusion-like” syndrome, major intoxication (alcohol, lithium), maintained severe intra-abdominal hypertension, and myocardial infarction, or occlusion syndrome, and major vessel occlusion. The application-sacrifice periods were ligation times of 0–30 min, 0–5 h, 0–24 h (cured periods, early regimen) and 4.30 h–5 h, 5 h–24 h (cured periods, delayed regimen). Otherwise, bile duct-ligated rats commonly presented intracranial (superior sagittal sinus), portal and caval hypertension and aortal hypotension, gross brain swelling, hemorrhage and lesions, heart dysfunction, lung lesions, liver and kidney failure, gastrointestinal lesions, and severe arterial and venous thrombosis, peripherally and centrally. Unless antagonized with the key effect of BPC 157 regimens, reversal of the inferior caval and superior mesenteric vein congestion and reversal of the failed azygos vein activated azygos vein-recruited direct delivery to rescue the inferior-superior caval vein pathway; these were all antecedent to acute pancreatitis major lesions (i.e., acinar, fat necrosis, hemorrhage). These lesions appeared in the later period, but were markedly attenuated/eliminated (i.e., hemorrhage) in BPC 157-treated rats. To summarize, while the innate vicious cycle may be peripheral (bile duct ligation), or central (rapidly developed brain disturbances), or peripheral and central, BPC 157 resolved acute pancreatitis and its adjacent syndrome
Stable Gastric Pentadecapeptide BPC 157 and Striated, Smooth, and Heart Muscle
First, we review the definitively severed myotendinous junction and recovery by the cytoprotective stable gastric pentadecapeptide BPC 157 therapy, its healing that might combine both transected and detached tendon and transected muscle, ligament and bone injuries, applied alone, as native peptide therapy, effective in rat injury, given intraperitoneally or in drinking water or topically, at the site of injury. As a follow up, we reviewed that with the BPC 157 therapy, its cytoprotective ability to organize simultaneous healing of different tissues of and full recovery of the myotendinous junction might represent the particular muscle therapy against distinctive etiopathology muscle disabilities and weakness. In this, BPC 157 therapy might recover many of muscle disabilities (i.e., succinylcholine, vascular occlusion, spinal cord compression, stroke, traumatic brain injury, severe electrolyte disturbances, neurotoxins, neuroleptics, alcohol, serotonin syndrome and NO-system blockade and tumor-cachexia). These might provide practical realization of the multimodal muscle-axis impact able to react depending on the condition and the given agent(s) and the symptoms distinctively related to the prime injurious cause symptoms in the wide healing concept, the concept of cytoprotection, in particular. Further, the BPC 157 therapy might be the recovery for the disabled heart functioning, and disabled smooth muscle functioning (various sphincters function recovery). Finally, BPC 157, native and stable in human gastric juice, might be a prototype of anti-ulcer cytoprotective peptide for the muscle therapy with high curing potential (very safe profile (lethal dose not achieved), with suited wide effective range (µg-ng regimens) and ways of application)