Complex Syndrome of the Complete Occlusion of the End of the Superior Mesenteric Vein, Opposed with the Stable Gastric Pentadecapeptide BPC 157 in Rats

Abstract

Background. Gastric pentadecapeptide BPC 157 therapy in rats compensated irremovable occlusion of various vessels and counteracted the consequent multiorgan dysfunction syndromes by activation of the corresponding collateral bypassing loops. Thus, we used BPC 157 therapy against the irremovable occlusion of the end of the superior mesenteric vein. Methods. Assessments, for 30 min (gross recording, venography, ECG, pressure, microscopy, biochemistry, and oxidative stress) include the portal and caval hypertension, aortal hypotension, and centrally, the superior sagittal sinus hypertension, systemic arterial and venous thrombosis, ECG disturbances, MDA-tissue increase, and heart, lung, liver, kidney and gastrointestinal tract, in particular, and brain (cortex (cerebral, cerebellar), hypothalamus/thalamus, hippocampus) lesions. Rats received BPC 157 medication (10 µg/kg, 10 ng/kg) intraperitoneally at 1 or 15 min ligation time. Results. BPC 157 rapidly activated the superior mesenteric vein–inferior anterior pancreati-coduodenal vein–superior anterior pancreaticoduodenal vein–pyloric vein–portal vein pathway, reestablished superior mesenteric vein and portal vein connection and reestablished blood flow. Simultaneously, toward inferior caval vein, an additional pathway appears via the inferior mesenteric vein united with the middle colic vein, throughout its left colic branch to ascertain alternative bypassing blood flow. Consequently, BPC 157 acts peripherally and centrally, and counteracted the intracranial (superior sagittal sinus), portal and caval hypertension, aortal hypotension, ECG disturbances attenuated, abolished progressing venous and arterial thrombosis. Additionally, BPC 157 counteracted multiorgan dysfunction syndrome, heart, lung, liver, kidney and gastrointestinal tract, and brain lesions, and oxidative stress in tissues. Conclusion. BPC 157 therapy may be specific management also for the superior mesenteric vein injuries.

Robert’s Intragastric Alcohol-Induced Gastric Lesion Model as an Escalated General Peripheral and Central Syndrome, Counteracted by the Stable Gastric Pentadecapeptide BPC 157

“…We have theorized and reinforced the observation that the stable gastric pentadecapeptide BPC 157 has cytoprotective effects for the epithelium/endothelium against lesions induced by intragastric alcohol [4] and NSAIDs [9] due to the modulation of prostaglandins [9], the nitric oxide (NO) system [10] and the effects of vascular recovery on collateral pathways (for a review, see [5,6]). Overall, BPC 157 counteracts in this way the syndromes induced in rat models, in which major peripheral or central vessels were occluded [11][12][13][14][15][16][17]. Thus, we assumed that intragastric alcohol administration causes similar widespread dysfunction to that observed in rats after the occlusion of peripheral [11][12][13][14][15][16] and central [17] vessels.…”

“…Overall, BPC 157 counteracts in this way the syndromes induced in rat models, in which major peripheral or central vessels were occluded [11][12][13][14][15][16][17]. Thus, we assumed that intragastric alcohol administration causes similar widespread dysfunction to that observed in rats after the occlusion of peripheral [11][12][13][14][15][16] and central [17] vessels. These peripheral and central deficits include severe gastric lesions [4], intracranial (superior sagittal sinus) hypertension, brain swelling and lesions, portal and vena caval hypertension, aortal hypotension, peripheral and central thrombosis, inferior and superior vena caval congestion, azygos vein failure, electrocardiogram (ECG) disturbances, and heart, lung, liver and kidney lesions.…”

“…Therefore, we suggest that intragastric alcohol-induced endothelial lesions exhibit Virchow's triad-endothelial lesions, hypercoagulability and stasis-which should be counteracted by therapy provided inside and outside the stomach and gastrointestinal tract [5,6]. Indeed, BPC 157 treatment ameliorates Virchow's triad: it maintains the stomach's endothelial integrity against noxious agents [31]; prevents and reverses the development of thrombosis after abdominal aorta anastomosis [32], major vein occlusion [11,12,[14][15][16][17], artery occlusion [13] or combined vein and artery occlusion [16]; maintains thrombocyte function, without interfering with coagulation pathways [33][34][35]; and evidently counteracts the syndrome induced by major vessel occlusion [11][12][13][14][15][16][17].…”

“…For the reliable counteraction of intragastric absolute alcohol application leading to a full syndrome like that described in rats, with the occlusion of major vessels [11][12][13][14][15][16][17], BPC 157 served as a 'bypassing key' that can be applied to the injurious occlusion. This effect has been observed in inferior vena caval syndrome [11], the Pringle maneuver (portal triad temporary occlusion), ischemia/reperfusion [12], Budd-Chiari syndrome (suprahepatic inferior vena cava occlusion) [14], superior mesenteric artery occlusion syndrome [13,16], superior mesenteric vein occlusion syndrome [15,16], superior mesenteric artery and vein occlusion syndrome [16], and superior sagittal sinus occlusion syndrome [17].…”

“…For the reliable counteraction of intragastric absolute alcohol application leading to a full syndrome like that described in rats, with the occlusion of major vessels [11][12][13][14][15][16][17], BPC 157 served as a 'bypassing key' that can be applied to the injurious occlusion. This effect has been observed in inferior vena caval syndrome [11], the Pringle maneuver (portal triad temporary occlusion), ischemia/reperfusion [12], Budd-Chiari syndrome (suprahepatic inferior vena cava occlusion) [14], superior mesenteric artery occlusion syndrome [13,16], superior mesenteric vein occlusion syndrome [15,16], superior mesenteric artery and vein occlusion syndrome [16], and superior sagittal sinus occlusion syndrome [17]. The rapid vessel recruitment and the activation of collateral pathways (i.e., the left ovarian vein [11], inferior mesenteric vein [12,14], azygos vein [14], inferior and superior pancreaticoduodenal veins and pyloric vein [15], the inferior anterior pancreaticoduodenal artery and inferior mesenteric artery [13,16]) re-establish blood flow, thereby compensating for vessel occlusion [11][12][13][14][15][16][17][36][37][38][39].…”