Abstract
We revealed that the stable gastric pentadecapeptide BPC 157, a useful peptide therapy against isoprenaline myocardial infarction, as well as against isoprenaline myocardial reinfarction, may follow the counteraction of the recently described occlusion-like syndrome, induced peripherally and centrally, which was described for the first time in isoprenaline-treated rats. BPC 157 (10 ng/kg, 10 µg/kg i.p.), L-NAME (5 mg/kg i.p.), and L-arginine (200 mg/kg i.p.) were given alone or together at (i) 30 min before or, alternatively, (ii) at 5 min after isoprenaline (75 or 150 mg/kg s.c.). At 30 min after isoprenaline 75 mg/kg s.c., we noted an early multiorgan failure (brain, heart, lung, liver, kidney and gastrointestinal lesions), thrombosis, intracranial (superior sagittal sinus) hypertension, portal and caval hypertension, and aortal hypotension, in its full presentation (or attenuated by BPC 157 therapy (given at 5 min after isoprenaline) via activation of the azygos vein). Further, we studied isoprenaline (75 or 150 mg/kg s.c.) myocardial infarction (1 challenge) and reinfarction (isoprenaline at 0 h and 24 h, 2 challenges) in rats (assessed at the end of the subsequent 24 h period). BPC 157 reduced levels of all necrosis markers, CK, CK-MB, LDH, and cTnT, and attenuated gross (no visible infarcted area) and histological damage, ECG (no ST-T ischemic changes), and echocardiography (preservation of systolic left ventricular function) damage induced by isoprenaline. Its effect was associated with a significant decrease in oxidative stress parameters and likely maintained NO system function, providing that BPC 157 interacted with eNOS and COX2 gene expression in a particular way and counteracted the noxious effect of the NOS-blocker, L-NAME.
Highlights
Isoprenaline myocardial infarction in rats is known to be a rapid, simple and noninvasive method that produces myocardial damage similar to that seen in acute myocardial infarction in humans [1]
BPC 157, we challenge the possibility that the stable gastric pentadecapeptide BPC 157, as a useful peptide therapy against isoprenaline myocardial infarction, as well as against isoprenaline myocardial reinfarction, should follow the activation of the collateral rescuing pathways seeable for the counteraction of the recently described occlusion-like syndrome, induced peripherally and centrally, that would appear in the isoprenaline-treatedrats, being decisive for further full myocardial infarction development
Our approach was the BPC 157 therapy effect in the study of the permanent occlusion of major vessels-induced occlusion syndromes [14,15,16,17,18,19,20], the “occlusion-like” syndrome induced by severe intoxication [21,22] or maintained severe intra-abdominal hypertension [23] recovered with the activation of the collateral pathways [14,15,16,17,18,19,20,21,22,23]
Summary
Isoprenaline myocardial infarction in rats is known to be a rapid, simple and noninvasive method that produces myocardial damage similar to that seen in acute myocardial infarction in humans [1]. There is a rapid effect of BPC 157 therapy on heart disturbances in studies of the permanent occlusion of major vessels-induced occlusion syndromes [14,15,16,17,18,19,20], “occlusion-like” syndrome induced by severe intoxication (alcohol, lithium) [21,22] and intra-abdominal hypertension [23], recovered with the activation of the collateral pathways to compensate vascular failure [14,15,16,17,18,19,20,21,22,23]. There is compelling evidence that BPC 157 therapy exerted both a prophylactic and curative effect
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