engleski

BPC 157 counteracts gastric lesions developed in rats along with lithium-induced intracranial, portal and caval hypertension, liver, kidney and lung congestion, and venous and arterial thrombosis

im. We focused on the severe gastric lesions developed in rats along with over-dose lithiuminduced intracranial, portal and caval hypertension, liver, kidney, and lung congestion and arterial and venous thrombosis, and therapy with stable gastric pentadecapeptide BPC 157. Recently, we demonstrated that BPC 157 may counteract the adverse effects of the administration of the huge dose of lithium sulfate (500 mg/kg ip) in rats, which immediately produced severe syndrome (severe muscular weakness and prostration, reduced muscle fibers, myocardial infarction, and edema of various brain areas, the most prominent in the cerebral cortex). The worsening, which appeared with subsequent lithium applications was also counteracted by concomitant BPC 157 application (FASEB J, 33, S1, 822.4- 822.4). Methods. We applied lithium sulfate (500 mg/kg/day, ip, once daily through 3 subsequent days), and after lithium, medication (/kg, ip) (BPC 157, 10μg, 10 ng, or saline, 5 mL/kg), and assessments were carried out at 3 h after each lithium administration. Results. Lithium consistently (day 1, 3h – day 2 – day 3) induced intracranial hypertension (12±2 - 10±2 - 12±3 mmHg in superior sagittal sinus), portal (33±4 - 30±3 - 28±3 mmHg), and caval (21±3 – 18±2 – 22±2 mmHg) hypertension and aortal hypotension (63±3 - 70±3 - 75±5 mmHg). Grossly, we noted largely congested stomach and major hemorrhagic lesions (sum of the longest diameters 15±3 - 19±3 - 21±2 mm). Inferior caval and superior mesenteric veins were congested (volume over 120% of normal (day 3)), clot formation appeared in superior mesenteric vein (SMV) (0.01222±0.002 - 0.01452±0.007 - 0.0158±0.007 g) and superior mesenteric artery (SMA) (0.0065±0.0008 - 0.0099±0.0009 - 0.010±0.008 g). Furthermore, along with the severe muscular weakness and prostration, myocardial infarction, and edema of various brain areas, we noted, microscopically, in liver, cystic dilatation, and central veins congestion, in lung, large area of congestion and hemorrhage, and in kidney, degeneration of proximal and distal tubuli with cytoplasmic vacuolization. BPC 157 administration largely attenuated or even eliminated all lithium- induced disturbances (i.e., microscopically, only mild lung and liver congestion), intracranial hypertension in superior sagittal sinus (-5±2 - -6±2 - -7 ±2 mmHg), portal (6±2 - 7±2 - 8±2 mmHg), and caval (4±2 - 5±2 - 5±2 mmHg) hypertension and aortal hypotension (85±5 - 88±5 - 97±2 mmHg) and stomach hemorrhagic lesions (2±1 - 2±1 - 3±1 mm), venous and arterial thrombosis (0.0052±0.0009 - 0.0075±0.0007 - 0.0078±0.0007 g (SMV), 0.0042±0.0006 - 0.0015±0.0007 - 0.0012±0.0007 g (SMA)). Conclusion. BPC 157 counteracts gastric lesions along with lithium-induced intracranial, portal and caval hypertension, and aortal hypotension, liver, kidney and lung congestion, and venous and arterial thrombosis.

BPC 157 ; lithium toxicity ; gastric lesion ; thrombosis

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