Doxorubicine-congestive heart failure-increased big endothelin-1 plasma concentration: reversal by amlodipine, losartan, and gastric pentadecapeptide BPC157 in rat and mouse.

  title={Doxorubicine-congestive heart failure-increased big endothelin-1 plasma concentration: reversal by amlodipine, losartan, and gastric pentadecapeptide BPC157 in rat and mouse.},
  author={Martina Lovri{\'c}-Ben{\vc}i{\'c} and Predrag Sikiric and Jadranka {\vS}eparovi{\'c} Han{\vz}eva{\vc}ki and Sven Seiwerth and Dunja Rogi{\'c} and Vesna Ku{\vs}ec and Gorana Aralica and Pa{\vs}ko Konjevoda and Lovorka Batelja and Alenka B. Blagaic},
  journal={Journal of pharmacological sciences},
  volume={95 1},
Overall, doxorubicine-congestive heart failure (CHF) (male Wistar rats and NMRI mice; 6 challenges with doxorubicine (2.5 mg/kg, i.p.) throughout 15 days and then a 4-week-rest period) is consistently deteriorating throughout next 14 days, if not reversed or ameliorated by therapy (/kg per day): a stable gastric pentadecapeptide BPC157 (GEPPPGKPADDAGLV, MW 1419, promisingly studied for inflammatory bowel disease (Pliva; PL 10, PLD-116, PL 14736)) (10 microg, 10 ng), losartan (0.7 mg… 

Tables from this paper

Mortal Furosemide-Hypokalemia-Disturbances in Rats NO-System Related Shorten Survival by L-NAME. Therapy Benefit with BPC 157 Peptide More Than With L-Arginine

L-NAME/L-arginine was mutual counteraction while BPC 157 completely eliminated L-NAME (arrhythmias, myoclonus, mortality), without an additive benefit when combined with L-argInine, which showed potentially effective therapeutic interventions for acute hypokalemia.

Stable Gastric Pentadecapeptide BPC 157 May Counteract Myocardial Infarction Induced by Isoprenaline in Rats

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.

Stable Gastric Pentadecapeptide BPC 157 Therapy for Monocrotaline-Induced Pulmonary Hypertension in Rats Leads to Prevention and Reversal

Pentadecapeptide BPC 157 prevents and counteracts monocrotaline-induced pulmonary arterial hypertension and cor pulmonale in rats.

Therapy Effect of the Stable Gastric Pentadecapeptide BPC 157 on Acute Pancreatitis as Vascular Failure-Induced Severe Peripheral and Central Syndrome in Rats

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.

Over-Dose Lithium Toxicity as an Occlusive-like Syndrome in Rats and Gastric Pentadecapeptide BPC 157

BPC 157 therapy overwhelmed high-dose lithium intoxication in rats and counteracted muscular weakness and prostration, in addition to edema and lesions in various brain areas, attenuating oxidative stress.

Pentadecapeptide BPC 157, in clinical trials as a therapy for inflammatory bowel disease (PL14736), is effective in the healing of colocutaneous fistulas in rats: role of the nitric oxide-system.

BPC 157 accelerated parenterally or perorally the healing of colonic and skin defect, leading to the suitable closure of the fistula, macro/microscopically, biomechanically, and functionally (larger water volume sustained without fistula leaking).

Pentadecapeptide BPC 157 Reduces Bleeding and Thrombocytopenia after Amputation in Rats Treated with Heparin, Warfarin, L-NAME and L-Arginine

Investigation of the effects of BPC 157 on the L-NAME- and L-arginine-induced hemostatic actions under different pathological condition and rescue against two different anticoagulants implicate a B PC 157 modulatory and balancing role with rescued NO-hemostatic mechanisms.



Role of endogenous endothelin in chronic heart failure: effect of long-term treatment with an endothelin antagonist on survival, hemodynamics, and cardiac remodeling.

Long-term treatment with an ET antagonist markedly increases survival in this rat model of CHF, and this increase in survival is associated with decreases in both preload and afterload and an increase in cardiac output as well as decreased LV hypertrophy, LV dilatation, and cardiac fibrosis.

Effects of amlodipine on nitric oxide synthase mRNA expression and coronary microcirculation in prolonged nitric oxide blockade-induced hypertensive rats.

NOS activity and eNOS mRNA were significantly increased by amlodipine in the left ventricle of L-NAME-induced hypertensive rats, and it was concluded that these increase NOSactivity and e NOS mRNA expression may play a role in the amelioration of coronary reserve and microvascular remodeling.

Beneficial effects of amlodipine in a murine model of congestive heart failure induced by viral myocarditis. A possible mechanism through inhibition of nitric oxide production.

Amlodipine appears to have a protective effect against myocardial injury in this animal model of congestive heart failure and may be in part resulting from inhibition of overproduction of NO.

Long-term 1-carnitine treatment prolongs the survival in rats with adriamycin-induced heart failure.

Preservation of the myocardial level of carnitine by 1-carnitine treatment prolonged survival of rats with adriamycin-induced failure by improving theMyocardial metabolism of fatty acids.

Endothelin concentrations in experimental sepsis: profiles of big endothelin and endothelin 1-21 in lethal peritonitis in rats.

In rats with peritonitis the profiles of big ET and ET 1-21 closely followed mortality, and blood concentrations of bacteria, endotoxin, TNF, IL-6, and lactate were closely followed.

The effects of losartan and enalapril therapies on the levels of nitric oxide, malondialdehyde, and glutathione in patients with essential hypertension.

Both losartan and enalapril may be regulators between oxidant stress and the antioxidant system and both systolic and diastolic pressure were significantly reduced.

Amlodipine releases nitric oxide from canine coronary microvessels: an unexpected mechanism of action of a calcium channel-blocking agent.

Amlodipine releases NO from blood vessels unlike nifedipine and diltiazem, and causes a dose-dependent increase in nitrite production that was similar in magnitude to that of either of the ACE inhibitors.