title: Does pantoprazole protect against reperfusion injury following myocardial ischemia in rats?
abstract: BACKGROUND
  Myocardial ischemia is inadequate perfusion due to reduced blood flow. Sudden onset of reperfusion could result with damage to the myocytes that have not been affected during ischemia called ischemia reperfusion (I/R) injury. Extracellular accumulation of H+ ions resulting in tissue acidosis is one of the underlying mechanisms. Inhibition of myocardial H+/K+-ATPase, namely proton pump, may lead to intracellular acidification via decreasing the extracellular H+ transport.
  
  
  OBJECTIVE
  The aim of this study is to investigate the effects of a proton pump inhibitor pantoprazole in intact rat I/R models.
  
  
  METHODS
  A total of 30 adult male Wistar albino rats weighing 200-300 g were studied. Rats were allocated into four groups: sham (n=6), ischemia (n=8), control (n=8), and pantoprazole (n=8). Left anterior descending coronary artery was occluded for 30 minutes and then reperfused for two hours. Pantoprazole was administered via jugular vein at the dose of 9 mg/kg starting from 30 minutes before ischemia, to the first 30 minutes of reperfusion. Haemodynamic parameters were recorded and serum CK-MB levels were measured. After reperfusion, heart was removed for the measurement of myocardial infarct size. Myocardial infarct area was measured using triphenyltetrazolium chloride (TTC) staining technique. Myocardial infarction size were expressed as the percentage of the total left ventricular weight.
  
  
  RESULTS
  Compared with other groups, plasma concentrations of CK-MB at the end of ischemia and reperfusion and myocardial infarct size were significantly lower in pantoprazole group (p < 0.008).
  
  
  CONCLUSIONS
  Pantoprazole preconditioning induces delayed cardioprotection in intact rat I/R model, which may be triggered via H+/K+-ATPase ion channels.
authors: Department of Cardiology, Bezmialem Foundation University, Istanbul, Turkey. ahmetbacaxiz@gmail.com
authors: A
authors: A
authors: Bacaksiz
authors: M E
authors: ME
authors: Teker
authors: N
authors: N
authors: Buyukpinarbasili
authors: O
authors: O
authors: Inan
authors: A
authors: A
authors: Tasal
authors: O
authors: O
authors: Sonmez
authors: E
authors: E
authors: Erdogan
authors: M
authors: M
authors: Turfan
authors: O C
authors: OC
authors: Akdemir
authors: G
authors: G
authors: Ertas
mesh_terms: D053799:2-Pyridinylmethylsulfinylbenzimidazoles / Q000627:therapeutic use*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D052279:Creatine Kinase, MB Form / Q000097:blood; D017506:H(+)-K(+)-Exchanging ATPase / Q000502:physiology; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D017202:Myocardial Ischemia / Q000188:drug therapy* / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D000077402:Pantoprazole; D054328:Proton Pump Inhibitors; D051381:Rats; D017208:Rats, Wistar
chemical_list: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D054328:Proton Pump Inhibitors; D000077402:Pantoprazole; D052279:Creatine Kinase, MB Form; D017506:H(+)-K(+)-Exchanging ATPase