Revista da Associacao Medica Brasileira (1992) · 2025
Cardiotoxic effects of pantoprazole in Wistar rats submitted to cardiac ischemia and reperfusion.
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Santos Adilson Costa Dos, Silva Celia Maria Camelo, Araújo Erisvaldo Amarante de, Sassi Lucas de Oliveira, Caixeta Adriano, Taha Murched Omar, Pires-Oliveira Marcelo, Caricati-Neto Afonso, Lopes Renato Delascio, Tallo Fernando Sabia, Menezes-Rodrigues Francisco Sandro
Аннотация
OBJECTIVE: The aim of the study was to evaluate the cardiotoxic effects of pantoprazole in Wistar rats submitted to cardiac ischemia and reperfusion.
METHODS: Cardiac ischemia and reperfusion was induced in rats through tourniquet of the left anterior descending coronary artery (10 min) followed by reperfusion (75 min). The incidences of ventricular arrhythmias, atrioventricular block, and lethality were evaluated by electrocardiogram analysis and compared between the control group (saline solution+cardiac ischemia and reperfusion) and the animals treated with pantoprazole 36 mg/kg (pantoprazole+cardiac ischemia and reperfusion), intravenously, immediately before cardiac ischemia (pantoprazole+cardiac ischemia and reperfusion) or before cardiac reperfusion (pantoprazole+cardiac reperfusion).
RESULTS: There were no differences between the incidences of ventricular arrhythmias in the groups studied. Treatment with pantoprazole before cardiac ischemia and reperfusion increased the incidence of atrioventricular block and lethality and myocardial injuries compared to the saline solution+cardiac ischemia and reperfusion group, but treatment of animals with pantoprazole before cardiac reperfusion decreased these parameters and serum creatine kinase-MB levels.
CONCLUSION: Our results indicate that when pantoprazole is administered before cardiac ischemia and reperfusion, it promotes cardiotoxicity; however, when administered before cardiac reperfusion, it promotes cardioprotection in Wistar rats.
METHODS: Cardiac ischemia and reperfusion was induced in rats through tourniquet of the left anterior descending coronary artery (10 min) followed by reperfusion (75 min). The incidences of ventricular arrhythmias, atrioventricular block, and lethality were evaluated by electrocardiogram analysis and compared between the control group (saline solution+cardiac ischemia and reperfusion) and the animals treated with pantoprazole 36 mg/kg (pantoprazole+cardiac ischemia and reperfusion), intravenously, immediately before cardiac ischemia (pantoprazole+cardiac ischemia and reperfusion) or before cardiac reperfusion (pantoprazole+cardiac reperfusion).
RESULTS: There were no differences between the incidences of ventricular arrhythmias in the groups studied. Treatment with pantoprazole before cardiac ischemia and reperfusion increased the incidence of atrioventricular block and lethality and myocardial injuries compared to the saline solution+cardiac ischemia and reperfusion group, but treatment of animals with pantoprazole before cardiac reperfusion decreased these parameters and serum creatine kinase-MB levels.
CONCLUSION: Our results indicate that when pantoprazole is administered before cardiac ischemia and reperfusion, it promotes cardiotoxicity; however, when administered before cardiac reperfusion, it promotes cardioprotection in Wistar rats.