Pantoprazol oferece proteção miocárdica semelhante ao pré-condicionamento isquêmico

Gomes, Otoni Moreira; Magalhães, Mônica de Mônico; Abrantes, Rafael Diniz; Kallás, Elias

doi:10.5935/1678-9741.20110019

Rev Bras Cir Cardiovasc

2011

DOI: 10.5935/1678-9741.20110019

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Pantoprazol oferece proteção miocárdica semelhante ao pré-condicionamento isquêmico

Otoni Moreira Gomes¹,

Mônica de Mônico Magalhães²,

Rafael Diniz Abrantes³

et al.

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Cited by 5 publications

References 28 publications

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Chronic Pantoprazole Administration and Ischemia–Reperfusion Arrhythmias In Vivo in Rats—Antiarrhythmic or Arrhythmogenic?

Kawy

2015

Cardiovascular Therapeutics

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SUMMARYBackground: The safety of all proton pump inhibitors (PPIs) in patients with intrinsic cardiac disease has not been well studied. In the present study, the effect of PPI pantoprazole on ventricular arrhythmias induced by either ischemia or ischemia-reperfusion (I/R) was studied. Methods: The left main coronary artery (LAD) was ligated for 30 or 10 min followed by a 30-min reperfusion in anesthetized rats. Rats were pretreated with pantoprazole (1.3 mg/kg) or vehicle by gastric gavage (daily for 3 weeks) before ligation. Serum electrolytes levels were measured by the end of the third week before coronary ligation. Lactate dehydrogenase (LDH) activity and nitric oxide (NO) concentrations were measured at the end of the ischemia and IR injury. Results: Pantoprazole caused significant hyperkalemia by the end of third week compared with vehicle-treated rats. After LAD ligation (30 min), ventricular premature contractions (VPC), ventricular tachycardia (VT) and ventricular fibrillation (VF) were recorded in rats of the vehicle ischemia group. Pantoprazole pretreatment aggravate these arrhythmias and increased mortality. A 10-min period of ischemia followed by a 30-min reperfusion induced high incidence of VT (100%) and VF (80%) in the vehicle-treated group. The group of rats administered pantoprazole had significantly lower incidence and durations of VT and VF together with reduction of mortality rate. Pantoprazole significantly reduced serum LDH activity and NO release from myocardial tissue after both ischemia and I/R injury. Conclusion: Pantoprazole aggravated ischemia-induced arrhythmias but had a significant antiarrhythmic effect on I/R-induced ventricular arrhythmias.

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Chronic Pantoprazole Administration and Ischemia–Reperfusion Arrhythmias In Vivo in Rats—Antiarrhythmic or Arrhythmogenic?

Kawy

2015

Cardiovascular Therapeutics

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The protective effect of acute pantoprazole pretreatment on renal ischemia/reperfusion injury in rats

Kohansal

Mohajer

Dehpour

et al. 2019

Fundamemntal Clinical Pharma

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Renal ischemia/reperfusion injury (IRI), which occurs in many pathological conditions, is associated with high rate of morbidity and mortality. Activation of inflammatory responses and oxidative stress contribute to induce organ damage following IRI. Pantoprazole, a proton pump inhibitor, which is mostly prescribed for gastroesophageal reflux disease (GERD) has been shown to exert anti‐inflammation effects. In order to evaluate the effects of pantoprazole on renal ischemia/reperfusion injury, four different doses of pantoprazole (4.5, 9, 18, and 36 mg/kg) were administered 30 min before the induction of IRI in male Wistar rats. Serum concentration of creatinine and blood urea nitrogen (BUN) were measured to assess renal function. Histopathological changes, malondialdehyde (MDA) level and toll‐like receptor 4 (TLR‐4) expression in renal tissue were determined and compared to control group. The results revealed that pretreatment with 18 and 36 mg/kg of pantoprazole leads to the significant decline in serum creatinine and BUN levels and the severity of necrosis grade in comparison with control group (P < 0.05). Pantoprazole also reduced the MDA level and TLR‐4 expression in renal tissue. In summary, pantoprazole attenuates renal injury following ischemia/reperfusion. This effect is mediated partially through inhibition of oxidative stress and TLR‐4 signaling pathway.

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The role of aldosterone inhibitors in cardiac ischemia–reperfusion injury

Dragasevic

Jakovljević

Živković

et al. 2021

Can. J. Physiol. Pharmacol.

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Myocardial ischaemia-reperfusion (I/R) injury is well known term for paradoxal exacerbation of cellular destruction and dysfunction, after the restoration of blood flow to previously ischaemic heart. A vast number of studies that has demonstrated the role of mineralocorticoids in cardiovascular diseases is based on the use of pharmacological mineralocorticoid receptor antagonists (MRA) such as spironolactone and eplerenone. This review paper aimed to summarize current knowledge on the effects of MR antagonists on myocardial I/R injury, as well as post-infarction remodeling. Animal models, predominantly Langendorff technique and left anterior descending coronary artery occlusion (LAD) have confirmed the potency of MRA as preconditioning and postconditioning agents in limiting infarct size and postinfarction remodeling. Several preclinical studies in rodents have established and proved possible mechanisms of cardioprotection by MRA, such as reduction of oxidative stress, reduction of inflammation and apoptosis, therefore limiting infarct zone. However, the results of some clinical trials are inconsistent with these results since they reported no benefit of MRA in acute myocardial infarction. Due to this, further studies and the results of on-going clinical trials regarding MRA administration in patients with acute myocardial infarction are being awaited with great interest.

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Pantoprazol oferece proteção miocárdica semelhante ao pré-condicionamento isquêmico

Cited by 5 publications

References 28 publications

Chronic Pantoprazole Administration and Ischemia–Reperfusion Arrhythmias In Vivo in Rats—Antiarrhythmic or Arrhythmogenic?

Chronic Pantoprazole Administration and Ischemia–Reperfusion Arrhythmias In Vivo in Rats—Antiarrhythmic or Arrhythmogenic?

The protective effect of acute pantoprazole pretreatment on renal ischemia/reperfusion injury in rats

The role of aldosterone inhibitors in cardiac ischemia–reperfusion injury

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