Sevoflurane preconditioning during myocardial ischemia-reperfusion reduces infarct size and preserves autonomic control of circulation in rats

Pasqualin, Rubens Campana; Mostarda, Cristiano Teixeira; Souza, Leandro Franco de; Vane, Matheus Fachini; Sirvente, Raquel; Otsuki, Denise Aya; Torres, Marcelo Luís Abramides; Irigoyen, Maria Cláudia; Auler, José Otávio Costa

doi:10.1590/s0102-865020160050000008

Cited by 18 publications

(14 citation statements)

References 30 publications

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“…Hemodynamic measurements were not performed, but they exhibit good correlations with echocardiography parameters [ 12 ]. Of note, our left ventricular ejection fraction figures for ablated and sham animals are comparable to other reports concerning infarcted rats and controls [ [29] , [30] , [31] , [32] ]. Mild systolic ventricular dysfunction was consistently induced in our model.…”

Section: Discussionsupporting

confidence: 90%

Atrial fibrillation promotion in a rat model of heart failure induced by left ventricle radiofrequency ablation

Santos

Antônio

Serra

et al. 2018

IJC Heart & Vasculature

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BackgroundAtrial fibrillation (AF) frequently coexists with congestive heart failure (CHF). The increased susceptibility to AF in CHF has been attributed to a variety of structural and electrophysiological changes in the atria, particularly dilation and interstitial fibrosis. We evaluated atrial remodeling and AF vulnerability in a rat model of CHF induced by left ventricle (LV) radiofrequency (RF) ablation.MethodsWistar rats were divided into 3 groups: RF-induced CHF (Ab, n = 36), CHF animals treated with spironolactone (AbSpi, n = 20) and sham controls (Sham, n = 29). After 12 weeks, animals underwent echocardiographic and electrophysiological evaluation and were sacrificed for histological (atrial fibrosis) and Western blotting (TGF-β1, collagen I/III, connexin 43 and CaV1.2) analysis.ResultsMild LV dysfunction and marked atrial enlargement were noted in both ablated groups. AF inducibility (episodes ≥2 s) increased in the Ab group compared to sham animals (31/36, 86%; vs. 15/29, 52%; p = 0.005), but did not differ from the AbSpi group (16/20, 80%; p = NS). Sustained AF (>30 s) was also more frequent in the Ab group compared to shams (56% vs. 28%; p = 0.04). Spironolactone reduced atrial fibrosis (p < 0.01) as well as TGF-β1 (p < 0.01) and collagen I/III (p < 0.01) expression but did not affect connexin 43 and CaV1.2 expression.ConclusionsRats with RF-induced CHF exhibit pronounced atrial structural remodeling and enhanced AF vulnerability. This model may be useful for studying AF substrate in CHF.

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Section: Discussionsupporting

confidence: 90%

Atrial fibrillation promotion in a rat model of heart failure induced by left ventricle radiofrequency ablation

Santos

Antônio

Serra

et al. 2018

IJC Heart & Vasculature

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“…• Neuregulin-1 [134][135][136][137][138] • Ghrelin [139] • Vasopressin [140] • Anesthetic preconditioning [141] Non-pharmacological interventions…”

Section: Pharmacological Interventionsmentioning

confidence: 99%

Autonomic Nervous System and Neurocardiac Physiopathology

Kingma¹,

Simard²,

Rouleau³

2018

Autonomic Nervous System

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The autonomic nervous system regulates multiple physiological functions; how distinct neurons in peripheral autonomic and intrathoracic ganglia communicate remains to be established. Increasing focus is being paid to functionality of the neurocardiac axis and crosstalk between the intrinsic nervous system and diverse organ systems. Current findings indicate that progression of cardiovascular disease comprises peripheral and central aspects of the cardiac nervous system hierarchy. Indeed, autonomic neuronal dysfunction is known to participate in arrhythmogenesis and sudden cardiac death; diverse interventions (pharmacological, non-pharmacological) that affect neuronal remodeling in the heart following injury caused by cardiovascular disease (congestive heart failure, etc.) or acute myocardial infarction are being investigated. Herein we examine recent findings from clinical and animal studies on the role of the intrinsic cardiac nervous system on regulation of myocardial perfusion and the consequences of cardiac injury. We also discuss different interventions that target the autonomic nervous system, stimulate neuronal remodeling and adaptation, and thereby optimize patient outcomes.

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“…Restora-tion of blood flow to an ischemic heart is necessary to salvage the ischemic myocardium, but reperfusion of an ischemic region can result in myocardial ischemia/reperfusion (IR) injury due to oxidative stress [2]. Studies have shown that sevoflurane postconditioning (SPostC) could protect the myocardium against reperfusion-induced injury and reduce myocardial infarct size [3,4]. However, patients with diabetes have a remarkably higher mortality rate owing to increased IR injury and the beneficial effects of SPostC almost completely disappeared [5][6][7].…”

Section: Introductionmentioning

confidence: 99%

Inactivation of TOPK Caused by Hyperglycemia Blocks Diabetic Heart Sensitivity to Sevoflurane Postconditioning by Impairing the PTEN/PI3K/Akt Signaling

Gao

Wang

Dong

et al. 2021

Oxidative Medicine and Cellular Longevity

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The cardioprotective effect of sevoflurane postconditioning (SPostC) is lost in diabetes that is associated with cardiac phosphatase and tensin homologue on chromosome 10 (PTEN) activation and phosphoinositide 3-kinase (PI3K)/Akt inactivation. T-LAK cell-originated protein kinase (TOPK), a mitogen-activated protein kinase- (MAPKK-) like serine/threonine kinase, has been shown to inactivate PTEN (phosphorylated status), which in turn activates the PI3K/Akt signaling (phosphorylated status). However, the functions of TOPK and molecular mechanism underlying SPostC cardioprotection in nondiabetes but not in diabetes remain unknown. We presumed that SPostC exerts cardioprotective effects by activating PTEN/PI3K/Akt through TOPK in nondiabetes and that impairment of TOPK/PTEN/Akt blocks diabetic heart sensitivity to SPostC. We found that in the nondiabetic C57BL/6 mice, SPostC significantly attenuated postischemic infarct size, oxidative stress, and myocardial apoptosis that was accompanied with enhanced p-TOPK, p-PTEN, and p-Akt. These beneficial effects of SPostC were abolished by either TOPK kinase inhibitor HI-TOPK-032 or PI3K/Akt inhibitor LY294002. Similarly, SPostC remarkably attenuated hypoxia/reoxygenation-induced cardiomyocyte damage and oxidative stress accompanied with increased p-TOPK, p-PTEN, and p-Akt in H9c2 cells exposed to normal glucose, which were canceled by either TOPK inhibition or Akt inhibition. However, either in streptozotocin-induced diabetic mice or in H9c2 cells exposed to high glucose, the cardioprotective effect of SPostC was canceled, accompanied by increased oxidative stress, decreased TOPK phosphorylation, and impaired PTEN/PI3K/Akt signaling. In addition, TOPK overexpression restored posthypoxic p-PTEN and p-Akt and decreased cell death and oxidative stress in H9c2 cells exposed to high glucose, which was blocked by PI3K/Akt inhibition. In summary, SPostC prevented myocardial ischemia/reperfusion injury possibly through TOPK-mediated PTEN/PI3K/Akt activation and impaired activation of this signaling pathway may be responsible for the loss of SPostC cardioprotection by SPostC in diabetes.

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Sevoflurane preconditioning during myocardial ischemia-reperfusion reduces infarct size and preserves autonomic control of circulation in rats

Cited by 18 publications

References 30 publications

Atrial fibrillation promotion in a rat model of heart failure induced by left ventricle radiofrequency ablation

Atrial fibrillation promotion in a rat model of heart failure induced by left ventricle radiofrequency ablation

Autonomic Nervous System and Neurocardiac Physiopathology

Inactivation of TOPK Caused by Hyperglycemia Blocks Diabetic Heart Sensitivity to Sevoflurane Postconditioning by Impairing the PTEN/PI3K/Akt Signaling

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