Role of erythropoietin in ischemic postconditioning induced cardioprotection in hyperlipidemic rat heart

Varshney, Vibhav; Goyal, Ahsas; Gupta, Jeetendra Kumar; Yadav, Harlokesh Narayan

doi:10.1016/j.jicc.2017.03.003

Cited by 8 publications

(6 citation statements)

References 36 publications

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“…These findings are as per our laboratory's previous published study. 13 Heme-oxygenase 1 (HO-1) has been located in plasma membrane caveolae, where caveolin interacts. 39 HO-1 triggers eNOS by the caveolin-eNOS complex disruption as well as promoting the release of nitric oxide, which is well known endogenous molecules that produce cardioprotection against I/R injury.…”

Section: Discussionmentioning

confidence: 99%

“…Isolated rat heart preparation for sham control, I/R control and IPOC control groups were followed by the previous publication of our lab. 13 Briefly, global ischemia was produced for 30 min by blocking the inflow of Kreb's-Henseleit (K-H; (NaCl 118 mM; KCl 4.7 mM; CaCl 2 2.5 mM; MgSO 4 .7H 2 0 1.2 mM; KH 2 PO 4 1.2 mM; C 6 H 12 O 6 11 mM) buffer solution, which was followed by 160 min of reperfusion. IPOC was produced by 5 min of reperfusion followed by 5 min of ischemia by closing the inflow of K-H buffer solution.…”

Section: Experimental Designmentioning

confidence: 99%

“…[7][8][9][10][11] Nevertheless, in many cases, the cardioprotective function of IPOC is attenuated. [12][13][14][15] One of the main threat of ischemic heart disease is diabetes mellitus. Heme oxygenase-1 (HO-1) activates the oxidative breakdown of the cell heme for free iron, biliverdin, carbon monoxide (CO) and is also known as a rate-limiting enzyme.…”

Section: Introductionmentioning

confidence: 99%

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Role of Heme Oxygenase- 1(HO-1) and Endothelin-1 (ET-1) in Modulation of Cardioprotective Effect of Ischemic Postconditioning in Diabetic Rat Heart

Rohilla¹,

Goyal²,

Varshney³

et al. 2020

IJPER

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Background:We have recently reported that heme oxygenase-1 (HO-1) is involved in ischemic preconditioning-mediated cardioprotection by promoting nitric oxide (NO) release into diabetic rat heart (DRH). The upregulation of HO-1 decreases the endothelin-1 (ET-1) production, which is a negative regulator of NO. In diabetes, the level of HO-1 is reduced while the level of ET-1 gets elevated. Thus, the present analysis was aimed to explore the concept of HO-1 and ET-1 in the abrogated cardioprotective role of ischemic post conditioning (IPOC) in the DRH. Materials and Methods: To explore the concept, a selective HO-1 inducer hemin, 18 hrs prior and a selective ETA receptor antagonist BQ-123, one week prior, were administered to DRH before isolation. DRH was removed and then mounted on Langendorff's apparatus, subjected to 10 min stabilization followed by 30 min ischemia. IPOC had been induced by four cycles of 5 min reperfusion along with 5 min ischemia followed by further 120 min of reperfusion. The extent of the infarct was measured and the coronary effluent was tested for the LDH, CK-MB and NO release. Results: In DRH, cardioprotection mediated by the IPOC was significantly attenuated. Hemin and BQ-123 reinstated the impact of IPOC in DRH and also increased the release of NO. In BQ-123 pre-treated diabetic rat, the administration of hemin was unable to produce the additive cardioprotective effect of IPOC. Conclusion: Thus, it is suggested that hemin and BQ-123 restore the attenuated cardioprotective effect of IPOC in the DRH, which may be due to increased NO release.

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Section: Discussionmentioning

confidence: 99%

Section: Experimental Designmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Role of Heme Oxygenase- 1(HO-1) and Endothelin-1 (ET-1) in Modulation of Cardioprotective Effect of Ischemic Postconditioning in Diabetic Rat Heart

Rohilla¹,

Goyal²,

Varshney³

et al. 2020

IJPER

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“…A commercially available kit (Coral Clinical System Pvt. Ltd., India) was used to estimate the amounts of lactate dehydrogenase (LDH) and creatine kinase-myoglobin binding (CK-MB) responsible for coronary drainage to quantify the extent of cell injury [ 24 ].…”

Section: Methodsmentioning

confidence: 99%

Modulation of Inula racemosa Hook Extract on Cardioprotection by Ischemic Preconditioning in Hyperlipidaemic Rats

Tiwari

Gupta

Prasad³

et al. 2022

J Pharmacopuncture

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Objectives: Hyperlipidemia (HL) is a major cause of ischemic heart diseases. The size-limiting effect of ischemic preconditioning (IPC), a cardioprotective phenomenon, is reduced in HL, possibly because of the opening of the mitochondrial permeability transition pore (MPTP). The objective of this study is to see what effect pretreatment with Inula racemosa Hook root extract (IrA) had on IPC-mediated cardioprotection on HL Wistar rat hearts. An isolated rat heart was mounted on the Langendorff heart array, and then ischemia reperfusion (I/R) and IPC cycles were performed. Atractyloside (Atr) is an MPTP opener. Methods: The animals were divided into ten groups, each consisting of six rats (n = 6), to investigate the modulation of I. racemosa Hook extract on cardioprotection by IPC in HL hearts: Sham control, I/R Control, IPC control, I/R + HL, I/R + IrA + HL, IPC + HL, IPC + NS + HL, IPC + IrA+ HL, IPC + Atr + oxidative stress, mitochondrial function, integrity, and hemodynamic parameters are evaluated for each group. Results: The present experimental data show that pretreatment with IrA reduced the LDH, CK-MB, size of myocardial infarction, content of cardiac collagen, and ventricular fibrillation in all groups of HL rat hearts. This pretreatment also reduced the oxidative stress and mitochondrial dysfunction. Inhibition of MPTP opening by Atr diminished the effect of IrA on IPC-mediated cardioprotection in HL rats. Conclusion:The study findings indicate that pretreatment with IrA e restores IPC-mediated cardioprotection in HL rats by inhibiting the MPTP opening.

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“…As understanding of the mechanisms involved with tissue injury following arterial occlusion (ischemia), and then subsequent appreciation of additional injury associated with relieving the occlusion (reperfusion) advanced (4-6), it became clear that periods of intermittent ischemia that either immediately preceded the ischemic event (ischemic preconditioning), or immediately preceded the reperfusion event (ischemic post-conditioning) could induce multiple pathways that could limit the extent of injury and improve recovery (4-7). Pre-and post-conditioning effects were associated with erythropoietin, the heme-oxygenase system, and atrial natriuretic peptide among many others (8)(9)(10), and those effects could I turn depend on underlying conditions such as diabetes, hyperlipidemia, and estrogen status (8)(9)(10). Practically though, both pre-conditioning and post-conditioning have had limited success, simply due to the inherent challenges of creating controlled, intentional ischemia.…”

Section: Introductionmentioning

confidence: 99%

Influence of Intrinsic Aerobic Exercise Capacity and Sex on Cardiac Injury Following Acute Myocardial Ischemia and Reperfusion

Alsahly

Zakari

Koch

et al. 2021

Front. Cardiovasc. Med.

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Purpose: Previous reports have suggested that active exercise aside, intrinsic aerobic running capacity (Low = LCR, high = HCR) in otherwise sedentary animals may influence several cardiovascular health-related indicators. Relative to the HCR phenotype, the LCR phenotype is characterized by decreased endothelial reactivity, increased susceptibility to reperfusion-induced arrhythmias following short, non-infarction ischemia, and increased diet-induced insulin resistance. More broadly, the LCR phenotype has come to be characterized as a “disease prone” model, with the HCRs as “disease resistant.” Whether these effects extend to injury outcomes in an overt infarction or whether the effects are gender specific is not known. This study was designed to determine whether HCR/LCR phenotypic differences would be evident in injury responses to acute myocardial ischemia-reperfusion injury (AIR), measured as infarct size and to determine whether sex differences in infarction size were preserved with phenotypic selection.Methods: Regional myocardial AIR was induced in vivo by either 15 or 30 min ligation of the left anterior descending coronary artery, followed by 2 h of reperfusion. Global ischemia was induced in isolated hearts ex vivo using a Langendorff perfusion system and cessation of perfusion for either 15 or 30 min followed by 2 h of reperfusion. Infarct size was determined using 2, 3, 5–triphenyltetrazolium chloride (TTC) staining, and normalized to area at risk in the regional model, or whole heart in the global model. Portions of the tissue were paraffin embedded for H&E staining and histology analysis.Results: Phenotype dependent differences in infarct size were seen with 15 min occlusion/2 h reperfusion (LCR > HCR, p < 0.05) in both regional and global models. In both models, longer occlusion times (30 min/2 h) produced significantly larger infarctions in both phenotypes, but phenotypic differences were no longer present (LCR vs. HCR, p = n.s.). Sex differences in infarct size were present in each phenotype (LCR male > LCR female, p < 0.05; HCR male > HCR female, p < 0.05 regardless of length of occlusion, or ischemia model.Conclusions: There is cardioprotection afforded by high intrinsic aerobic capacity, but it is not infinite/continuous, and may be overcome with sufficient injury burden. Phenotypic selection based on endurance running capacity preserved sex differences in response to both short and longer term coronary occlusive challenges. Outcomes could not be associated with differences in system characteristics such as circulating inflammatory mediators or autonomic nervous system influences, as similar phenotypic injury patterns were seen in vivo, and in isolated crystalloid perfused heart ex vivo.

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Role of erythropoietin in ischemic postconditioning induced cardioprotection in hyperlipidemic rat heart

Cited by 8 publications

References 36 publications

Role of Heme Oxygenase- 1(HO-1) and Endothelin-1 (ET-1) in Modulation of Cardioprotective Effect of Ischemic Postconditioning in Diabetic Rat Heart

Role of Heme Oxygenase- 1(HO-1) and Endothelin-1 (ET-1) in Modulation of Cardioprotective Effect of Ischemic Postconditioning in Diabetic Rat Heart

Modulation of Inula racemosa Hook Extract on Cardioprotection by Ischemic Preconditioning in Hyperlipidaemic Rats

Influence of Intrinsic Aerobic Exercise Capacity and Sex on Cardiac Injury Following Acute Myocardial Ischemia and Reperfusion

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