scholarly journals Both Castration and Goserelin Acetate Ameliorate Myocardial Ischemia Reperfusion Injury and Apoptosis in Male Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Najah R. Hadi ◽  
Fadhil G. Yusif ◽  
Maitham Yousif ◽  
Karrar K. Jaen
Keyword(s):  
Myocardial Ischemia ◽  
Myocardial Injury ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Male Rats ◽  
Control Group ◽  
Goserelin Acetate ◽  
Myocardial Ischemia Reperfusion

Although reperfusion of an ischemic organ is essential to prevent irreversible tissue damage, it may amplify tissue injury. This study investigates the role of endogenous testosterone in myocardial ischemia reperfusion and apoptosis in male rats. Material and method. Twenty four male rats were randomized into 4 equal groups: Group (1), sham group, rats underwent the same anesthetic and surgical procedure as the control group except for LAD ligation; Group (2), Active control group, rats underwent LAD ligation; Group (3), castrated, rats underwent surgical castration, left 3wks for recovery, and then underwent LAD ligation; and Group (4), Goserelin acetate treated, rats received 3.6 mg of Goserelin 3 wks before surgery and then underwent LAD ligation. At the end of experiment, plasma cTn I, cardiac TNF-α, IL1-β, ICAM-1, and Apoptosis level were measured and histological examination was made. Results. Compared to sham group, the levels of myocardial TNF-α, IL-1β, ICAM-1, apoptosis, and plasma cTn I were significantly increased (P<0.05) in control group and all rats showed significant myocardial injury (P<0.05). Castration and Goserelin acetates significantly counteract the increase in myocardial levels of TNF-α, IL-1β, ICAM-1, plasma cTn I, and apoptosis (P<0.05) and significantly reduce (P<0.05) the severity of myocardial injury. We conclude that castration and Goserelin acetates ameliorate myocardial I/R injury and apoptosis in rats via interfering with inflammatory reactions.

scholarly journals The cardioprotective potential of Tadalafil in myocardial ischemia/reperfusion

2020 ◽  
Vol 8 (2) ◽  
pp. 87-100
Author(s):  
Najah R. Hadi ◽  
Fadhil G. Al-Amran
Keyword(s):  
Myocardial Ischemia ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Male Rats ◽  
Control Group ◽  
Inflammatory Reactions ◽  
Tnf Α ◽  
Myocardial Ischemia Reperfusion

The objective of this study is to assess the potential protective effect of Tadalafil on myocardial ischemia reperfusion injury induced by LAD ligation, 28 male rats were randomized into 4 groups (7 rats per group); Sham, rats underwent the same anesthetic and surgical procedure except for LAD ligation; control, rats underwent LAD ligation for 30 minutes and reperfusion for 2 hours; vehicle, rats treated with 10% DMSO, the Tadalafil solvent 30 minutes before the ligation; Tadalafil group, rats pretreated with Tadalafil1mg/kg i.p 30 minutes before ligation. In control group, as compared with sham, tissue TNF-α, IL-6, IL-10, caspase-3 and BAX, plasma cTn-T and serum MDA significantly increased (P<0.05), while serum GSH significantly decreased (P<0.05). Histopathologically, control group showed a significant cardiac injury (P<0.05) compared with sham group. Tadalafil significantly counteracted (P<0.05) the increase of TNF-α, IL-6, caspase-3 and BAX and counteracted the increase in plasma cTn-T and serum MDA. Tadalafil produces a significant elevation (P<0.05) in cardiac IL-10 and serum GSH with significant reduction in (P<0.05) cardiac injury. In We concluded that Tadalafil attenuates myocardial I/R injury in male rats through interfering with inflammatory reactions and apoptosis .

scholarly journals Effects of Thyroid Hormone Analogue and a Leukotrienes Pathway-Blocker on Reperfusion Injury Attenuation after Heart Transplantation

2013 ◽  
Vol 2013 ◽  
pp. 1-8
Author(s):  
Fadhil G. Al-Amran ◽  
Najah R. Hadi ◽  
Haider S. H. Al-Qassam
Keyword(s):  
Myocardial Ischemia ◽  
Heart Transplantation ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Treated Group ◽  
Control Group ◽  
Group I ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Background. Global myocardial ischemia reperfusion injury after heart transplantation is believed to impair graft function and aggravate both acute and chronic rejection episodes. Objectives. To assess the possible protective potential of MK-886 and 3,5-diiodothyropropionic acid DITPA against global myocardial ischemia reperfusion injury after heart transplantation. Materials and Methods. Adult albino rats were randomized into 6 groups as follows: group I sham group; group II, control group; groups III and IV, control vehicles (1,2); group V, MK-886 treated group. Donor rats received MK-886 30 min before transplantation, and the same dose was repeated for recipients upon reperfusion; in group VI, DITPA treated group, donors and recipients rats were pretreated with DITPA for 7 days before transplantation. Results. Both MK-886 and DITPA significantly counteract the increase in the levels of cardiac TNF-α, IL-1β, and ICAM-1 and plasma level of cTnI (). Morphologic analysis showed that both MK-886 and DITPA markedly improved () the severity of cardiac injury in the heterotopically transplanted rats. Conclusions. The results of our study reveal that both MK-886 and DITPA may ameliorate global myocardial ischemia reperfusion injury after heart transplantation via interfering with inflammatory pathway.

scholarly journals Noninvasive Delayed Limb Ischemic Preconditioning Attenuates Myocardial Ischemia-Reperfusion Injury in Rats by a Mitochondrial KATP Channel-Dependent Mechanism

2011 ◽  
pp. 271-279 ◽  
Author(s):  
Y.-N. WU ◽  
H. YU ◽  
X.-H. ZHU ◽  
H.-J. YUAN ◽  
Y. KANG ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemic Preconditioning ◽  
Katp Channel ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion ◽  
Dependent Mechanism

We previously demonstrated in rats that noninvasive delayed limb ischemic preconditioning (LIPC) induced by three cycles of 5-min occlusion and 5-min reperfusion of the left hind limb per day for three days confers the same cardioprotective effect as local ischemic preconditioning of the heart, but the mechanism has not been studied in depth. The aim of this project was to test the hypothesis that delayed LIPC enhances myocardial antioxidative ability during ischemia-reperfusion by a mitochondrial KATP channel (mito KATP)-dependent mechanism. Rats were randomized to five groups: ischemia-reperfusion (IR)-control group, myocardial ischemic preconditioning (MIPC) group, LIPC group, IR-5HD group and LIPC-5HD group. The MIPC group underwent local ischemic preconditioning induced by three cycles of 5-min occlusion and 5-min reperfusion of the left anterior descending coronary arteries. The LIPC and LIPC-5HD groups underwent LIPC induced by three cycles of 5-min occlusion and 5-min reperfusion of the left hind limb using a modified blood pressure aerocyst per day for three days. All rats were subjected to myocardial ischemia-reperfusion injury. The IR-5HD and LIPC-5HD groups received the mito KATP channel blocker 5-hydroxydecanoate Na (5-HD) before and during the myocardial ischemia-reperfusion injury. Compared with the IR-control group, both the LIPC and MIPC groups showed an amelioration of ventricular arrhythmia, reduced myocardial infarct size, increased activities of total superoxide dismutase, manganese-superoxide dismutase (Mn-SOD) and glutathione peroxidase, increased expression of Mn-SOD mRNA and decreased xanthine oxidase activity and malondialdehyde concentration. These beneficial effects of LIPC were prevented by 5-HD. In conclusion, delayed LIPC offers similar cardioprotection as local IPC. These results support the hypothesis that the activation of mito KATP channels enhances myocardial antioxidative ability during ischemia-reperfusion, thereby contributing, at least in part, to the anti-arrhythmic and anti-infarct effects of delayed LIPC.

scholarly journals Study on the Protective Effect of Edaravone on Myocardial Ischemia Reperfusion Injury

2013 ◽  
Vol 2 ◽  
pp. 10
Author(s):  
Hui Hou
Keyword(s):  
Treatment Group ◽  
Myocardial Ischemia ◽  
Protective Effect ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Acute Myocardial Ischemia ◽  
Control Group ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

<div><p><strong>Objective: </strong>Discussion the role of edaravone as a free radical scavenger in protective effect of thrombolysis in acute myocardial ischemia reperfusion injury. Besides compared with the control group and analyze the possible mechanism which is widely used in clinical setting. <strong>Method: </strong>80 patients hospitalized within year 2012−2013 with acute myocardial infarction (AMI) were treated with intravenous thrombolytic therapy, and were divided into treatment group (n = 41) and control group (n = 39). Edaravone injection 30 mg + 0.9% normal saline solution 100 mL with intravenous drip, BID for 14 days was given to the treatment group before and after thrombolytic treatment. Whereas, control group was treated with intravenous drip of placebo. Both groups were monitored by echocardiography and hemodynamic monitoring, and the myocardium was measured by echocardiography. Coronary artery CT was used to determine the degree of obstruction. <strong>Results: </strong>Compared with the control group, pain and reperfusion arrhythmia in treatment group was reduced. The area of myocardial wall movement disorder was significantly decreased (<em>p</em> &lt; 0.05), the difference was statistically significant. CT result comparing treatment group and control group and show that rate of coronary recanalization increases 1.7 times (<em>p </em>&lt; 0.01), the differences were statistically significant. <strong>Conclusion: </strong>For acute myocardial ischemia injection of edaravone before reperfusion and combine with pharmacological treatment can alleviate myocardial ischemia reperfusion injury, effectively scavenge oxygen free radicals and improve the ability of antioxidant. Both improve the thrombolytic treatment and protective effect for acute myocardial ischemia were significant. Hence, edaravone can is a kind of new milestone in the clinical cardiovascular drugs.</p></div>

Abstract 453: The Role of PD-1/PDL-1 in Myocardial Ischemia Reperfusion Injury.

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Mahmood Mozaffari ◽  
Jun Yao Liu ◽  
Babak Baban
Keyword(s):  
Cell Death ◽  
Myocardial Ischemia ◽  
Inflammatory Response ◽  
Ischemia Reperfusion Injury ◽  
Tissue Injury ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Cardiac Cells ◽  
Interleukin 17 ◽  
Myocardial Ischemia Reperfusion

Programmed Death-1 (PD-1) and its ligand, PDL-1, are expressed on immune cells and have emerged as negative regulators of immune and inflammatory mechanisms. Aside from the contribution of systemic immune and inflammatory mechanisms to myocardial ischemia reperfusion (IR) injury, isolated heart studies have shown that the myocardium is capable of mounting a robust inflammatory response to an IR insult. However, potential involvement of PD-1/PDL-1 in the setting of cardiac IR injury is not established. We tested the hypothesis that an IR insult downregulates PD-1/PDL-1 pathway thereby exacerbating the inflammatory response and cell death. According, Langendorff-perfused rat hearts were subjected to 40 min of ischemia and 15 min of reperfusion; normoxic hearts served as controls. Thereafter, cardiac cells were prepared and subjected to flow-cytometry-based assays. The ischemic-reperfused hearts displayed a marked increase in the pro-inflammatory cytokine interleukin-17 in association with disruption of mitochondrial membrane potential (JC-1 assay) and apoptotic and necrotic cell death. Importantly, the ischemic-reperfused hearts showed a significant increase in PD-1 and PDL-1 positive cells. The results suggest that cardiac PD-1/ PDL-1 pathway likely constitutes an endogenous mechanism whose upregulation in the ischemic-reperfused heart curbs the inflammatory response and associated tissue injury.

Protective effect of Shengmai injection on myocardial endothelial cell glycoprotein detachment after myocardial ischemia-reperfusion injury in isolated rat hearts

Perfusion ◽  
2020 ◽  
pp. 026765912096592
Author(s):  
Qi Chen ◽  
Ping Zhang ◽  
Qiu-Xia Xiao ◽  
Qing Liu ◽  
Ying Zhang
Keyword(s):  
Endothelial Cell ◽  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Stress Injury ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Objective: To investigate effects of Shengmai injection (SMI) postconditioning on myocardial ischemia-reperfusion injury (MIRI) in isolated rat hearts. Materials and methods: A total of thirty isolated hearts were randomly divided into three groups: Sham group, I/R group and SMI group. Sham group was continuously perfused with K-H solution for 120 minutes. I/R group and SMI group were given balanced perfusion for 30 min followed by reperfusion for 60 min, with an interval of 30 min, and those in the SMI group were given postconditioning with 1% SMI during the first 10 min of reperfusion. The left ventricular function, markers of myocardial injury, endothelial cell injury and oxidative stress injury were measured at 30 minutes after equilibration (t0), 30 minutes after ischemia (t2) and 60 minutes after reperfusion (t3). Results: The results showed that there was no significant difference for all observation indexes at t0. Compared with the Sham group, real portfolio project and coronary arterial flow rate and the activity of superoxide dismutase were significantly decreased in the I/R group, whereas those in the SMI group were significantly higher. Left ventricular end-diastolic pressure, the concentrate of malondialdehyde, lactate dehydrogenase, cTn-I, hyaluronic acid, heparin sulphate, syndecan-1 in the I/R group were markedly higher than those in the Sham group, whereas those in the SMI group were significantly lower. Conclusion: In summary, the present study indicated that 1% SMI postconditioning can alleviate the detachment of endothelial cell glycoprotein envelope induced by myocardial ischemia-reperfusion injury, and its mechanism is probably related to the inhibition of the oxidative stress injury.

scholarly journals Visnagin ameliorates myocardial ischemia/reperfusion injury through the promotion of autophagy and the inhibition of apoptosis

2020 ◽  
Vol 64 (s2) ◽  
Author(s):  
Hai-rong Fu ◽  
Xiao-shan Li ◽  
Yong-hui Zhang ◽  
Bin-bin Feng ◽  
Lian-hong Pan
Keyword(s):  
Myocardial Ischemia ◽  
Cardiac Function ◽  
Protective Effect ◽  
Reperfusion Injury ◽  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Tunel Staining ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Visnagin is a furanochromone and one of the main compounds of Ammi visnaga L. that had been used to treat nephrolithiasis in Ancient Egypt. Nowadays, visnagin was widely used to treat angina pectoris, urolithiasis and hypertriglyceridemia. The potential mechanisms of visnagin involved in inflammation and cardiovascular disease were also identified. But the protective effect of visnagin on myocardial ischemia/reperfusion injury has not been confirmed. Our aim was, for the first time, to investigate the potential protective effect of visnagin on cardiac function after myocardial ischemia-reperfusion injury in a rat model, and to identify its underlying mechanism involving the inhibition of apoptosis and induction of autophagy. Thirty SD rats were randomly divided into sham group, ischemia/reperfusion group (IR), ischemia/reperfusion with visnagin (IR + visnagin) group. Myocardial ischemia/Reperfusion injury model was established. Hemodynamic measurements and echocardiography were used to analyze cardiac function, TUNEL staining and caspase activity, LC3 dots were detected with immunofluorescence staining, LC3 expression was evaluated by western blot analysis, transmission electron microscopy (TEM) was used to detect autophagosomes. Compared with the sham group and visnagin group, the cardiac dysfunction, LC3II, autophagy flow in the IR+ visnagin group increased significantly (P<0.01), but the activity of caspase-3 and caspase-9 and the apoptotic in the IR + visnagin group decreased significantly (P<0.01). In conclusion, visnagin may play a protective role in ischemia/reperfusion injury by inducing autophagy and reducing apoptosis.

15-F2t-isoprostane exacerbates myocardial ischemia-reperfusion injury of isolated rat hearts

2005 ◽  
Vol 289 (4) ◽  
pp. H1366-H1372 ◽  
Author(s):  
Zhengyuan Xia ◽  
Kuo-Hsing Kuo ◽  
David V. Godin ◽  
Michael J. Walker ◽  
Michelle C. Y. Tao ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Saline Control ◽  
Control Group ◽  
Endothelin 1 ◽  
Rat Hearts ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

Reactive oxygen species induce formation of 15-F2t-isoprostane (15-F2t-IsoP), a specific marker of in vivo lipid peroxidation, which is increased after myocardial ischemia and during the subsequent reperfusion. 15-F2t-IsoP possesses potent bioactivity under pathophysiological conditions. However, it remains unknown whether 15-F2t-IsoP, by itself, can influence myocardial ischemia-reperfusion injury (IRI). Adult rat hearts were perfused by the Langendorff technique with Krebs-Henseleit (KH) solution at a constant flow rate of 10 ml/min. 15-F2t-IsoP (100 nM), SQ-29548 (1 μM, SQ), a thromboxane receptor antagonist that can abolish the vasoconstrictor effect of 15-F2t-IsoP, 15-F2t-IsoP + SQ in KH, or KH alone (vehicle control) was applied for 10 min before induction of 40 min of global ischemia followed by 60 min of reperfusion. During ischemia, saline (control), 15-F2t-IsoP, 15-F2t-IsoP + SQ, or SQ in saline was perfused through the aorta at 60 μl/min. 15-F2t-IsoP, 15-F2t-IsoP + SQ, or SQ in KH was infused during the first 15 min of reperfusion. Coronary effluent endothelin-1 concentrations were significantly higher in the group treated with 15-F2t-IsoP than in the control group during ischemia and also in the later phase of reperfusion ( P < 0.05). Infusion of 15-F2t-IsoP increased release of cardiac-specific creatine kinase, reduced cardiac contractility during reperfusion, and increased myocardial infarct size relative to the control group. SQ abolished the deleterious effects of 15-F2t-IsoP. 15-F2t-IsoP exacerbates myocardial IRI and may, therefore, act as a mediator of IRI. 15-F2t-IsoP-induced endothelin-1 production during cardiac reperfusion may represent a mechanism underlying the deleterious actions of 15-F2t-IsoP.

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