scholarly journals Homocysteine Exposure Impairs Myocardial Resistance to Ischaemia Reperfusion and Oxidative Stress

2015 ◽  
Vol 37 (6) ◽  
pp. 2265-2274 ◽  
Author(s):  
Amer Almashhadany ◽  
Dareuosh Shackebaei ◽  
Thomas Van der Touw ◽  
Graham L. Jones ◽  
M.-Saadeh Suleiman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Calcium Transient ◽  
Rate Pressure Product ◽  
Rat Cardiomyocytes ◽  
Ischaemia Reperfusion ◽  
Rat Hearts ◽  
Before And After ◽  
Cardiomyocyte Contractility ◽  
Perfused Rat Hearts ◽  
And Oxidative Stress

Background/Aims: Hyperhomocysteinaemia is recognised as a strong independent risk factor for developing cardiovascular disease. This study investigated how an acute homocysteine dose affected cardiac performance during ischaemia reperfusion and cardiomyocyte contractility and morphology under normal conditions and during oxidative stress. Methods: Cardiac function was measured in isolated and perfused rat hearts before and after 40 minutes' global normothermic ischaemia. Where used, 0.1 mM L-homocysteine was present prior to, and throughout ischaemia, before wash out after 10 minutes' reperfusion. Calcium transients under normal conditions and changes in contractile synchronicity during oxidative stress (exposure to 0.2 mM H2O2) were measured in freshly isolated rat cardiomyocytes incubated for 60 minutes ± 0.1 mM L-homocysteine. Results: During ischaemia reperfusion 0.1 mM L-homocysteine significantly reduced the rate pressure product during reperfusion (10,038 ± 749 vs. 5955 ± 567 mmHg bpm, p < 0.001), but did not affect time to ischaemic contracture. Incubation of freshly isolated cardiomyocytes with 0.1 mM L-homocysteine significantly decreased the amplitude of the calcium transient and slowed the time to half relaxation. Conclusions: These findings suggest that homocysteine exposure affected myocardial recovery from ischaemia and contractile homeostasis although the exact mechanisms for these changes remain to be determined.

scholarly journals Effects of Monomeric and Oligomeric Flavanols on Kidney Function, Inflammation and Oxidative Stress in Runners: A Randomized Double-Blind Pilot Study

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1634 ◽  
Author(s):  
Khrystyna O. Semen ◽  
Antje R. Weseler ◽  
Marcel J. W. Janssen ◽  
Marie-José Drittij-Reijnders ◽  
Jos L. M. L. le Noble ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Kidney Function ◽  
Randomized Study ◽  
Kidney Injury ◽  
Strenuous Exercise ◽  
Vitis Vinifera L ◽  
Grape Seeds ◽  
Double Blind ◽  
Before And After ◽  
And Oxidative Stress

Nonsteroidal anti-inflammatory drugs are frequently used by athletes in order to prevent musculoskeletal pain and improve performance. In combination with strenuous exercise, they can contribute to a reduction of renal blood flow and promote development of kidney damage. We aimed to investigate whether monomeric and oligomeric flavanols (MOF) could reduce the severity of kidney injuries associated with the intake of 400-mg ibuprofen followed by the completion of a half-marathon in recreational athletes. In this double-blind, randomized study, the original MOF blend of extracts from grape seeds (Vitis vinifera L.) and pine bark (Pinus pinaster L.) or placebo were taken for 14 days preceding the ibuprofen/half-marathon. Urine samples were collected before and after the ibuprofen/half-marathon, and biomarkers of kidney injury, inflammation and oxidative stress were assessed. Intake of MOF significantly reduced the incidence of post-race hematuria (p = 0.0004) and lowered concentrations of interleukin (IL)-6 in the urine (p = 0.032). Urinary neutrophil-associated lipocalin, creatine, albumin, IL-8 and malondialdehyde tended to decrease. The supplementation with MOF in recreational runners appears to safely preserve kidney function, reduce inflammation and promote antioxidant defense during strenuous exercise and intake of a single dose of ibuprofen.

scholarly journals Antioxidant Solution in Combination with Angiotensin-(1-7) Provides Myocardial Protection in Langendorff-Perfused Rat Hearts

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Michaela Andrä ◽  
Miriam Russ ◽  
Susanne Jauk ◽  
Mariana Lamacie ◽  
Ingrid Lang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Protection ◽  
Ischemia Reperfusion Injury ◽  
Organ Procurement ◽  
Ischemia Reperfusion ◽  
Morphological Alteration ◽  
Organ Shortage ◽  
Cold Ischemia ◽  
Rat Hearts ◽  
Perfused Rat Hearts

As progressive organ shortage in cardiac transplantation demands extension of donor criteria, effort is needed to optimize graft survival. Reactive oxygen and nitrogen species, generated during organ procurement, transplantation, and reperfusion, contribute to acute and late graft dysfunction. The combined application of diverse substances acting via different molecular pathways appears to be a reasonable approach to face the complex mechanism of ischemia reperfusion injury. Thus, an antioxidant solution containing α-ketoglutaric acid, 5-hydroxymethylfurfural, N-acetyl-L-methionine, and N-acetyl-selenium-L-methionine was combined with endogenous angiotensin-(1-7). Its capacity of myocardial protection was investigated in isolated Langendorff-perfused rat hearts subjected to warm and cold ischemia. The physiological cardiac parameters were assessed throughout the experiments. Effects were evaluated via determination of the oxidative stress parameters malondialdehyde and carbonyl proteins as well as immunohistochemical and ultrastructural tissue analyses. It was shown that a combination of 20% (v/v) antioxidant solution and 220 pM angiotensin-(1-7) led to the best results with a preservation of heart tissue against oxidative stress and morphological alteration. Additionally, immediate cardiac recovery (after warm ischemia) and normal physiological performance (after cold ischemia) were recorded. Overall, the results of this study indicate substantial cardioprotection of the novel combination with promising prospective for future clinical use.

Ischemic preconditioning affects hexokinase activity and HKII in different subcellular compartments throughout cardiac ischemia-reperfusion

2009 ◽  
Vol 106 (6) ◽  
pp. 1909-1916 ◽  
Author(s):  
Ebru Gürel ◽  
Kirsten M. Smeele ◽  
Otto Eerbeek ◽  
Anneke Koeman ◽  
Cihan Demirci ◽  
...  
Keyword(s):  
Protein Content ◽  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Glycolytic Enzyme ◽  
Cardiac Ischemia ◽  
Biphasic Response ◽  
Control Groups ◽  
Rat Hearts ◽  
Before And After ◽  
Perfused Rat Hearts

The glycolytic enzyme hexokinase (HK) is suggested to play a role in ischemic preconditioning (IPC). In the present study we determined how ischemic preconditioning affects HK activity and HKI and HKII protein content at five different time points and three different subcellular fractions throughout cardiac ischemia-reperfusion. Isolated Langendorff-perfused rat hearts (10 groups of 7 hearts each) were subjected to 35 min ischemia and 30 min reperfusion (control groups); the IPC groups were pretreated with 3 times 5-min ischemia. IPC was without effect on microsomal HK activity, and only decreased cytosolic HK activity at 35 min ischemia, which was mimicked by decreased cytosolic HKII, but not HKI, protein content. In contrast, mitochondrial HK activity at baseline and during reperfusion was elevated by IPC, without changes during ischemia. No effect of IPC on mitochondrial HK I protein content was observed. However, mitochondrial HK II protein content during reperfusion was augmented by IPC, albeit not following the IPC stimulus. It is concluded that IPC results in decreased cytosolic HK activity during ischemia that could be explained by decreased HKII protein content. IPC increased mitochondrial HK activity before ischemia and during reperfusion that was only mimicked by increased HK II protein content during reperfusion. IPC was without effect on the phosphorylation status of HK before ischemia. We conclude that IPC is associated with 1) a biphasic response of increased mitochondrial HK activity before and after ischemia, 2) decreased cytosolic HK activity during ischemia, and 3) cellular redistribution of HKII but not HKI.

Effect of diazoxide on flavoprotein oxidation and reactive oxygen species generation during ischemia-reperfusion: a study on Langendorff-perfused rat hearts using optic fibers

2008 ◽  
Vol 294 (5) ◽  
pp. H2088-H2097 ◽  
Author(s):  
Philippe Pasdois ◽  
Bertrand Beauvoit ◽  
Liliane Tariosse ◽  
Béatrice Vinassa ◽  
Simone Bonoron-Adèle ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Reactive Oxygen Species Generation ◽  
Left Ventricular ◽  
Rate Pressure Product ◽  
Control Group ◽  
Rat Hearts ◽  
Perfused Rat Hearts ◽  
Optic Fibers ◽  
The One ◽  
Isolated Perfused Rat Hearts

This study analyzed the oxidant generation during ischemia-reperfusion protocols of Langendorff-perfused rat hearts, preconditioned with a mitochondrial ATP-sensitive potassium channel (mitoKATP) opener (i.e., diazoxide). The autofluorescence of mitochondrial flavoproteins, and that of the total NAD(P)H pool on the one hand and the fluorescence of dyes sensitive to H2O2 or O2•− [i.e., the dihydrodichlorofluoroscein (H2DCF) and dihydroethidine (DHE), respectively] on the other, were noninvasively measured at the surface of the left ventricular wall by means of optic fibers. Isolated perfused rat hearts were subjected to an ischemia-reperfusion protocol. Opening mitoKATP with diazoxide (100 μM) 1) improved the recovery of the rate-pressure product after reperfusion (72 ± 2 vs. 16.8 ± 2.5% of baseline value in control group, P < 0.01), and 2) attenuated the oxidant generation during both ischemic (−46 ± 5% H2DCF oxidation and −40 ± 3% DHE oxidation vs. control group, P < 0.01) and reperfusion (−26 ± 2% H2DCF oxidation and −23 ± 2% DHE oxidation vs. control group, P < 0.01) periods. All of these effects were abolished by coperfusion of 5-hydroxydecanoic acid (500 μM), a mitoKATP blocker. During the preconditioning phase, diazoxide induced a transient, reversible, and 5-hydroxydecanoic acid-sensitive flavoprotein and H2DCF (but not DHE) oxidation. In conclusion, the diazoxide-mediated cardioprotection is supported by a moderate H2O2 production during the preconditioning phase and a strong decrease in oxidant generation during the subsequent ischemic and reperfusion phases.

scholarly journals Different mechanisms of mitochondrial proton leak in ischaemia/reperfusion injury and preconditioning: implications for pathology and cardioprotection

2006 ◽  
Vol 395 (3) ◽  
pp. 611-618 ◽  
Author(s):  
Sergiy M. Nadtochiy ◽  
Andrew J. Tompkins ◽  
Paul S. Brookes
Keyword(s):  
Reperfusion Injury ◽  
Kinase Inhibitor ◽  
Adenine Nucleotide ◽  
Treatment Strategies ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Rat Hearts ◽  
Perfused Rat Hearts

The mechanisms of mitochondrial proton (H+) leak under various pathophysiological conditions are poorly understood. In the present study it was hypothesized that different mechanisms underlie H+ leak in cardiac IR (ischaemia/reperfusion) injury and IPC (ischaemic preconditioning). Potential H+ leak mechanisms examined were UCPs (uncoupling proteins), allosteric activation of the ANT (adenine nucleotide translocase) by AMP, or the PT (permeability transition) pore. Mitochondria isolated from perfused rat hearts that were subjected to IPC exhibited a greater H+ leak than did controls (202±27%, P<0.005), and this increased leakage was completely abolished by the UCP inhibitor, GDP, or the ANT inhibitor, CAT (carboxyattractyloside). Mitochondria from hearts subjected to IR injury exhibited a much greater amount of H+ leak than did controls (411±28%, P<0.001). The increased leakage after IR was weakly inhibited by GDP, but was inhibited, >50%, by carboxyattractyloside. In addition, it was inhibited by cardioprotective treatment strategies including pre-IR perfusion with the PT pore inhibitors cyclosporin A or sanglifehrin A, the adenylate kinase inhibitor, AP5A (diadenosine pentaphosphate), or IPC. Together these data suggest that the small increase in H+ leak in IPC is mediated by UCPs, while the large increase in H+ leak in IR is mediated by the ANT. Furthermore, under all conditions studied, in situ myocardial O2 efficiency was correlated with isolated mitochondrial H+ leak (r2=0.71). In conclusion, these data suggest that the modulation of H+ leak may have important implications for the outcome of IR injury.

scholarly journals Study the Haematological parameters and Oxidative stress before and after disbudding in Calves

2021 ◽  
pp. 62-69
Author(s):  
Shiv Swaroop ◽  
Pramanik PS ◽  
Singh KD ◽  
Subodh Kumar ◽  
Verma AK
Keyword(s):  
Oxidative Stress ◽  
Animal Husbandry ◽  
Lipid Peroxides ◽  
Haematological Parameters ◽  
Veterinary Science ◽  
Treatment Groups ◽  
Significant Difference ◽  
Haematological Profile ◽  
Before And After ◽  
And Oxidative Stress

The aim of the present investigation was to examine the haematological profile and oxidative stress before and after disbudding in calves. The study was carried out at Livestock Farm Complex, College of Veterinary Science and Animal Husbandry, ANDUAT, Kumarganj, Ayodhya and nearby villages. Twenty four cattle calves were utilized to study haematological parameters that are Haemoglobin (Hb (gm/dl), Neutrophil (%), Basophil (%), PCV (%), Lymphocyte (%), Monocyte (%), TLC (103/ µl), Eosinophil (%), N/L ratio) and oxidative stress before and after disbudding in to four groups viz. control (T0), lignocaine (TL), tremadol (TT) and lignocaine+tremadol (TL-T). After medication calves were disbudded by hot iron method. The blood samples were collected for haematological parameters & for estimation of LPO (lipid peroxides) as per method described by [1] just before (0h) and after disbudding on 6h, 24h and 72h. The results showed that, at 24h, T0 group showed significantly lowest Hb (10.66±0.49%) which was statistically similar to TT and TL-T groups. At 0h, 6h and 72h means of PCV% were significantly different among treatment groups. The lowest lymphocytes (64.00±1.00) was observed in TT group at 6h. The T0 group showed significantly lowest basophil (0.00±0.00) which was statistically similar to TT and TL-T groups but significantly different from TL group at 6h. At the same interval, T0 group showed significantly lowest monocytes (4.66±0.61) which was significantly different with TL, TT and TL-T groups. At 6h, T0 group showed significantly lowest N/ L ratio (0.15±0.01) which was statistically similar to TT and TL-T groups but significantly different from TL group. At 0h, 6h and 24h LPO was significantly different among groups. At 0h, T0 group showed significantly highest (106.59±0.63) which was significantly different from TL, TT and TL-T groups. It may be concluded that no significant difference was observed in eosinophil%, TLC, neutrophil% and monocyte% counts between control and treatment groups. However, Hb%, basophil%, PCV% and lymphocyte% were significantly different between control and treatment groups. N/L ratio was significant only at 6h. Most of the cases TL-T group showed comparatively better performance. At 0h, 6h and 24h LPO was significantly different among groups. At 0h, T0 group showed significantly highest (106.59±0.63) which was significantly different from TL, TT and TL-T groups.

Tadalafil in Increasing Doses: The Influence on Coronary Blood Flow and Oxidative Stress in Isolated Rat Hearts

Pharmacology ◽  
2021 ◽  
pp. 1-10
Author(s):  
Nada M. Banjac ◽  
Velibor M. Vasović ◽  
Nebojša P. Stilinović ◽  
Dušan V. Prodanović ◽  
Ana D. Tomas Petrović ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Anion ◽  
Coronary Flow ◽  
Albino Rats ◽  
Dependent Manner ◽  
Superoxide Anion Production ◽  
Nitrite Oxide ◽  
Rat Hearts ◽  
And Oxidative Stress ◽  
Isolated Rat

<b><i>Introduction:</i></b> This study aimed to assess the influence of different doses of tadalafil on coronary flow and oxidative stress in isolated rat hearts. <b><i>Methods:</i></b> The hearts of male Wistar albino rats (<i>n</i> = 48) were retrogradely perfused according to the Langendorff technique at gradually increased constant perfusion pressure (CPP) (40–120 mm Hg). Coronary flow and oxidative stress markers: nitrite oxide (NO) outflow and superoxide anion production in coronary effluent were measured. The experiments were performed during control conditions and in the presence of tadalafil (10, 20, 50, and 200 nM) alone or with Nω-nitro-L-arginine monomethyl ester (L-NAME) (30 μM). <b><i>Results:</i></b> Tadalafil administration significantly increased coronary flow at all CPP values at all administered doses. Tadalafil led to an increase in the NO levels, but a statistically significant NO release increase was found only at the highest dose and highest CPP. Tadalafil did not significantly affect the release of O<sup>2−</sup>. After inhibiting the nitrite oxide synthase system by L-NAME, tadalafil-induced changes in cardiac flow and NO levels were reversed. L-NAME administration had no pronounced effect on the O<sup>2−</sup> release. <b><i>Conclusion:</i></b> Tadalafil causes changes in the heart vasculature in a dose-dependent manner. It does not lead to a significant increase in the production of superoxide anion radicals.

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