Glutathione disulfide as an index of oxidative stress during postischemic reperfusion in isolated rat hearts

1995 ◽  
Vol 144 (1) ◽  
pp. 85-93 ◽  
Author(s):  
Robert J. A. M. Verbunt ◽  
Willem G. van Dockum ◽  
E. M. Lars Bastiaanse ◽  
Janneke M. Egas ◽  
Arnoud van der Laarse
1995 ◽  
Vol 146 (2) ◽  
pp. 187-187
Author(s):  
Robert J. A. M. Verbunt ◽  
Willem G. van Dockum ◽  
E. M. Lars Bastiaanse ◽  
Janneke M. Egas ◽  
Arnoud van der Laarse

2017 ◽  
Vol 40 (5) ◽  
pp. 640-654 ◽  
Author(s):  
Eun-Seok Park ◽  
Do-Hyun Kang ◽  
Jun Chul Kang ◽  
Yong Chang Jang ◽  
Min-Ju Lee ◽  
...  

2006 ◽  
Vol 283 (1-2) ◽  
pp. 147-152 ◽  
Author(s):  
Ségolène Gambert ◽  
Catherine Vergely ◽  
Rodolphe Filomenko ◽  
Daniel Moreau ◽  
Ali Bettaieb ◽  
...  

2001 ◽  
Vol 280 (5) ◽  
pp. H2189-H2195 ◽  
Author(s):  
Jan G. Van Emous ◽  
Carmen L. A. M. Vleggeert-Lankamp ◽  
Marcel G. J. Nederhoff ◽  
Tom J. C. Ruigrok ◽  
Cees J. A. Van Echteld

Normalization of intracellular sodium (Na[Formula: see text]) after postischemic reperfusion depends on reactivation of the sarcolemmal Na+-K+-ATPase. To evaluate the requirement of glycolytic ATP for Na+-K+-ATPase function during postischemic reperfusion, 5-s time-resolution23Na NMR was performed in isolated perfused rat hearts. During 20 min of ischemia, Na[Formula: see text] increased approximately twofold. In glucose-reperfused hearts with or without prior preischemic glycogen depletion, Na[Formula: see text]decreased immediately upon postischemic reperfusion. In glycogen-depleted pyruvate-reperfused hearts, however, the decrease of Na[Formula: see text] was delayed by ∼25 s, and application of the pyruvate dehydrogenase (PDH) activator dichloroacetate (DA) did not shorten this delay. After 30 min of reperfusion, Na[Formula: see text]had almost normalized in all groups and contractile recovery was highest in the DA-treated hearts. In conclusion, some degree of functional coupling of glycolytic ATP and Na+-K+-ATPase activity exists, but glycolysis is not essential for recovery of Na[Formula: see text] homeostasis and contractility after prolonged reperfusion. Furthermore, the delayed Na+-K+-ATPase reactivation observed in pyruvate-reperfused hearts is not due to inhibition of PDH.


Pharmacology ◽  
2021 ◽  
pp. 1-10
Author(s):  
Nada M. Banjac ◽  
Velibor M. Vasović ◽  
Nebojša P. Stilinović ◽  
Dušan V. Prodanović ◽  
Ana D. Tomas Petrović ◽  
...  

<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.


2013 ◽  
Vol 19 (3) ◽  
pp. 186-194 ◽  
Author(s):  
Hitoshi Inafuku ◽  
Yukio Kuniyoshi ◽  
Satoshi Yamashiro ◽  
Katsuya Arakaki ◽  
Takaaki Nagano ◽  
...  

1997 ◽  
Vol 85 (3) ◽  
pp. 245-257 ◽  
Author(s):  
Anders Winnerkvist ◽  
Björn Wiman ◽  
Guro Valen ◽  
Jarle Vaage

2001 ◽  
Vol 79 (4) ◽  
pp. 489-497 ◽  
Author(s):  
M'hammed Aouffen ◽  
Joanne Paquin ◽  
Eric De Grandpré ◽  
Réginald Nadeau ◽  
Mircea-Alexandru Mateescu

Ceruloplasmin (CP), an important serum antioxidant, is a blue copper glycoprotein with ferroxidase and oxidase activities. Among other physiological actions, plasma CP was shown to protect isolated rat hearts and cultured P19 neurons exposed to oxidative stress conditions, raising the possibility of using this protein in the treatment of cardiac and neuronal diseases related to oxidative damage. However, since therapeutic applications of CP must be compatible with restrictions in the administration of blood derivatives to humans, there is a need to produce the protein by genetic engineering. To help in the choice of adequate expression systems, we undertook this study to determine if the carbohydrate moiety on the protein is essential for its functions. CP was completely deglycosylated using N-glycosidase F under nondenaturing conditions. Deglycosylated CP was found to retain most of the conformational, antioxidant, and enzymatic properties of the native protein in vitro. Moreover, both forms of the protein had similar cardioprotective and neuronoprotective effects against oxidative stress as evaluated with isolated rat hearts undergoing ischemia–reperfusion and with cultured P19 neurons exposed to xanthine – xanthine oxidase. The data thus indicate that the carbohydrate moiety of CP is not essential for its enzymatic and protective actions. Accordingly, even the use of expression systems that do not glycosylate mammalian proteins could provide a recombinant CP that retains its therapeutic potential.Key words: copperproteins, protein-linked carbohydrates, ischemia-reperfusion, isolated rat hearts, cultured P19 neurons.


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