<i>S</i>‐Nitrosoglutathione induces formation of nitrosylmyoglobin in isolated hearts during cardioplegic ischemia — an electron spin resonance study

Konorev, Eugene; Joseph, Joy; Kalyanaraman, B.

doi:10.1016/0014-5793(95)01429-2

Cited by 26 publications

(14 citation statements)

References 35 publications

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“…Significantly, at least two other groups have detected the presence of nitrosomyoglobin in cardiac tissue. (19,20) To summarize, in the tissue at physiologically relevant concentrations, no evidence for significant reaction of NO with myoglobin species was found (Fig. 3B).…”

Section: Quantitative Production Of Nomentioning

confidence: 86%

The Catabolic Fate of Nitric Oxide

Pearce¹,

Kanai²,

Birder³

et al. 2002

Journal of Biological Chemistry

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Stimulation of cardiomyocytes to endogenously evolve nitric oxide is shown by microsensor measurements on single cells to lead to transient nitric oxide concentrations of a few hundred nanomolar. At these submicromolar concentrations, no evidence could be found for the expected reaction between nitric oxide generated and the oxymyoglobin present in the cells: nitric oxide ؉ oxymyoglobin 3 nitrate ؉ metmyoglobin. No metmyoglobin formation was detected by electron paramagnetic resonance spectroscopy, and microsensor measurements revealed near quantitative conversion of the nitric oxide to nitrite rather than nitrate ion. Moreover, the rate of nitrite formation is shown to be too rapid to be accounted for by non-enzymatic means. The essentially quantitative and rapid catabolism of nitric oxide to nitrite ion can plausibly be explained on the basis of a cycle of reactions catalyzed by cytochrome c oxidase. It is demonstrated with the purified hemoproteins in vitro that the terminal oxidase can outcompete oxymyoglobin for available nitric oxide. It is proposed that under normal physiological and most pathological (non-inflammatory) conditions, reaction with cytochrome c oxidase is the major route by which NO is removed from mitochondria-rich cells.It has been widely accepted that the reactions of nitric oxide (NO) with either oxyhemoglobin or oxymyoglobin to form nitrate ion, and respectively, methemoglobin or metmyoglobin constitute the major catabolic pathways by which excess NO is removed from tissues in vivo. The in vitro reactions are facile with second-order rate constants at pH 7.0 and 20 -25°C of about 4 ϫ 10 7

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Section: Quantitative Production Of Nomentioning

confidence: 86%

The Catabolic Fate of Nitric Oxide

Pearce¹,

Kanai²,

Birder³

et al. 2002

Journal of Biological Chemistry

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“…Myoglobin which is abundant in muscle cells, has previously been used to trap -NO in myocardial cells (Konorev et al, 1996). The formation of the MGD-Fe2+-NO adduct indicated -NO trapping in the extracellular space.…”

Section: Discussion -No As An Endogenous Protective Agent In Myocardimentioning

confidence: 99%

The mechanism of cardioprotection by S‐nitrosoglutathione monoethyl ester in rat isolated heart during cardioplegic ischaemic arrest

Konorev

Joseph

Tarpey

et al. 1996

British J Pharmacology

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1 This study was designed (i) to assess the effect of S-nitrosoglutathione monoethyl ester (GSNO-MEE), a membrane-permeable analogue of S-nitrosoglutathione (GSNO), on rat isolated heart during cardioplegic ischaemia, and (ii) to monitor the release of nitric oxide (-NO) from GSNO-MEE in intact hearts using endogenous myoglobin as an intracellular -NO trap and the hydrophilic N-methyl glucamine dithiocarbamate-iron During aerobic reperfusion, denitrosylation of the MbNO complex slowly occurred as shown by the decrease in ESR spectral intensity. GSNO-MEE treatment did not affect ubisemiquinone radical formation during reperfusion. 5 GSNO-MEE (20,l`-) treatment elevated the myocardial cyclic GMP during ischaemia (47 + 3 in control vs. 153 + 34 pmol g-' dry wt. after 35 min ischaemia, P< 0.05). The cyclic GMP levels decreased in the control group during ischaemia from 100 + 6 after induction of cardioplegia to 47 + 3 pmol g' dry wt. at the end of ischaemic duration. 6 Glycogen levels were lower in GSNO-MEE (20 pmol 1-1)-treated hearts throughout the ischaemic duration (26.7 + 3.1 in control vs. 19.7 + 2.4 pmol g dry-' wt. in GSNO-MEE-treated group at the end of ischaemic duration), because of rapid depletion of glycogen during induction of cardioplegia. During ischaemia, the amounts of glycogen consumed in both groups were similar. Equivalent amounts of lactate were produced in both groups (148 + 4 in control vs. 141 + 4 umol g' dry wt. in GSNO-MEEtreated group after 35 min in ischaemia). 7 The mechanism(s) of myocardial protection by GSNO-MEE against ischaemic injury may involve preischaemic glycogen reduction and/or elevated cyclic GMP levels in myocardial tissue during ischaemia.

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“…With the spectroscopic detection of MbNO during ischemia in isolated rat hearts two years later (Konorev et al, 1996), it finally became clear that also in the heart, at least under pathophysiological conditions, the same species could be involved as during the curing process (i.e. MbNO).…”

Section: From Trophism To Cardiovascular Physiologymentioning

confidence: 99%