Low-Dose Sodium Nitrite Attenuates Myocardial Ischemia and Vascular Ischemia-Reperfusion Injury in Human Models

Ingram, Thomas E.; Fraser, Alan G.; Bleasdale, Robert A.; Ellins, Elizabeth A; Mărgulescu, Andrei D.; Halcox, Julian; James, Philip E.

doi:10.1016/j.jacc.2013.03.050

Cited by 52 publications

(47 citation statements)

References 40 publications

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“…38,39,44,45 First clinical trials are under way for cardiac arrest survivors as well as patients with diabetic ulcer and myocardial ischemia. 40,46,47 Considering the results of our rat study in conjunction with the reasonable adverse-effect profile in humans, it seems appropriate to determine the potential of low-dose nitrite to alleviate, if not prevent, CIAKI through clinical trials.…”

Section: Discussionmentioning

confidence: 99%

Low-Dose Nitrite Alleviates Early Effects of an X-ray Contrast Medium on Renal Hemodynamics and Oxygenation in Rats

Seeliger

Cantow

Arakelyan³

et al. 2014

Investigative Radiology

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Low-dose nitrite infusion greatly alleviates early adverse effects of CM on renal tissue oxygenation in rats. Nitrite's beneficial effect probably relies on its reduction to nitric oxide in hypoxic tissue with ensuing vasodilation. Our nitrite dose resulted in a negligible increase in methemoglobin and did not induce hypotension. Thus, low-dose nitrite infusion might prove to be a reasonably specific measure to reduce the risk for CM-induced AKI.

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Section: Discussionmentioning

confidence: 99%

Low-Dose Nitrite Alleviates Early Effects of an X-ray Contrast Medium on Renal Hemodynamics and Oxygenation in Rats

Seeliger

Cantow

Arakelyan³

et al. 2014

Investigative Radiology

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“…In particular, mitochondrial protein S- nitrosation (SNO) reversibly inhibits mitochondrial respiration, prevents mtROS production by reverse electron transfer (RET) at complex I of the ETS [25], and shields protein cysteine residues from irreversible oxidation [34,35]. Enhancement of mitochondrial SNO either by ischemic preconditioning [36] or treatment with NO donor [37–40] has been found to be protective in models of myocardial infarction; however, whether such strategies are applicable for conditions of neuromuscular injuries in skeletal muscle and how enhanced mitochondrial SNO might lead to the protection are unknown. In the present study, we utilized a clinically relevant model of tourniquet-induced IR injury in mouse hindlimb to test whether pharmacological augmentation of mitochondrial SNO could preserve muscle and/or motor nerve structural integrity and function with improved recovery from IR.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial protein S-nitrosation protects against ischemia reperfusion-induced denervation at neuromuscular junction in skeletal muscle

Wilson

Drake

Cui

et al. 2018

Free Radical Biology and Medicine

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Deterioration of neuromuscular junction (NMJ) integrity and function is causal to muscle atrophy and frailty, ultimately hindering quality of life and increasing the risk of death. In particular, NMJ is vulnerable to ischemia reperfusion (IR) injury when blood flow is restricted followed by restoration. However, little is known about the underlying mechanism(s) and hence the lack of effective interventions. New evidence suggests that mitochondrial oxidative stress plays a causal role in IR injury, which can be precluded by enhancing mitochondrial protein S-nitrosation (SNO). To elucidate the role of IR and mitochondrial protein SNO in skeletal muscle, we utilized a clinically relevant model and showed that IR resulted in significant muscle and motor nerve injuries with evidence of elevated muscle creatine kinase in the serum, denervation at NMJ, myofiber degeneration and regeneration, as well as muscle atrophy. Interestingly, we observed that neuromuscular transmission improved prior to muscle recovery, suggesting the importance of the motor nerve in muscle functional recovery. Injection of a mitochondria-targeted S-nitrosation enhancing agent, MitoSNO, into ischemic muscle prior to reperfusion reduced mitochondrial oxidative stress in the motor nerve and NMJ, attenuated denervation at NMJ, and resulted in accelerated functional recovery of the muscle. These findings demonstrate that enhancing mitochondrial protein SNO protects against IR-induced denervation at NMJ in skeletal muscle and accelerates functional regeneration. This could be an efficacious intervention for protecting neuromuscular injury under the condition of IR and other related pathological conditions.

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“…Sodium nitrite is a selective nitric oxide donor that causes vasodilatation in ischaemic (acidotic) tissue 19. It has been proven to reduce infarct size in mice by up to 67%.…”

Section: Methods To Reduce Infarct Sizementioning

confidence: 99%

Infarct size reduction in acute myocardial infarction

McAlindon

Bucciarelli-Ducci

Suleiman

et al. 2014

Heart

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Low-Dose Sodium Nitrite Attenuates Myocardial Ischemia and Vascular Ischemia-Reperfusion Injury in Human Models

Abstract: Low-dose NaNO₂ improves functional responses in ischemic myocardium but has no effect on normal regions. Low-dose NaNO₂ protects against vascular ischemia-reperfusion injury only when it is given before the onset of ischemia.

Cited by 52 publications

References 40 publications

Low-Dose Nitrite Alleviates Early Effects of an X-ray Contrast Medium on Renal Hemodynamics and Oxygenation in Rats

Low-Dose Nitrite Alleviates Early Effects of an X-ray Contrast Medium on Renal Hemodynamics and Oxygenation in Rats

Mitochondrial protein S-nitrosation protects against ischemia reperfusion-induced denervation at neuromuscular junction in skeletal muscle

Infarct size reduction in acute myocardial infarction

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