Does nitric oxide generation contribute to the mechanism of remote ischemic preconditioning?

Nn, Petrishchëv; Власов, Т. Д.; Sipovsky, V G; Kurapeev, Dmitry; Galagudza, M. M.

doi:10.1016/s0928-4680(00)00058-4

Cited by 32 publications

(25 citation statements)

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“…Gho et al [31] found transient ischemia-reperfusion of small intestine could reduce the area of subsequent ischemic myocardial infarction, but permanent obstruction of mesenteric artery could not alleviate myocardial damage. Similar results were obtained in the study on the protective effect of renal ischemia preconditioning on cardiac muscles [32]. These results suggested that the protective effects of longdistance preconditioning on remote organs might be mediated by some humoral factors released during the reperfusion of preconditioned organs rather than nerve way.…”

Section: Discussionsupporting

confidence: 87%

The Role of Nitric Oxide in the Neuroprotection of Limb Ischemic Preconditioning in Rats

et al. 2007

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Brief limb ischemia was reported to protect neurons against injury induced by subsequent cerebral ischemia-reperfusion, and this phenomenon is known as limb ischemic preconditioning (LIP). To explore the role of nitric oxide (NO) in neuroprotection of LIP in rats, we observed changes in the content of nitric oxide (NO) and activity of NO synthase (NOS) in the serum and CA1 hippocampus of rats after transient limb ischemic preconditioning (LIP), and the influence of N(G)-nitro-L-arginine methylester (L-NAME), a NOS inhibitor, on the neuroprotection of LIP against cerebral ischemia-reperfusion injury. Results showed that NO content and NOS activity in serum increased significantly after LIP compared with the sham group. The increase showed a double peak pattern, in which the first one appeared at time 0 (immediate time point) and the second one appeared at 48 h after the LIP (P < 0.01). The NO content and NOS activity in the CA1 hippocampus in LIP group showed similar change pattern with the changes in the serum, except for the first peak of up-regulation of NO content and NOS activity appeared at 6 h after LIP. Pretreatment with L-NAME before LIP blocked the neuroprotection of LIP against subsequent cerebral ischemic insult. The blocking effect of L-NAME was abolished with pretreatment of L-Arg. These findings indicated that NO may be associated with the tolerance of pyramidal cells in the CA1 hippocampus to ischemia induced by LIP in rats.

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Section: Discussionsupporting

confidence: 87%

The Role of Nitric Oxide in the Neuroprotection of Limb Ischemic Preconditioning in Rats

et al. 2007

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“…In an early study in a rat model of RC, induced by ischaemia of the small intestine, NOS inhibition by Nω-nitro-L-arginine (L-NNA) did not affect cardioprotection (Petrishchev et al, 2001). Similarly, in rabbits preconditioned by pulmonary ischaemia, the NOS inhibitor L-NAME did not affect cardioprotection (Tang et al, 2014).…”

Section: Endogenous No In Remote Conditioningmentioning

confidence: 99%

The role of gasotransmitters NO, H₂S and CO in myocardial ischaemia/reperfusion injury and cardioprotection by preconditioning, postconditioning and remote conditioning

Andreadou

Iliodromitis

Rassaf

et al. 2014

British J Pharmacology

186

153

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Ischaemic heart disease is one of the leading causes of morbidity and mortality worldwide. The development of cardioprotective therapeutic agents remains a partly unmet need and a challenge for both medicine and industry, with significant financial and social implications. Protection of the myocardium can be achieved by mechanical vascular occlusions such as preconditioning (PC), when brief episodes of ischaemia/reperfusion (I/R) are experienced prior to ischaemia; postconditioning (PostC), when the brief episodes are experienced at the immediate onset of reperfusion; and remote conditioning (RC), when the brief episodes are experienced in another vascular territory. The elucidation of the signalling pathways, which underlie the protective effects of PC, PostC and RC, would be expected to reveal novel molecular targets for cardioprotection that could be modulated by pharmacological agents to prevent reperfusion injury. Gasotransmitters including NO, hydrogen sulphide (H2S) and carbon monoxide (CO) are a growing family of regulatory molecules that affect physiological and pathological functions. NO, H2S and CO share several common properties; they are beneficial at low concentrations but hazardous in higher amounts; they relax smooth muscle cells, inhibit apoptosis and exert anti-inflammatory effects. In the cardiovascular system, NO, H2S and CO induce vasorelaxation and promote cardioprotection. In this review article, we summarize current knowledge on the role of the gasotransmitters NO, H2S and CO in myocardial I/R injury and cardioprotection provided by conditioning strategies and highlight future perspectives in cardioprotection by NO, H2S, CO, as well as their donor molecules. LINKED ARTICLESThis article is part of a themed section on Pharmacology of the Gasotransmitters. To view the other articles in this section visit http://dx. Abbreviations 3MP, 3-mercaptopyruvate; 3-MST, 3-mercaptopyruvate transferase; BCA, cyano-L-alanine; CBS, cystathionine β-synthase; CHD, coronary heart disease; CK, creatinine kinase; CORM, carbon monoxide-releasing molecule; CSE, cystathionine γ-lyase; CyPD, cyclophilin D; HPDTT, 5-(4-hydroxyphenyl)-3H-1,2-dithiole-3-thione; eNOS, endothelial nitric oxide synthase; FeTPPS, 5,10,15, porphyrinato iron; GYY4137, morpholin-4-ium 4-methoxyphenyl-morpholino-phosphinodithioate; HNO, nitroxyl; HO, haem oxygenase; I/R, ischaemia/reperfusion; iNOS, inducible nitric oxide synthase; L-NAME, N-nitro-L-arginine methylester; L-NNA, Nω-nitro-l-arginine; LV, left ventricular; MitoSNO, mitochondria-targeted S-nitrosothiols; mPTP, mitochondria permeability transition pore; nNOS, neuronal nitric oxide synthase; Nrf2, nuclear factor (erythroid-derived 2)-like 2; NSAIDs, non-steroidal antiinflammatory drugs; ONOO − , peroxynitrite; PRG, DL-propargylglycine; PC, preconditioning; PostC, postconditioning; RC, remote conditioning; RISK, reperfusion injury salvage kinase; ROS, reactive oxygen species; SAC, S-allylcysteine; SAFE, survivor activating factor enhancement; SOD, superoxide dismutase; XOR, xanthin...

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“…For example, a brief occlusion of the mesenteric artery triggered cardioprotection in the rat (6,17,32,38,52,54) and the rabbit (44). A brief occlusion of a renal artery in the rabbit (33,43) and a femoral artery or the infrarenal aorta in the rat (34,53) also induced cardioprotection against infarction. However, these remote IPC techniques are invasive and thus have limited clinical application.…”

mentioning

confidence: 99%

Mitochondrial K_ATPchannels in hindlimb remote ischemic preconditioning of skeletal muscle against infarction

Moses¹,

Addison²,

Neligan³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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Mitochondrial KATP channels in hindlimb remote ischemic preconditioning of skeletal muscle against infarction. Am J Physiol Heart Circ Physiol 288: H559 -H567, 2005. First published September 30, 2004 doi:10.1152/ajpheart.00845.2004.-We previously demonstrated in the pig that instigation of three cycles of 10 min of occlusion and reperfusion in a hindlimb by tourniquet application (ϳ300 mmHg) elicited protection against ischemia-reperfusion injury (infarction) in multiple distant skeletal muscles subsequently subjected to 4 h of ischemia and 48 h of reperfusion, but the mechanism was not studied. The aim of this project was to test our hypothesis that mitochondrial ATP-sensitive potassium (K ATP) (mKATP) channels play a central role in the trigger and mediator mechanisms of hindlimb remote ischemic preconditioning (IPC) of skeletal muscle against infarction in the pig. We observed in the pig that hindlimb remote IPC reduced the infarct size of latissimus dorsi (LD) muscle flaps (8 ϫ 13 cm) from 45 Ϯ 2% to 22 Ϯ 3% (n ϭ 10; P Ͻ 0.05). The nonselective K ATP channel inhibitor glibenclamide (0.3 mg/kg) or the selective mK ATP channel inhibitor 5-hydroxydecanoate (5-HD, 5 mg/kg), but not the selective sarcolemmal K ATP (sKATP) channel inhibitor HMR-1098 (3 mg/kg), abolished the infarct-protective effect of hindlimb remote IPC in LD muscle flaps (n ϭ 10, P Ͻ 0.05) when these drugs were injected intravenously at 10 min before remote IPC. In addition, intravenous bolus injection of glibenclamide (1 mg/kg) or 5-HD (10 mg/kg) at the end of hindlimb remote IPC also abolished the infarct protection in LD muscle flaps (n ϭ 10; P Ͻ 0.05). Furthermore, intravenous injection of the specific mK ATP channel opener BMS-191095 (2 mg/kg) at 10 min before 4 h of ischemia protected the LD muscle flap against infarction to a similar extent as hindlimb remote IPC, and this infarct-protective effect of BMS-191095 was abolished by intravenous bolus injection of 5-HD (5 mg/kg) at 10 min before or after intravenous injection of BMS-191095 (n ϭ 10; P Ͻ 0.05). The infarct protective effect of BMS-191095 was associated with a higher muscle content of ATP at the end of 4 h of ischemia and a decrease in muscle neutrophilic myeloperoxidase activity at the end of 1.5 h of reperfusion compared with the time-matched control (n ϭ 10, P Ͻ 0.05). These observations led us to conclude that mK ATP channels play a central role in the trigger and mediator mechanisms of hindlimb remote IPC of skeletal muscle against infarction in the pig, and the opening of mK ATP channels in ischemic skeletal muscle is associated with an ATP-sparing effect during sustained ischemia and attenuation of neutrophil accumulation during reperfusion. pig skeletal muscle; remote ischemic preconditioning; trigger and mediator mechanism MURRY ET AL. (20) reported that ischemic preconditioning (IPC) of dog myocardium with four cycles of 5 min of coronary artery occlusion interspersed with 5 min of reperfusion attenuated myocardial infarction by 75% when the preconditioned myocardium...

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Does nitric oxide generation contribute to the mechanism of remote ischemic preconditioning?

Cited by 32 publications

References 12 publications

The Role of Nitric Oxide in the Neuroprotection of Limb Ischemic Preconditioning in Rats

The Role of Nitric Oxide in the Neuroprotection of Limb Ischemic Preconditioning in Rats

The role of gasotransmitters NO, H₂S and CO in myocardial ischaemia/reperfusion injury and cardioprotection by preconditioning, postconditioning and remote conditioning

Mitochondrial K_ATPchannels in hindlimb remote ischemic preconditioning of skeletal muscle against infarction

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Does nitric oxide generation contribute to the mechanism of remote ischemic preconditioning?

Cited by 32 publications

References 12 publications

The Role of Nitric Oxide in the Neuroprotection of Limb Ischemic Preconditioning in Rats

The Role of Nitric Oxide in the Neuroprotection of Limb Ischemic Preconditioning in Rats

The role of gasotransmitters NO, H2S and CO in myocardial ischaemia/reperfusion injury and cardioprotection by preconditioning, postconditioning and remote conditioning

Mitochondrial KATPchannels in hindlimb remote ischemic preconditioning of skeletal muscle against infarction

Contact Info

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The role of gasotransmitters NO, H₂S and CO in myocardial ischaemia/reperfusion injury and cardioprotection by preconditioning, postconditioning and remote conditioning

Mitochondrial K_ATPchannels in hindlimb remote ischemic preconditioning of skeletal muscle against infarction