Adenosine A2-receptor activation inhibits neutrophil-mediated injury to coronary endothelium

Zhi, Zhao; Sato, Hiroki; Williams, Mark W.; Fernandez, Antony; Vinten-Johansen, J.

doi:10.1152/ajpheart.1996.271.4.h1456

Cited by 48 publications

(64 citation statements)

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“…Our findings indicated that the baseline superoxide responses to PAF were double that to fMLP. This difference in response was also shown by Zhao et al 23 in their study using canine neutrophils, and it may reflect a difference in receptor density on the surface of the neutrophil membrane for the two agonists.…”

Section: Discussionsupporting

confidence: 79%

Persistance et voie de l’inhibition de la production de superoxyde par les neutrophiles induite par isoflurane

Saad

Eom

et al. 2009

Can J Anesth/J Can Anesth

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Background Our previous work has demonstrated that treatment with isoflurane has a preconditioning-like inhibitory effect on superoxide production (SOP) by polymorphonuclear neutrophils. The current objectives were to determine persistency of this effect and to clarify where in the signalling pathway this inhibition of SOP occurred. The latter was accomplished using two receptor-dependent neutrophil agonists, platelet activating factor (PAF) and formyl-methionyl-leucyl-phenylalanine (fMLP), and two receptor-independent neutrophil stimuli, the protein-kinase C stimulator, phorbol myristate acetate (PMA), and the calcium ionophore, A23187.Methods Arterial blood samples were obtained from eight dogs under baseline condition (conscious state), during isoflurane (1 MAC) administration, and 24 and 48 hr post-isoflurane (also in conscious state). Neutrophils were isolated and stimulated with 1 lM concentrations of PAF, fMLP, PMA, and A23187. SOP was measured spectrophotometrically. Results Isoflurane administration caused (1) an approximate 50% decrease in SOP during PAF or fMLP (P \ 0.01 vs baseline), which remained evident from 24 to 48 hr following isoflurane; (2) an initial 29% decrease in SOP during PMA (P \ 0.05 vs baseline), which returned to baseline by 24 hr following isoflurane; and (3) no change in SOP during A23187 (P [ 0.05 vs baseline). Conclusions Isoflurane administration caused prolonged (from 24 to 48 hr) decreases in agonist-induced SOP by neutrophils. This effect involved inhibition at site(s)

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Section: Discussionsupporting

confidence: 79%

Persistance et voie de l’inhibition de la production de superoxyde par les neutrophiles induite par isoflurane

Saad

Eom

et al. 2009

Can J Anesth/J Can Anesth

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“…It has been reported that adenosine reduces the neutrophil-induced endothelial injury by A 2 -receptor-mediated inhibition of O 2 generation and adherence. 18 In addition, caution must be applied before extrapolating these results to other organs. In summary, this work indicates that the optimal ischemic time window to induce preconditioning in liver is defined by the balance between the tissue concentrations of adenosine and xanthine.…”

Section: Discussionmentioning

confidence: 99%

Hepatic preconditioning in rats is defined by a balance of adenosine and xanthine

et al. 1998

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The present work investigates the relationship between adenosine, nitric oxide (NO), and free radicals during ischemic preconditioning in rat liver. For this purpose, we evaluated: 1) the efficacy of different periods of preconditioning; 2) the changes in the concentration of adenine nucleotides during preconditioning; 3) the importance of adenosine and xanthine concentrations in the induction of preconditioning; and 4) the possible effect of xanthine oxidase-derived superoxide anion on NO during preconditioning. Results show that just a 10-to 15-minute period of ischemia followed by 10-minute reperfusion prevents the ischemic damage that would be induced by a subsequent 90 minutes of ischemia followed by 90 minutes of reperfusion. Administration of xanthine or metabolization of endogenous adenosine abolishes the protective effect of preconditioning. When rats have been subjected to a period of preconditioning not within the effective time window (10-15 minutes), and thus offering no protection, the administration of a NO donor was found to restore the protection. The dose needed to restore protection appears to be proportional to the endogenous xanthine concentration. In addition, when xanthine oxidase was inhibited, preconditioning effectively offered protection in front of ischemia and reperfusion, independently of the xanthine concentration. Altogether, this indicates that the time window of ischemia capable to induce preconditioning in liver is defined by the relative tissue concentrations of adenosine and xanthine. The lower limit of this window (10 minutes) is defined by the amount of adenosine able to induce NO generation. Its upper limit (15 minutes) is defined by the concentration of xanthine able to remove the generated NO. (HEPATOLOGY 1998;28:768-773.)In 1986, Murry et al. discovered that short periods of ischemia and reperfusion render the myocardium resistant to a subsequent more-sustained ischemic insult. 1 This phenomenon, called ischemic preconditioning, has been commonly studied in the heart, but few studies have been performed on intestine 2 or liver. 3 The mechanism underlying preconditioning remains unknown and is currently under intense investigation. It has been suggested that protection depends on the release of substances by the organ helping to protect it against injury. Along this line, potential mediators include nitric oxide (NO) 2,4 and adenosine. 5 Vegh et al. 6 reported that the protection conferred by preconditioning in dog heart in vivo disappeared after NO inhibition. Nevertheless, other authors 7 found that endogenous NO is not a mediator in the ischemic preconditioning in the isolated rat heart. Recent work by our group, using a model of hepatic preconditioning in rat, demonstrated that inhibition of NO abolishes the effect of preconditioning. 8 In the same study, we suggested that NO production was stimulated by endogenous adenosine. It is known that pretreatment with adenosine or selective adenosine A 1 receptor agonists mimics the effect of preconditioning in heart. 10 Bot...

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“…The A 1 receptor is in-volved in the triggering mechanism of ischemic preconditioning, and selective A 1 receptor agonists applied before the onset of ischemia can mimic ischemic preconditioning to protect myocardium from ischemia/reperfusion injury (14,48,50). In contrast, the A 2a receptor has been documented to play an important role in preventing neutrophil-initiated reperfusion injury (38,78). Due to the lack of the selective agonists, the exact role of A 2b receptor in cardioprotection remains elusive, although a recent report has suggested a potential role for this receptor in postconditioning (57).…”

Section: Introductionmentioning

confidence: 99%

IB‐MECA and Cardioprotection

Xu¹,

Jang²,

Mueller³

et al. 2006

Cardiovascular Drug Reviews

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The adenosine A 3 receptor plays an important role in ischemic preconditioning. Activation of the adenosine A 3 receptor with its agonists induces both early and late pharmacological preconditioning through various mechanisms. As the first potent and selective adenosine A 3 receptor agonist, IB-MECA (N 6 -(3-iodobenzyl)-adenosine-5¢-N-methylcarboxamide) has been demonstrated to induce cardioprotection against myocardial ischemia/reperfusion injury when given before onset of ischemia by triggering pharmacological preconditioning. More importantly, IB-MECA can also protect the heart even when administered at the onset of reperfusion after ischemia, indicating a strong likelihood that the drug may be useful for the treatment of patients with acute myocardial infarction. However, since IB-MECA has been reported to have lethal effects at higher concentrations, and may cause systemic hypertension in some species, further studies are needed to find the best treatment strategy to increase its therapeutic potential.

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Adenosine A2-receptor activation inhibits neutrophil-mediated injury to coronary endothelium

Cited by 48 publications

References 0 publications

Persistance et voie de l’inhibition de la production de superoxyde par les neutrophiles induite par isoflurane

Persistance et voie de l’inhibition de la production de superoxyde par les neutrophiles induite par isoflurane

Hepatic preconditioning in rats is defined by a balance of adenosine and xanthine

IB‐MECA and Cardioprotection

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