Evidence map›Paper›PMID 27358482›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2016

Spinal Neuronal NOS Signaling Contributes to Morphine Cardioprotection in Ischemia Reperfusion Injury in Rats.

Lingling Jiang, Jun Hu, Shufang He, Li Zhang, Ye Zhang

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.2field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 15 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Lingling JiangDepartment of Anesthesiology, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, People's Republic of China (L.J., J.H., S.H., and Y. Z.); Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland (L.J. and L.Z.).
Jun HuDepartment of Anesthesiology, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, People's Republic of China (L.J., J.H., S.H., and Y. Z.); Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland (L.J. and L.Z.).
Shufang HeDepartment of Anesthesiology, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, People's Republic of China (L.J., J.H., S.H., and Y. Z.); Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland (L.J. and L.Z.).
Li ZhangDepartment of Anesthesiology, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, People's Republic of China (L.J., J.H., S.H., and Y. Z.); Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland (L.J. and L.Z.).
Ye ZhangDepartment of Anesthesiology, the Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui, People's Republic of China (L.J., J.H., S.H., and Y. Z.); Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland (L.J. and L.Z.) zhangye_hassan@sina.com.
National Institutes of Health · USAnhui Medical University · CNNational Institute on Alcohol Abuse and Alcoholism · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Morphine has been widely used as rescue treatment for heart attack and failure in humans for many decades. Relatively little has been known about the role of spinal opioid receptors in morphine cardioprotection. Recent studies have shown that intrathecal injection of morphine can reduce the heart injury caused by ischemia (I)/reperfusion (R) in rats. However, the molecular and cellular mechanisms underlying intrathecal morphine cardioprotection has not been determined. Here, we report that intrathecal morphine postconditioning (IMPOC) rescued mean artery pressure (MAP) and reduced myocardial injury in I/R. Pretreatment with either naloxone (NAL), a selective mu-opioid receptor antagonist, or nitric oxide synthase (NOS) inhibitors via intrathecal delivery completely abolished IMPOC cardioprotection, suggesting that the spinal mu-opioid receptor and its downstream NOS signaling pathway are involved in the mechanism of the morphine-induced effect. Consistent with this, IMPOC significantly enhanced spinal neural NOS phosphorylation, nitric oxide, and cGMP content in a similar time course. Intrathecal application of 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, a specific inhibitor of guanylate cyclase, completely ablated IMPOC-induced enhancement of cardioprotection and spinal cGMP content. IMPOC rescue of MAP and ischemic injury is correlated with IMPOC enhancement of NOS signaling. Collectively, these findings strengthen the concept of spinal mu-opioid receptors as a therapeutic target that mediates morphine-induced cardioprotection. We also provide evidence suggesting that the activation of spinal NOS signaling is essential for morphine cardioprotection.

Indexed as

AnimalsCardiotonic AgentsCyclic GMPIschemic PostconditioningMaleMorphineMyocardial Reperfusion InjuryNitric OxideNitric Oxide Synthase Type IRatsRats, Sprague-DawleyReceptors, Opioid, muSignal TransductionSpinal CordCardiotonic AgentsCyclic GMPMorphineNitric OxideNitric Oxide Synthase Type IReceptors, Opioid, mu

Identifiers

PMID27358482
PMCPMC4998671
OpenAlexW2472059215

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.