Evidence map›Paper›PMID 26911739›Full record

ArticleScientific reports2016

Hemoglobin induced NO/cGMP suppression Deteriorate Microcirculation via Pericyte Phenotype Transformation after Subarachnoid Hemorrhage in Rats.

Qiang Li, Yujie Chen, Bo Li, Chunxia Luo, Shilun Zuo, Xin Liu, John H Zhang, Huaizhen Ruan, Hua Feng

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 46 citations in OpenAlex.

  1. Haemorrhage, hypercoagulability and ischaemia: Evolution of brain injury after aneurysmal subarachnoid haemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
    Review
  2. Microthrombi and hypercoagulability's contribution to delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
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  13. Role of platelets in the pathogenesis of delayed injury after subarachnoid hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Qiang LiDepartment of Neurosurgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
Yujie ChenDepartment of Neurosurgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
Bo LiDepartment of Neurosurgery, Jinan Military General Hospital, Jinan, Shandong, China.
Chunxia LuoDepartment of Neurology, Southwest Hospital, Third Military Medical University, Chongqing, China.
Shilun ZuoDepartment of Neurosurgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
Xin LiuDepartment of Neurosurgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
John H ZhangDepartment of Physiology and Pharmacology, Loma Linda University, Loma Linda, California, USA.
Huaizhen RuanDepartment of Neurobiology, College of Basic Medical Sciences, Third Military Medical University, Chongqing, China.
Hua FengDepartment of Neurosurgery, Southwest Hospital, Third Military Medical University, Chongqing, China.
Army Medical University · CNJinan Military General Hospital · CNLoma Linda University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Subarachnoid hemorrhage (SAH) usually results from ruptured aneurysm, but how leaked hemoglobin regulates the microcirculation in the pathophysiology of early brain injury after SAH is still unclear. In the present study, we sought to investigate the role and possible mechanism of hemoglobin induced pericyte phenotype transformation in the regulation of microcirculation after SAH. Endovascular perforation SAH rat model, brain slices and cultured pericytes were used, and intervened with endothelial nitric oxide synthase (eNOS) antagonist L-NNA and its agonist scutellarin, hemoglobin, DETA/NO (nitric oxide(NO) donor), PITO (NO scavenger), 8-Br-cGMP (cGMP analog). We found modulating eNOS regulated pericyte α-SMA phenotype transformation, microcirculation, and neurological function in SAH rats. Modulating eNOS also affected eNOS expression, eNOS activity and NO availability after SAH. In addition, we showed hemoglobins penetrated into brain parenchyma after SAH. And hemoglobins significantly reduced the microvessel diameters at pericyte sites, due to the effects of hemoglobin inducing α-SMA expressions in cultured pericytes and brain slices via inhibiting NO/cGMP pathway. In conclusion, pericyte α-SMA phenotype mediates acute microvessel constriction after SAH possibly by hemoglobin suppressing NO/cGMP signaling pathway. Therefore, by targeting the eNOS and pericyte α-SMA phenotype, our present data may shed new light on the management of SAH patients.

Indexed as

MicrocirculationPhenotypeActinsAnimalsCyclic GMPDisease Models, AnimalEnzyme ActivationGene ExpressionHemoglobinsMaleNitric OxideNitric Oxide Synthase Type IIIPericytesRatsSignal TransductionSubarachnoid HemorrhageActinsCyclic GMPHemoglobinsNitric OxideNitric Oxide Synthase Type III

Identifiers

PMID26911739
PMCPMC4766506
OpenAlexW2417927954

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Registered trials

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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 OpenQuestion graph.