Evidence map›Paper›PMID 29257200›Full record

ArticleMolecular medicine reports2018

Protective effects of atorvastatin on cerebral vessel autoregulation in an experimental rabbit model of subarachnoid hemorrhage.

Jun-Hui Chen, Ting Wu, Li-Kun Yang, Lei Chen, Jie Zhu, Pei-Pei Li, Xu Hu, Yu-Hai Wang

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. 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 31 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 2 pooled it
0.9field-weighted citation impact, top 24% 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

31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Jun-Hui ChenDepartment of Neurosurgery, l0lst Hospital of PLA, Wuxi, Jiangsu 214044, P.R. China.
Ting WuDepartment of Cardiology, l0lst Hospital of PLA, Wuxi, Jiangsu 214044, P.R. China.
Li-Kun YangDepartment of Neurosurgery, l0lst Hospital of PLA, Wuxi, Jiangsu 214044, P.R. China.
Lei ChenDepartment of Neurosurgery, l0lst Hospital of PLA, Wuxi, Jiangsu 214044, P.R. China.
Jie ZhuDepartment of Neurosurgery, l0lst Hospital of PLA, Wuxi, Jiangsu 214044, P.R. China.
Pei-Pei LiDepartment of Neurosurgery, l0lst Hospital of PLA, Wuxi, Jiangsu 214044, P.R. China.
Xu HuDepartment of Neurosurgery, l0lst Hospital of PLA, Wuxi, Jiangsu 214044, P.R. China.
Yu-Hai WangDepartment of Neurosurgery, l0lst Hospital of PLA, Wuxi, Jiangsu 214044, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the present study was to assess the therapeutic effects of atorvastatin on cerebral vessel autoregulation and to explore the underlying mechanisms in a rabbit model of subarachnoid hemorrhage (SAH). A total of 48 healthy male New Zealand rabbits (weight, 2‑2.5 kg) were randomly allocated into SAH, Sham or SAH + atorvastatin groups (n=16/group). The Sham group received 20 mg/kg/d saline solution, whereas 20 mg/kg/d atorvastatin was administered to rabbits in the SAH + atorvastatin group following SAH induction. Changes in diameter, perimeter and basilar artery (BA) area were assessed and expression levels of the vasoactive molecules endothelin‑1 (ET‑1), von Willebrand factor (vWF) and thrombomodulin (TM) were measured. Neuronal apoptosis was analyzed 72 h following SAH by terminal deoxynucleotidyl-transferase‑mediated dUTP nick‑end labeling (TUNEL) staining. The mortality rate in the SAH group was 18.75, 25% in the SAH + atorvastatin treated group and 0% in the Sham group (n=16/group). The neurological score in the SAH + atorvastatin group was 1.75±0.68, which was significantly higher compared with the Sham group (0.38±0.49; P<0.05). The BA area in the SAH + atorvastatin group (89.6±9.11) was significantly lower compared with the SAH group (115.4±11.0; P<0.01). The present study demonstrated that SAH induction resulted in a significant increase in the diameter, perimeter and cross‑sectional area of the BA in the SAH + atorvastatin group. Administration of atorvastatin may significantly downregulate the expression levels of ET‑1, vWF and TM (all P<0.01) vs. sham and SAH groups. TUNEL staining demonstrated that neuronal apoptosis was remarkably reduced in the hippocampus of SAH rabbits following treatment with atorvastatin (P<0.05). Atorvastatin treatment may alleviate cerebral vasospasm and mediate structural and functional remodeling of vascular endothelial cells, in addition to promoting anti‑apoptotic signaling. These results provided supporting evidence for the use of atorvastatin as an effective and well‑tolerated treatment for SAH in various clinical settings and may protect the autoregulation of cerebral vessels.

Indexed as

AnimalsAnticholesteremic AgentsApoptosisAtorvastatinBasilar ArteryBrainEndothelin-1MaleNeuronsProtective AgentsRabbitsSubarachnoid HemorrhageVasospasm, IntracranialAnticholesteremic AgentsAtorvastatinEndothelin-1Protective Agents

Identifiers

PMID29257200
PMCPMC5780106
OpenAlexW2770890216

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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 OpenQuestion graph.