Evidence map›Paper›PMID 19138364›Full record

ArticleThe journal of sexual medicine2009

Fibrosis and loss of smooth muscle in the corpora cavernosa precede corporal veno-occlusive dysfunction (CVOD) induced by experimental cavernosal nerve damage in the rat.

Monica G Ferrini, Istvan Kovanecz, Sandra Sanchez, Chiome Umeh, Jacob Rajfer, Nestor F Gonzalez-Cadavid

Open access · greenAbstract readEvaluation Study
PubMed Full text at PMC Publisher
In one paragraph

Article in The journal of sexual medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 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

6 authors at 2 institutions in 1 country.

Monica G FerriniCharles Drew University, Department of Medicine, Los Angeles, CA 90059, USA. monicaferrini@cdrewu.edu
Istvan Kovanecz
Sandra Sanchez
Chiome Umeh
Jacob Rajfer
Nestor F Gonzalez-Cadavid
The Lundquist Institute · USUniversity of California, Los Angeles · US

Funding

RESEARCH INFORMATICS COREG12RR003026 · NCRR · CHARLES R. DREW UNIVERSITY OF MED &SCI · PI BAKER, RICHARD S. · 1986 to 2004
$11.5M
ERECTILE DYSFUNCTION AND NITRIC OXIDE SYNTHASE IN AGINGR01DK053069 · NIDDK · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI GONZALEZ-CADAVID, NESTOR F · 1999 to 2006
$1.6M
Nitric Oxide/cGMP Modulation of Corporal Fibrosis Caused by NeuropraxiaSC1NS064611 · NINDS · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI FERRINI, MONICA GABRIELA · 2008 to 2012
$1.4M
NCI NIH HHS N02 PC061300NCRR NIH HHS G12 RR003026NCRR NIH HHS G12RR-03026NIDDK NIH HHS R01 DK053069NIDDK NIH HHS R01DK-53069NINDS NIH HHS SC1 NS064611NINDS NIH HHS SC1NS064611
6 · The paper itself

Abstract

introductionCorporal veno-occlusive dysfunction (CVOD), which usually is associated with a loss of smooth muscle cells (SMC) and an increase in fibrosis within the corpora cavernosa, can be induced by an injury to the cavernosal nerves. The corporal tissue expresses inducible nitric oxide synthase (iNOS), presumably as an antifibrotic and SMC-protective response.

aimsWe studied the temporal relationship in the corpora between the expression of iNOS, other histological and biochemical changes, and the development of CVOD, after bilateral cavernosal nerve resection (BCNR) in the rat.

methodsRats underwent either BCNR or sham operation. Cavernosometry was performed 1, 3, 7, 15, 30, and 45 days (N = 8/groups) after surgery. Penile tissue sections were subjected to Masson trichrome staining for SMC and collagen, and immunodetection for alpha smooth muscle actin, iNOS, neuronal NOS (nNOS), endothelial NOS (eNOS), proliferating cell nuclear antigen (PCNA), and terminal transferase dUTP nick end labeling (TUNEL). Quantitative western blot analysis was done in homogenates.

main outcome measuresTime course on the development of fibrosis and CVOD.

resultsFollowing BCNR, CVOD was detectable 30 days later, and it became more pronounced by 45 days. In contrast, the SMC/collagen ratio in the BCNR corpora was reduced at 7 days and bottomed at 30 and 45 days, due in part to the reduction of SMC, presumably caused by an increase in apoptosis peaking at 3 days. PCNA also peaked at 3 days, but then decayed. nNOS was reduced early (3-7 days) and disappeared at 30 days, whereas eNOS was not affected. iNOS was induced at day 3, and steadily increased peaking at 30 days.

conclusionsCVOD develops in the BCNR rat as a result of the early loss of corporal SMC by the neuropraxia-induced apoptosis, which the initial cell replication response cannot counteract, followed by fibrosis. The time course of iNOS induction supports the antifibrotic role of iNOS.

Indexed as

PenisActinsAnimalsBlotting, WesternEndotheliumFibrosisIn Situ Nick-End LabelingMaleMuscle, SmoothNitric Oxide SynthasePeripheral NervesProliferating Cell Nuclear AntigenRandom AllocationRatsRats, Sprague-DawleyActinsNitric Oxide SynthaseProliferating Cell Nuclear Antigen

Identifiers

PMID19138364
PMCPMC2756287
OpenAlexW1990048810

What OpenQuestion holds

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LicenceTDM
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.