ArticleLipids in health and disease2010
Endothelial dysfunction of resistance vessels in female apolipoprotein E-deficient mice.
Article in Lipids in health and disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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.
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.
Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Cerebral arteriolar and neurovascular dysfunction after chemically induced menopause in mice.American journal of physiology. Heart and circulatory physiology · 2022Article
- Immune Mechanisms Linking Obesity and Preeclampsia.Biomolecules · 2015Review
- Sex Difference in Coronary Endothelial Dysfunction in Apolipoprotein E Knockout Mouse: Role of NO and A2A Adenosine Receptor.Microcirculation (New York, N.Y. : 1994) · 2015Article
- Endogenous female sex hormones delay the development of renal dysfunction in apolipoprotein E-deficient mice.Lipids in health and disease · 2014Article
- Inhibition of phosphodiesterase 5 restores endothelial function in renovascular hypertension.Journal of translational medicine · 2014Article
- Sildenafil restores endothelial function in the apolipoprotein E knockout mouse.Journal of translational medicine · 2013Article
- Mononuclear cell therapy reverts cuff-induced thrombosis in apolipoprotein E-deficient mice.Lipids in health and disease · 2012Article
- Cardiac and vascular phenotypes in the apolipoprotein E-deficient mouse.Journal of biomedical science · 2012Review
- Endothelial dysfunction in the apolipoprotein E-deficient mouse: insights into the influence of diet, gender and aging.Lipids in health and disease · 2011Review
- Impaired CXCR4 expression and cell engraftment of bone marrow-derived cells from aged atherogenic mice.Atherosclerosis · 2011Article
- Oral P. gingivalis infection alters the vascular reactivity in healthy and spontaneously atherosclerotic mice.Lipids in health and disease · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe effects of hypercholesterolemia on vasomotricity in apolipoprotein E-deficient (ApoE) mice, a murine model of spontaneous atherosclerosis, are still unclear. The studies were mostly performed in conductance vessels from male mice fed a high-fat diet. In the present study, we evaluated the endothelial function of resistance vessels from normal C57BL/6 (C57) and hypercholesterolemic (ApoE) female mice in both normal and ovariectomized conditions.
methodsTwenty week-old C57 and ApoE mice underwent ovariectomy or sham surgery and were studied 30 days later. The vascular reactivities to norepinephrine (NE, 10(-9) to 2 x 10(-3) mol/L), acetylcholine (ACh) and sodium nitroprusside (SNP) (10(-10) to 10(-3) mol/L) were evaluated in the isolated mesenteric arteriolar bed through dose-response curves.
resultsACh-induced relaxation was significantly reduced (P < 0.05) in ApoE compared with C57 animals, as indicated by both the maximal response (37 +/- 4% vs. 72 +/- 1%) and the LogEC50 (-5.67 +/- 0.18 vs. -6.23 +/- 0.09 mol/L). Ovariectomy caused a significant impairment in ACh-induced relaxation in the C57 group (maximal response: 61 +/- 4%) but did not worsen the deficient state of relaxation in ApoE animals (maximal response: 39 +/- 5%). SNP-induced vasorelaxation and NE-induced vasoconstriction were similar in ApoE and C57 female mice.
conclusionThese data show an impairment of endothelial function in the resistance vessels of spontaneously atherosclerotic (ApoE-deficient) female mice compared with normal (C57) female mice. The endothelial dysfunction in hypercholesterolemic animals was so marked that ovariectomy, which impaired endothelial function in C57 mice, did not cause additional vascular damage in ApoE-deficient mice.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.