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Above and Below: Impaired Endothelial Function in Rat Femoral Artery after Spinal Cord Injury is Reversed with Passive Exercise
Author(s) -
Zheng Mei Mu Zi,
Phillips Aaron A.,
Golbidi Saeid,
Laher Ismail,
Krassioukov Andrei V.
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1204.13
Subject(s) - medicine , endothelial dysfunction , electrical impedance myography , spinal cord injury , cardiology , brachial artery , vasodilation , endothelium , acetylcholine , spinal cord , anesthesia , blood pressure , psychiatry
Endothelial dysfunction is considered a highly sensitive marker of cardiovascular disease progression in humans, which is the leading cause of death in people with SCI. Reports on endothelial function (using flow mediated dilation) after SCI has been contentious to date, as those with SCI have reported unchanged endothelial function in the brachial artery (BA), with an unexpected increase in flow‐mediated dilation in the femoral artery (FA). It is suspected that this latter finding is confounded by a lack of appropriate adjustment for differences in resting arterial dimensions as well as shear rate between SCI and able‐bodied controls, which are critical factors when using this technique. The objective of the current study is to examine the endothelial function of conduit arteries above and below the level of spinal cord lesion using a method independent of arterial dimensions. Moreover, exercise has been linked with improved vascular function through increases in flood flow and shear stress. This study also aims to assess the effect of passive exercise on the endothelial function of conduit arteries of SCI animals. We examined endothelial function in animals with complete T3 spinal cord transection (SCI‐T3), T3 transection and passive exercise (PE), and uninjured controls. To obviate prior methodological concerns, in vitro wire myography was used to examine endothelial‐mediated vasodilation (acetylcholine, ACh) in the BA and FA of each rat. Femoral arteries from SCI animals exhibited impaired reactivity to ACh (i.e., requiring 5× greater ACh to reach 50% of maximal dilation; p <.01) compared to those of the controls. Passive exercise after SCI improved the sensitivity of FA ( p <.01) to be similar to that of uninjured animals. However, brachial arteries from all groups showed similar responses to ACh ( p =0.789). The results from ex vivo myography showed arterial endothelial dysfunction in arteries (i.e. FA) after disruption of supraspinal input by experimental SCI, however when supraspinal regulation is intact, endothelial function is preserved. We have shown, for the first time, the expected endothelial dysfunction in the inactive/supraspinally disconnected femoral artery after SCI, clarifying previously unexpected findings. Furthermore, passive exercise of the hind legs was effective in preventing endothelial dysfunction. Together, this study provides mechanistic insight into cardiovascular disease progression after SCI, as well as a potential therapeutic intervention. Support or Funding Information Study supported by CIHR Team Grant (TCA 118348); MMZZ is funded by CIHR Canada Graduate Scholarship. 1Dose response curves of brachial (BA; left) and femoral artery (FA; right) to cumulative additions of acetylcholine (ACh; 10‐9 M to 10‐5 M). The sensitivity to ACh (p=0.789) in BA is the same among the three groups. For FA, the SCI group showed impaired sensitivity to ACh compared to the control group(p<0.01), whereas the PE group showed improved sensitivity to ACh compared to the SCI group (p<0.01).