Preserved alpha-adrenergic tone in the leg vascular bed of spinal cord-injured individuals

Article

关键词: NITRIC-OXIDE SYNTHASE;    SMOOTH-MUSCLE CELLS;    BLOOD-FLOW;    CHRONIC SYMPATHECTOMY;    LUMBAR SYMPATHECTOMY;    SKELETAL-MUSCLE;    FEMORAL-ARTERY;    SHORT-TERM;    ENDOTHELIUM;    INHIBITION;   

DOI  :  10.1161/01.CIR.0000096480.55857.3C

来源: SCIE

【 摘 要 】

Background-Supraspinal sympathetic control of leg vascular tone is lost in spinal cord-injured individuals, but this does not result in a reduced leg vascular tone: Leg vascular resistance is even increased. The aim of this study was to assess the alpha-adrenergic contribution to the increased vascular tone in the lower extremity in patients without central sympathetic control of leg circulation. Methods and Results-Upper-leg vascular resistance responses to local infusion of incremental doses of phentolamine (a competitive antagonist of the alpha-adrenoceptor) into the femoral artery were determined in 10 spinal cord-injured individuals (SCI) and 8 healthy age-matched control subjects during local beta-adrenergic receptor blockade with propranolol. Basal leg vascular resistance was higher in SCI than in control subjects (41+/-6 arbitrary units [AU] versus 24+/-4 AU; P=0.034). The same accounts for minimal leg vascular resistance, assessed during reactive hyperemia, which was higher in SCI compared with control subjects (6.9+/-1.0 AU versus 2.5+/-0.2 AU; P<0.01). The maximal phentolamine-induced reduction in leg vascular resistance normalized to each individual's minimal resistance did not differ between the groups (68 +/- 17% and 51 +/- 4% for SCI and control subjects, respectively; P>0.1). A decline in mean arterial pressure was observed in both groups with increasing dosage of phentolamine. In response, baroreceptor-mediated vasoconstriction was observed in the noninfused leg of the control subjects, whereas in SCI individuals this reaction was absent. Conclusions-These results indicate that the alpha-adrenoceptor-mediated vascular tone in the leg is preserved in spinal cord-injured individuals without sympathetic supraspinal control.

【 授权许可】

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