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Vascular reactivity to L‐NAME administration in chronic tetraplegia
Author(s) -
La Fountaine Michael,
Radulovic Miroslav,
Wecht Jill,
Cardozo Chrstopher,
Spungen Ann,
De Meersman Ronald,
Bauman William
Publication year - 2008
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.22.1_supplement.737.6
Subject(s) - tetraplegia , medicine , baroreceptor , blood pressure , anesthesia , placebo , analysis of variance , baroreflex , endocrinology , cardiology , heart rate , spinal cord injury , spinal cord , alternative medicine , pathology , psychiatry
Nitric oxide (NO)‐dependent vascular reactivity, assessed by a change (Δ) in arterial resistance (AR), was evaluated in 5 persons with chronic tetraplegia and 5 age‐matched controls. AR was obtained by venous occlusion plethysmography, and blood pressure was obtained manually. AR was calculated as mean arterial pressure (MAP) divided by the arterial inflow slope. Measures were assessed at baseline (BL) and post intravenous infusion of a NO synthase (NOS) inhibitor, L‐NAME (1 mg/kg), or placebo (normal saline) on separate days. Unpaired t‐tests were used to identify group differences for BL dependent variables (MAP and AR). A one factor ANOVA with a Fisher's post‐hoc analysis was completed on the % Δ [(post‐pre)/pre*100)] of the dependent variables. MAP (74.3 ± 11.3 v. 86.5 ± 8.5, p = 0.01) and AR (19.9 ± 13.6 v. 46.6 ± 30.5, p = 0.02) were lower at BL in the tetraplegia group compared to controls. In the tetraplegia group after L‐NAME: the pressor effect was 58% > placebo ( p = 0.001) and 39% > controls ( p =0.0008) and AR was 92% > placebo ( p =0.004) and 73% > controls (p= 0.018). NOS‐inhibition in the tetraplegia group had an augmented effect to increase MAP, possibly due to the abolished baroreflex capacity. The heightened Δ in AR in those with tetraplegia suggests that enhanced vascular reactivity may be due to a NO‐mediated mechanism and the absence of modulation from interrupted sympathetic innervation. Funds: VA RR&D #B4335V