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Effects of hydrostatic distention on in vitro vasoreactivity of radial artery conduits
Chee Fui Chong1, Paul J L Ong, Neil Moat
1Department of Cardiothoracic Surgery, Royal Brompton and Harefield NHS Trust, London, United Kingdom. chong_chee_fui@hotmail.com <chong_chee_fui@hotmail.com>
Background:
Surgical preparation of coronary conduits may affect early and long-term patency through endothelial and smooth muscle injury. We investigated the effect of hydrostatic distention on the in vitro endothelial function and contractile properties of the human radial artery.
Methods:
Human radial arteries were harvested and distended to physiologic pressure or suprasystemic pressure (>300 mm Hg) by using heparinized whole blood for 2 minutes. Distal segments were retrieved and prepared into 3-mm rings. These were mounted and stretched to optimum resting tension in oxygenated Krebs solution at 37 degrees C. Contraction responses to potassium, norepinephrine, and serotonin and relaxation responses to acetylcholine and nitroprusside were evaluated. Undistended radial artery segments were used as controls.
Results:
Vasocontraction to all 3 contractile agonists was significantly different between groups. The radial artery subjected to suprasystemic pressure distention achieved the lowest percentage of maximum contraction (potassium, P <.001; norepinephrine, P <.05; serotonin, P <.05). The median effective concentration was also significantly reduced in this group, indicating increased sensitivity to all 3 agonists. Receptor-mediated contractility was significantly reduced in both distended groups when compared with controls. Relaxation to acetylcholine and nitroprusside was significantly reduced in the suprasystemic pressure-distended group, which had a tendency to vasospasm when exposed to a physiologic concentration of acetylcholine (10(-6) mol/L). Median effective concentrations for both acetylcholine and nitroprusside were not different between groups.
Conclusions:
Excessive distention of the radial artery leads to a significant reduction in vasoreactivity, which may be attributed to a disruption of the vascular endothelium and media, with a propensity for graft spasm with exposure to acetylcholine.
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