Taylor Jessica C, Li Zeyi, Yang H T, Laughlin M Harold, Terjung Ronald L
Department of Biomedical Sciences, E102 Vet. Medical Bldg, University of Missouri, Columbia, MO 65211, USA.
J Physiol. 2008 Mar 15;586(6):1649-67. doi: 10.1113/jphysiol.2007.149567. Epub 2008 Jan 24.
This study evaluated whether alpha-adrenergic activation contributes to collateral circuit vascular resistance in the hindlimb following acute unilateral occlusion of the femoral artery in rats. Blood pressures (BPs) were measured above (caudal artery) and below (distal femoral artery) the collateral circuit. Arterial BPs were reduced (15-35 mmHg) with individual (prazosin, rauwolscine) or combined (phentolamine) alpha-receptor inhibition. Blood flows (BFs) were measured using microspheres before and after alpha inhibition during the same treadmill speed. alpha(1) inhibition increased blood flow by approximately 40% to active muscles that were not affected by femoral occlusion, whereas collateral-dependent BFs to the calf muscles were reduced by 29 +/- 8.4% (P < 0.05), due to a decrease in muscle conductance with no change in collateral circuit conductance. alpha(2) inhibition decreased both collateral circuit (39 +/- 6.0%; P < 0.05) and calf muscle conductance (36 +/- 7.3%; P < 0.05), probably due to residual alpha(1) activation, since renal BF was markedly reduced with rauwolscine. Most importantly, inhibiting alpha(2) receptors in the presence of alpha(1) inhibition increased (43 +/- 12%; P < 0.05) collateral circuit conductance. Similarly, non-selective alpha inhibition with phentolamine increased collateral conductance (242 +/- 59%; P < 0.05). We interpret these findings to indicate that both alpha(1)- and alpha(2)-receptor activation can influence collateral circuit resistance in vivo during the high flow demands caused by exercise. Furthermore, we observed a reduced maximal conductances of active muscles that were ischaemic. Our findings imply that in the presence of excessive sympathetic activation, which can occur in the condition of intermittent claudication during exertion, an exaggerated vasoconstriction of the existing collateral circuit and active muscle will occur.
本研究评估了α-肾上腺素能激活是否会导致大鼠股动脉急性单侧闭塞后后肢侧支循环血管阻力增加。在侧支循环上方（尾动脉）和下方（股动脉远端）测量血压（BP）。使用哌唑嗪、萝芙木碱单独或酚妥拉明联合抑制α受体后，动脉血压降低（15 - 35 mmHg）。在相同跑步机速度下，于α抑制前后使用微球测量血流量（BF）。α(1)受体抑制使未受股动脉闭塞影响的活跃肌肉血流量增加约40%，而小腿肌肉依赖侧支循环的血流量减少29±8.4%（P<0.05），这是由于肌肉传导性降低，而侧支循环传导性未改变。α(2)受体抑制使侧支循环（39±6.0%；P<0.05）和小腿肌肉传导性均降低（36±7.3%；P<0.05），这可能是由于存在残余的α(1)受体激活，因为使用萝芙木碱后肾血流量显著降低。最重要的是，在α(1)受体抑制的情况下抑制α(2)受体可增加侧支循环传导性（43±12%；P<0.05）。同样，酚妥拉明非选择性抑制α受体可增加侧支循环传导性（242±59%；P<0.05）。我们认为这些发现表明，在运动引起的高流量需求期间，α(1)和α(2)受体激活均可在体内影响侧支循环阻力。此外，我们观察到缺血活跃肌肉的最大传导性降低。我们的研究结果表明，在存在过度交感神经激活的情况下，如在运动性间歇性跛行时可能发生的情况，现有侧支循环和活跃肌肉会出现过度的血管收缩。
