Davis T R, Wood M B
Mayo Graduate School of Medicine, Rochester, Minnesota.
J Orthop Res. 1993 Nov;11(6):834-9. doi: 10.1002/jor.1100110609.
This study used an ex vivo perfusion model to investigate the direct effects of acidosis and alkalosis on the vascular resistance of the canine tibia. Baseline vascular resistance (BVR) and the vascular smooth muscle response to bolus doses of norepinephrine (NE) (0.025-3.2 nmol) and periarterial sympathetic nerve stimulation (NS) (10-25 Hz: 9 V, 2 ms pulses, 10 s) were studied. In Group I, these parameters were measured at normal pH (duration 7.34-7.44) and then during acidosis (pH 7.2-7.33). In Group II, they were measured at normal pH and then during alkalosis (pH 7.47-7.58). In Group III (control), they were measured serially at a normal pH. Alkalosis increased BVR by 56% (p < 0.0001). Acidosis attenuated (18% reduction) and alkalosis enhanced (66% increase) the vasoconstrictor action of NE (p < 0.0001). Acidosis also attenuated (11% reduction) the effect of sympathetic NS (p = 0.012). It is concluded that perfusion pH influences the sensitivity of long bone resistance vessels to circulating NE and sympathetic NS. Thus, local concentration of hydrogen ions may provide bone with a mechanism to autoregulate blood flow.
本研究采用离体灌注模型，以研究酸中毒和碱中毒对犬胫骨血管阻力的直接影响。研究了基线血管阻力（BVR）以及血管平滑肌对大剂量去甲肾上腺素（NE）（0.025 - 3.2 nmol）和动脉周围交感神经刺激（NS）（10 - 25 Hz：9 V，2 ms脉冲，10 s）的反应。在第一组中，在正常pH值（持续时间7.34 - 7.44）下测量这些参数，然后在酸中毒（pH 7.2 - 7.33）期间测量。在第二组中，在正常pH值下测量这些参数，然后在碱中毒（pH 7.47 - 7.58）期间测量。在第三组（对照组）中，在正常pH值下连续测量这些参数。碱中毒使BVR增加了56%（p < 0.0001）。酸中毒减弱了NE的血管收缩作用（降低18%），而碱中毒增强了NE的血管收缩作用（增加66%）（p < 0.0001）。酸中毒还减弱了交感神经刺激的作用（降低11%）（p = 0.012）。结论是灌注pH值影响长骨阻力血管对循环NE和交感神经刺激的敏感性。因此，局部氢离子浓度可能为骨骼提供一种自动调节血流的机制。
