Pancera P, Minuz P, Rossi L, Ribul M, Arosio E, Lechi A
Chair of Internal Medicine, University of Verona, Italy.
Angiology. 1997 Feb;48(2):149-55. doi: 10.1177/000331979704800208.
The physiological basis of postischemic hyperemia is not yet fully understood. The present study investigated the effects of pharmacologic manipulation of the prostaglandin system on local hemodynamics. Strain-gauge plethysmography was used to study 8 normal subjects and 9 patients with obliterating arterial disease of the lower limbs. Hemodynamic evaluations were performed before treatment, after seven days of low-dose acetylsalicylic acid (100 mg/day) to inhibit platelet thromboxane synthesis, and after acute infusion of 1 g of acetylsalicylic acid to inhibit endothelial prostacyclin synthesis. In patients with arterial disease, the hemodynamic study was also carried out after infusion of iloprost, a synthetic prostacyclin analogue. Acute infusion of acetylsalicylic acid significantly reduced basal blood flow in normal subjects, but not in patients with arterial disease. In the latter group, iloprost affected neither basal nor maximal postischemic flow. The study also evaluated the role of endothelin in musculocutaneous hemodynamic regulation, both in physiological conditions and in atherosclerosis. This part of the study addressed the possibility that the hemodynamic effects of vasodilator prostanoids like prostacyclin might affect endothelin release in vivo. During reactive hyperemia, plasma endothelin was reduced in normal subjects (-1.02 pg/mL, 95% CI: -2.23, 0.08), but not in patients with atherosclerosis (-0.35 pg/mL, 95% CI: -1.45, 0.75). In both groups, plasma endothelin was not affected by aspirin. These findings confirm the role of prostacyclin in local hemodynamic regulation. In the normal subject, musculocutaneous blood flow seems to depend at least in part on the action of vasodilator prostanoids and endothelin. This is not the case in patients with arterial disease, in whom plasma endothelin does not seem to be affected by postischemic changes in blood flow. A possible explanation for this difference could be alteration of the endothelial function in patients with arterial disease, related to the functional and structural characteristics of the artery wall in atherosclerosis.
缺血后充血的生理基础尚未完全明确。本研究调查了前列腺素系统的药物调控对局部血流动力学的影响。使用应变片体积描记法对8名正常受试者和9名下肢动脉闭塞性疾病患者进行研究。在治疗前、给予低剂量阿司匹林（100毫克/天）以抑制血小板血栓素合成7天后以及急性输注1克阿司匹林以抑制内皮前列环素合成后进行血流动力学评估。在动脉疾病患者中，还在输注依洛前列素（一种合成前列环素类似物）后进行血流动力学研究。急性输注阿司匹林显著降低了正常受试者的基础血流量，但对动脉疾病患者则无此影响。在后者组中，依洛前列素对基础血流和缺血后最大血流均无影响。该研究还评估了内皮素在生理状况和动脉粥样硬化中对肌肉皮肤血流动力学调节的作用。研究的这一部分探讨了前列环素等血管舒张性前列腺素的血流动力学效应可能影响体内内皮素释放的可能性。在反应性充血期间，正常受试者的血浆内皮素降低（-1.02皮克/毫升，95%置信区间：-2.23，0.08），但动脉粥样硬化患者未降低（-0.35皮克/毫升，95%置信区间：-1.45，0.75）。在两组中，血浆内皮素均不受阿司匹林影响。这些发现证实了前列环素在局部血流动力学调节中的作用。在正常受试者中，肌肉皮肤血流量似乎至少部分取决于血管舒张性前列腺素和内皮素的作用。动脉疾病患者则不然，其血浆内皮素似乎不受缺血后血流变化的影响。对此差异的一种可能解释是动脉疾病患者内皮功能的改变，这与动脉粥样硬化中动脉壁的功能和结构特征有关。
