CHANGES OF VASCULAR ARCHITECTURE-INDEPENDENT OF BLOOD-PRESSURE IN EXPERIMENTAL UREMIA
CHANGES OF VASCULAR ARCHITECTURE-INDEPENDENT OF BLOOD-PRESSURE IN EXPERIMENTAL UREMIA
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DOI：
10.1016/0895-7061(94)00248-a
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发表时间：
1995-04-01
影响因子：
3.2
通讯作者：
MALL, G
中科院分区：
文献类型：
--
作者：
AMANN, K;NEUSUSS, R;MALL, G
不同管径的动脉血管结构的显著改变是肾功能衰竭的一个众所周知的特征，但目前尚不清楚它们在多大程度上反映了高血压或尿毒症本身。为了进一步解决这个问题，我们研究了肾次全切除的大鼠，假手术并与匹配的对照组配对喂养。尿毒症持续14天后，对灌流固定的组织进行体视学测量。为了消除高血压的潜在影响，亚组动物分别在饮用水中服用速尿和肼丙嗪，日剂量分别为15 mg/kg和20 mg/kg。实验结束时，未治疗和治疗的尿毒症动物的收缩压(尾部体积图)分别为110±13.3(Mean+/-SD)mm Hg和99.4+/-8.1 mm Hg，未治疗和治疗的尿毒症动物分别为132±20.7 mm Hg和103±13.0 mm Hg。对照组心肌内小动脉壁/腔比分别为0.056±0.011和0.052±0.006。在未治疗和治疗的尿毒症动物中，相应的值分别为0.077+/-0.011和0.066+/-0.007(P<；0.01；对照尿毒症，方差分析)。心肌内动脉壁厚度也有类似的增加，但不受血压治疗的影响。肠系膜小动脉和静脉也有类似的变化。最后，尿毒症动物的主动脉中膜厚度显著高于对照组(138+/-29微米比103+/-14微米)(P<；0.005)。此外，主动脉中层和弹性内板显示出明显的结构异常。结果证明尿毒症动物的动脉(阻力和温氏)以及静脉血管的结构变化与压力无关。这些变化对肾功能衰竭的阻力和阻抗具有潜在的重要意义。
Striking alterations of the structure of arterial vessels of different caliber are a well-known feature of renal failure, but it is currently unknown to what extent they are a reflection of hypertension or of uremia per se. To address this issue further we studied subtotally nephrectomized rats, sham-operated and pair-fed with matched controls. After uremia of 14 days' duration, stereologic measurements were carried out on perfusion-fixed tissue. To eliminate a potential influence of hypertension, subgroups of animals received furosemide and hydralazine in the drinking fluid to yield daily doses of 15 mg/kg and 20 mg/kg, respectively.At the end of the experiment, systolic blood pressure (tail plethysmography) was 110 +/- 13.3 (mean +/- SD) mm Hg and 99.4 +/- 8.1 mm Hg in untreated and treated controls, respectively, and 132 +/- 20.7 mm Hg and 103 +/- 13.0 mm Hg in untreated and treated uremic animals, respectively (n = 5 to 10 animals per group).The wall:lumen ratio of intramyocardial small arteries was 0.056 +/- 0.011 and 0.052 +/- 0.006 in untreated and treated controls, respectively. In untreated and treated uremic animals, the corresponding values were 0.077 +/- 0.011 and 0.066 +/- 0.007 (P < .01; control v uremia, ANOVA). A similar increase, unaffected by blood pressure treatment, was found for wall thickness of intramyocardial arteries. Analogous changes were also noted in mesenteric arterioles and veins.Finally, aorta media thickness was significantly (P < .005) higher in uremic animals than in controls (138 +/- 29 mu m v 103 +/- 14 mu m). Additionally, aortic media and lamina elastica interna showed significant architectural abnormalities. The results document pressure-independent structural alterations in arterial (resistance and Windkessel) as well as venous vessels of uremic animals. The changes are of potential importance for resistance and impedance in renal failure.