Videomicroscopic demonstration of defective cholinergic arteriolar vasodilation in atherosclerotic rabbit.
Videomicroscopic demonstration of defective cholinergic arteriolar vasodilation in atherosclerotic rabbit.
复制标题
动脉粥样硬化兔胆碱能小动脉血管舒张缺陷的视频显微镜演示。
DOI：
10.1172/jci113516
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Henry,PD
中科院分区：
文献类型：
--
作者：
Yamamoto,H;Bossaller,C;CartwrightJr,J;Henry,PD
在动脉粥样硬化兔（SCLER）中，血管阻力对乙酰胆碱（ACH）（一种内皮依赖性药物）的反应性降低被抑制，而对硝普钠（NP）（一种内皮非依赖性血管扩张剂）的反应性降低被保留。为了确定是否有缺陷的SCLER血管舒张与阻力血管的反应性改变，我们可视化兔提睾肌的小动脉通过视频显微镜。在局部（灌流）输送ACh和NO，不影响全身血流动力学的干预措施，监测小动脉直径。对NP（0.01-100.0 μ M）反应的直径变化在SCLER和对照组之间没有差异;最大扩张达到110 +/- 10%（平均值+/- SE）。相比之下，对ACH（0.001-100 μ M）的反应不同; SCLER的最大扩张平均为54 +/- 4%，对照组为124 +/- 9%（P <0.001）。在用酚妥拉明、普萘洛尔和吲哚美辛阻断后，这些差异仍然存在。非尼酮和氢醌阻断剂的内皮依赖性血管舒张，抑制小动脉扩张的ACH，而不影响NP。动脉内药物引起的微血管反应与局部药物引起的反应相似。因此，家兔的高胆固醇血症和动脉粥样硬化似乎产生微血管缺陷，其特征在于内皮依赖性扩张受损和内皮非依赖性扩张保留。这种缺陷可能在限制动脉粥样硬化的血管舒张储备中发挥作用。
In atherosclerotic rabbits (SCLER), decreases in vascular resistance in response to acetylcholine (ACH), an endothelium-dependent agent, are suppressed, whereas those to nitroprusside (NP), an endothelium-independent vasodilator, are preserved. To determine whether defective vasodilation in SCLER is related to altered reactivity of resistance vessels, we visualized arterioles of rabbit cremaster muscle by videomicroscopy. Arteriolar diameter was monitored during topical (superfusional) delivery of ACh and NO, interventions that did not affect systemic hemodynamics. Diameter changes in response to NP (0.01-100.0 microM) did not differ between SCLER and controls; maximal dilations amounted to 110 +/- 10% (mean +/- SE). In contrast, responses to ACH (0.001-100 microM) differed; maximal dilations averaged 54 +/- 4% in SCLER and 124 +/- 9% in controls (P less than 0.001). These differences persisted after blockade with phentolamine, propranolol, and indomethacin. Phenidone and hydroquinone blockers of endothelium-dependent vasodilation, inhibited arteriolar dilation to ACH without affecting that to NP. Microvascular responses to intra-arterial drug were similar to those elicited by topical drug. Thus, hypercholesterolemia and atherosclerosis in the rabbit appear to produce a microvascular defect characterized by an impaired endothelium-dependent dilation and a preserved endothelium-independent dilation. This defect could play a role in limiting vasodilator reserve in atherosclerosis.Images