Heterogeneous microvascular coronary alpha-adrenergic vasoconstriction.
Heterogeneous microvascular coronary alpha-adrenergic vasoconstriction.
复制标题
异质微血管冠状动脉α-肾上腺素能血管收缩。
DOI：
10.1161/01.res.64.2.376
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发表时间：
1989
影响因子：
20.1
通讯作者：
Marcus,ML
中科院分区：
文献类型：
--
作者：
Chilian,WM;Layne,SM;Eastham,CL;Marcus,ML
我们检验了冠状动脉循环中体液或神经源性α-肾上腺素能激活会产生异质性血管反应的假设。为了实现这一点，心外膜冠状动脉微循环观察通过活体显微镜使用频闪epi-illumination。在β-肾上腺素能阻滞期间，在对照条件下测量微血管直径（普萘洛尔1 mg/kg）和β-肾上腺素能阻滞伴起搏;在存在β-肾上腺素能阻滞的情况下，输注三种剂量的去甲肾上腺素时冠状动脉α-肾上腺素能激活期间（0.1、0.5和1.0-2.0 μ g/kg/min）或三种频率的双侧星状神经刺激（2，10和20 Hz）;和在联合α-和β-肾上腺素能阻滞（酚妥拉明2 mg/kg和普萘洛尔1 mg/kg）。在β-肾上腺素能阻滞期间，动脉和静脉血管的直径均减小，但起搏后恢复至基线。在最低水平的去甲肾上腺素输注或双侧星状核刺激频率下，未观察到微血管收缩。在较高剂量的去甲肾上腺素下，观察到直径大于100 μ m的动脉血管直径降低-5.1 +/- 0.9%（1.0-2.0 μ g/kg/min）和-4.0 +/- 1.1%（0.5 μ g/kg/min）（p <0.05）。在10 Hz和20 Hz的星状刺激下，这些相对较大的血管的直径分别减小了-4.8 +/- 1.9%和-4.4 +/-2.1%。在最高水平的神经刺激（直径增加9.2 +/- 2.5%）或去甲肾上腺素输注速率（直径增加13.6 +/- 2.7%）期间，小冠状动脉（直径小于100微米）显著扩张（p <0.05）。这些收缩和扩张反应被取消后，联合α和β-肾上腺素能阻滞。去甲肾上腺素输注导致冠状静脉和小静脉直径减小（7.2 +/- 1.3%）（p <0.05），而星状刺激没有显著减小静脉和小静脉直径。总之，冠状静脉和小静脉血管系统对来自循环去甲肾上腺素的α-肾上腺素能激活有反应，但不受星状刺激的影响。相比之下，星状刺激和去甲肾上腺素输注在冠状动脉和小动脉微血管中引起类似的反应。收缩发生在直径大于100微米的血管中，而扩张主要发生在直径小于100微米的血管中。这种不均匀的动脉反应无疑会导致冠状血管阻力向更大的冠状动脉和小动脉重新分布。
We tested the hypothesis that humoral or neurogenic alpha-adrenergic activation in the coronary circulation would produce heterogeneous vascular reactions. To accomplish this, the epicardial coronary microcirculation was viewed through an intravital microscope using stroboscopic epi-illumination. Microvascular diameters were measured under control conditions during beta-adrenergic blockade (propranolol 1 mg/kg) and beta-adrenergic blockade with pacing; during coronary alpha-adrenergic activation in the presence of beta-adrenergic blockade with three doses of norepinephrine infusion (0.1, 0.5, and 1.0-2.0 micrograms/kg/min) or three frequencies of bilateral stellate nerve stimulation (2, 10, and 20 Hz); and during combined alpha- and beta-adrenergic blockade (phentolamine 2 mg/kg and propranolol 1 mg/kg). Diameters of both arterial and venous vessels were reduced during beta-adrenergic blockade but returned back to baseline with pacing. At the lowest level of norepinephrine infusion or frequency of bilateral stellate stimulation, microvessel constriction was not observed. At the higher doses of norepinephrine a -5.1 +/- 0.9% (1.0-2.0 micrograms/kg/min) and a -4.0 +/- 1.1% (0.5 micrograms/kg/min) decrease in diameter of arterial vessels greater than 100 microns in diameter were observed (p less than 0.05). At 10 Hz and 20 Hz of stellate stimulation, diameter decreased by -4.8 +/- 1.9% and -4.4 +/- 2.1%, respectively, in these relatively large vessels. Small coronary arterioles (less than 100 microns diameter) dilated significantly during the highest levels of nerve stimulation (9.2 +/- 2.5% increase in diameter) or infusion rate of norepinephrine (13.6 +/- 2.7% increase in diameter) (p less than 0.05). These constrictor and dilator responses were abolished following combined alpha- and beta-adrenergic blockade. Norepinephrine infusion resulted in a decrease in diameter of coronary veins and venules (7.2 +/- 1.3%) (p less than 0.05), whereas stellate stimulation did not significantly reduce venous and venular diameters. In summary, the coronary venous and venular vasculature responds to alpha-adrenergic activation from circulating norepinephrine but is not affected by stellate stimulation. In contrast, stellate stimulation and norepinephrine infusion elicit similar responses in the coronary arterial and arteriolar microvasculature. Constriction occurs in vessels greater than 100 microns in diameter, whereas dilation predominates in vessels less than 100 microns in diameter. Such heterogeneous arterial responses would undoubtedly result in a redistribution of coronary vascular resistance toward larger coronary arteries and arterioles.