大鼠眼脉络膜血流对动脉血压降低的代偿依赖于神经元型一氧化氮合酶，但对动脉血压升高的代偿则不依赖。
Choroidal blood flow compensation in rats for arterial blood pressure decreases is neuronal nitric oxide-dependent but compensation for arterial blood pressure increases is not.
机构信息
Department of Anatomy and Neurobiology, University of Tennessee Health Science Center, 855 Monroe Ave., Memphis, TN 38163, USA.
出版信息
Exp Eye Res. 2010 Jun;90(6):734-41. doi: 10.1016/j.exer.2010.03.006. Epub 2010 Mar 17.
Choroidal blood flow (ChBF) compensates for changes in arterial blood pressure (ABP) and thereby remains relatively stable within a +/-40 mmHg range of basal ABP in rabbits, humans and pigeons. In the present study, we investigated if ChBF can compensate for increases and decreases in ABP in rats. ChBF was continuously monitored using laser Doppler flowmetry in anesthetized rats, and ABP measured via the femoral artery. At multiple intervals over a 2-4 h period during which ABP varied freely, ChBF and ABP were sampled and the results compiled across rats. We found that ChBF remained near baseline over an ABP range from 40 mmHg above basal ABP (90-100 mmHg) to 40 mmHg below basal ABP, but largely followed ABP linearly below 60 mmHg. Choroidal vascular resistance increased linearly as BP increased above 100 mmHg, and decreased linearly as BP declined from basal to 60 mmHg, but resistance declined no further below 60 mmHg. Inhibition of nitric oxide (NO) formation by either a selective inhibitor of neuronal nitric oxide synthase (NOS) (N(omega)-propyl-L-arginine) or a nonselective inhibitor of both neuronal NOS and endothelial NOS (N(omega)-nitro-l-arginine methyl ester) did not affect compensation above 100 mmHg ABP, but did cause ChBF to linearly follow declines in BP below 90 mmHg. In NOS-inhibited rats, vascular resistance increased linearly with BP above 100 mmHg, but remained at baseline below 90 mmHg. These findings reveal that ChBF in rats, as in rabbits, humans and pigeons, compensates for rises and/or declines in arterial blood pressure so as to remain relatively stable within a physiological range of ABPs. The ChBF compensation for low ABP in rats is dependent on choroidal vasodilation caused by neuronal NO formation but not the compensation for elevated BP, implicating parasympathetic nervous system vasodilation in the ChBF compensation to low ABP.
脉络膜血流（ChBF）可补偿动脉血压（ABP）的变化，因此在兔子、人类和鸽子中，其在基础 ABP 的+/-40mmHg 范围内保持相对稳定。在本研究中，我们研究了 ChBF 是否可以补偿大鼠的 ABP 升高和降低。在麻醉大鼠中使用激光多普勒血流仪连续监测 ChBF，并通过股动脉测量 ABP。在 2-4 小时期间，ABP 自由变化，多次采样 ChBF 和 ABP，并在大鼠之间汇总结果。我们发现，在 ABP 范围从基础 ABP 以上 40mmHg（90-100mmHg）到基础 ABP 以下 40mmHg 的情况下，ChBF 保持在基线附近，但在 ABP 低于 60mmHg 时，ChBF 基本呈线性跟随 ABP。脉络膜血管阻力随着 ABP 升高而呈线性增加，随着 ABP 从基础值降至 60mmHg 而呈线性下降，但在 60mmHg 以下阻力不再下降。一氧化氮（NO）形成的抑制，无论是通过神经元型一氧化氮合酶（NOS）的选择性抑制剂（N（omega）-丙基-L-精氨酸）还是神经元型和内皮型 NOS 的非选择性抑制剂（N（omega）-硝基-L-精氨酸甲酯），都不会影响高于 100mmHg ABP 的补偿，但确实导致 ChBF 随低于 90mmHg 的 ABP 下降而呈线性下降。在 NOS 抑制大鼠中，血管阻力随着 ABP 高于 100mmHg 而呈线性增加，但在低于 90mmHg 时保持在基线水平。这些发现表明，大鼠的 ChBF 与兔子、人类和鸽子一样，可以补偿动脉血压的升高和/或降低，从而在 ABP 的生理范围内保持相对稳定。大鼠低 ABP 时的 ChBF 补偿依赖于神经元型 NO 形成引起的脉络膜血管扩张，但不依赖于高 ABP 的补偿，这暗示副交感神经系统的血管扩张参与了低 ABP 时的 ChBF 补偿。
Zotero 插件