Department of Bioengineering, University of Utah, 20 S. 2030 E., Salt Lake City, UT, 84112, USA.
Faculty of Life Sciences, Bar Ilan University, 5290002, Ramat-Gan, Israel.
J Neuroeng Rehabil. 2018 May 29;15(1):43. doi: 10.1186/s12984-018-0390-y.
Electrical vasoconstriction is a promising approach to control blood pressure or restrict bleeding in non-compressible wounds. We explore the neural and non-neural pathways of electrical vasoconstriction in-vivo.
Charge-balanced, asymmetric pulses were delivered through a pair of metal disc electrodes. Vasoconstriction was assessed by measuring the diameter of rat saphenous vessels stimulated with low-voltage (20 V, 1 ms) and high-voltage (150 V, 10 μs) stimuli at 10 Hz for 5 min. Activation pathways were explored by topical application of a specific neural agonist (phenylephrine, alpha-1 receptor), a non-specific agonist (KCl) and neural inhibitors (phenoxybenzamine, 25 mg/ml; guanethidine, 1 mg/ml). Acute tissue damage was assessed with a membrane permeability (live-dead) fluorescent assay. The Joule heating in tissue was estimated using COMSOL Multiphysics modeling.
During stimulation, arteries constricted to 41 ± 8% and 37 ± 6% of their pre-stimulus diameter with low- and high-voltage stimuli, while veins constricted to 80 ± 18% and 40 ± 11%, respectively. In arteries, despite similar extent of constriction, the recovery time was very different: about 30 s for low-voltage and 10 min for high-voltage stimuli. Neural inhibitors significantly reduced low-voltage arterial constriction, but did not affect high-voltage arterial or venous constriction, indicating that high-voltage stimuli activate non-neural vasoconstriction pathways. Adrenergic pathways predominantly controlled low-voltage arterial but not venous constriction, which may involve a purinergic pathway. Viability staining confirmed that stimuli were below the electroporation threshold. Modeling indicates that heating of the blood vessels during stimulation (< 0.2 °C) is too low to cause vasoconstriction.
We demonstrate that low-voltage stimuli induce reversible vasoconstriction through neural pathways, while high-voltage stimuli activate non-neural pathways, likely in addition to neural stimulation. Different stimuli providing precise control over the extent of arterial and venous constriction as well as relaxation rate could be used to control bleeding, perfusion or blood pressure.
电血管收缩是一种有前途的控制血压或限制非可压缩性伤口出血的方法。我们在体内探索电血管收缩的神经和非神经途径。
通过一对金属盘电极传递平衡电荷的不对称脉冲。通过测量低电压（20 V，1 ms）和高电压（150 V，10 μs）刺激下大鼠隐静脉的直径来评估血管收缩，刺激频率为 10 Hz，持续 5 分钟。通过局部应用特定的神经激动剂（苯肾上腺素，α-1 受体）、非特异性激动剂（KCl）和神经抑制剂（酚氧苄胺，25 mg/ml；胍乙啶，1 mg/ml）来探索激活途径。使用膜通透性（死活）荧光测定法评估急性组织损伤。使用 COMSOL Multiphysics 建模估计组织中的焦耳加热。
在刺激过程中，动脉分别收缩至刺激前直径的 41±8%和 37±6%，而静脉分别收缩至 80±18%和 40±11%。在动脉中，尽管收缩程度相似，但恢复时间却大不相同：低电压刺激约 30 秒，高电压刺激约 10 分钟。神经抑制剂显著降低了低电压动脉收缩，但不影响高电压动脉或静脉收缩，表明高电压刺激激活了非神经血管收缩途径。肾上腺素能途径主要控制低电压动脉但不控制静脉收缩，这可能涉及嘌呤能途径。存活染色证实刺激低于电穿孔阈值。建模表明，刺激期间血管的加热（<0.2°C）太低，不会引起血管收缩。
我们证明低电压刺激通过神经途径诱导可逆血管收缩，而高电压刺激激活非神经途径，可能除了神经刺激外还激活非神经途径。不同的刺激可以精确控制动脉和静脉收缩以及松弛速率，可用于控制出血、灌注或血压。
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