Karnes J L, Mendel F C, Fish D R, Burton H W
D'Youville College, Division of Rehabilitation Sciences, Buffalo, NY 14201-1084, USA.
Arch Phys Med Rehabil. 1995 Apr;76(4):381-6. doi: 10.1016/s0003-9993(95)80665-2.
Results from five independent studies from our laboratory indicate that cathodal high-voltage pulsed current (HVPC) significantly curbs posttraumatic edema formation in several animal models. Conversely, anodal HVPC did not curb edema formation. The mechanism by which HVPC reduces edema formation is unknown. We hypothesize that HVPC causes a decrease in local blood flow by active vasoconstriction of arterioles. Because we had previously observed positive effects with cathodal HVPC but not anodal HVPC, we further hypothesized that cathodal but not anodal HVPC would reduce diameters of histamine-dilated arterioles. Changes in diameters of resistance arterioles (5 to 30 microns internal diameter) were measured directly in cheek pouches of anesthetized hamsters, using in vivo video microscopy. Three minutes after superfusion with the inflammatory mediator (histamine) was begun, sensory-level HVPC at 120pps was applied concurrently for 30 minutes. Five animals received cathodal HVPC and five received anodal HVPC. Four other animals received 30-minute treatments of both cathodal and anodal HVPC in random order. Three control animals received histamine without HVPC for 30 minutes. Diameter changes of one arteriole from each cheek pouch was measured every 20 seconds throughout the treatment period. One-way analysis of variance (ANOVA) with repeated measures showed that diameters of histamine-dilated controls varied little over 30 minutes, and that adding cathodal HVPC did not significantly alter diameters of arterioles superfused with histamine. However, applying anodal HVPC to histamine-dilated arterioles significantly reduced arteriolar diameters. These results do not support the hypothesis that cathodal HVPC curbs edema formation by increasing arteriolar tone in the injured area.
我们实验室的五项独立研究结果表明,阴极高压脉冲电流(HVPC)在多种动物模型中能显著抑制创伤后水肿的形成。相反,阳极HVPC并不能抑制水肿形成。HVPC减轻水肿形成的机制尚不清楚。我们推测,HVPC通过使小动脉主动收缩从而导致局部血流减少。由于我们之前观察到阴极HVPC有积极效果而阳极HVPC没有,我们进一步推测,阴极而非阳极HVPC会减小组胺扩张后的小动脉直径。使用体内视频显微镜,直接在麻醉仓鼠的颊囊中测量阻力小动脉(内径5至30微米)的直径变化。在开始用炎症介质(组胺)灌注三分钟后,同时施加120次/秒的感觉水平HVPC,持续30分钟。五只动物接受阴极HVPC,五只接受阳极HVPC。另外四只动物以随机顺序接受阴极和阳极HVPC各30分钟的治疗。三只对照动物接受无HVPC的组胺治疗30分钟。在整个治疗期间,每隔20秒测量每个颊囊一根小动脉的直径变化。重复测量的单因素方差分析(ANOVA)表明,组胺扩张后的对照小动脉直径在30分钟内变化很小,并且添加阴极HVPC并没有显著改变用组胺灌注的小动脉直径。然而,对组胺扩张后的小动脉施加阳极HVPC会显著减小小动脉直径。这些结果不支持阴极HVPC通过增加损伤区域小动脉张力来抑制水肿形成的假设。