Liu K, Chen L E, Seaber A V, Johnson G W, Urbaniak J R
Department of Surgery, Duke University Medical Center, Durham, North Carolina 07902, USA.
J Orthop Res. 1999 Jan;17(1):88-95. doi: 10.1002/jor.1100170114.
Intermittent pneumatic compression has been established as a method of clinically preventing deep vein thrombosis, but the mechanism has not been documented. This study observed the effects of intermittent pneumatic compression of legs on the microcirculation of distant skeletal muscle. The cremaster muscles of 80 male rats were exposed, a specially designed intermittent pneumatic-compression device was applied to both legs for 60 minutes, and the microcirculation of the muscles was assessed by measurement of the vessel diameter in three categories (10-20, 21-40, and 41-70 microm) for 120 minutes. The results showed significant vasodilation in arterial and venous vessels during the application of intermittent pneumatic compression, which disappeared after termination of the compression. The vasodilation reached a maximum 30 minutes after initiation of the compression and could be completely blocked by an inhibitor of nitric oxide synthase, NG-monomethyl-L-arginine (10 micromol/min). A 120-minute infusion of NG-monomethyl-L-arginine, beginning coincident with 60 minutes of intermittent pneumatic compression, resulted in a significant decrease in arterial diameter that remained at almost the same level after termination of the compression. The magnitude of the decrease in diameter in the group treated with intermittent pneumatic compression and NG-monomethyl-L-arginine was comparable with that in the group treated with NG-monomethyl-L-arginine alone. The results imply that the production of nitric oxide is involved in the positive influence of intermittent pneumatic compression on circulation. It is postulated that the rapid increase in venous velocity induced by intermittent pneumatic compression produces strong shear stress on the vascular endothelium, which stimulates an increased release of nitric oxide and thereby causes systemic vasodilation.
间歇性气动压迫已被确立为临床上预防深静脉血栓形成的一种方法，但其机制尚未得到证实。本研究观察了腿部间歇性气动压迫对远处骨骼肌微循环的影响。暴露80只雄性大鼠的提睾肌，将特制的间歇性气动压迫装置应用于双下肢60分钟，通过测量三类血管直径（10 - 20、21 - 40和41 - 70微米）评估肌肉微循环120分钟。结果显示，在应用间歇性气动压迫期间，动脉和静脉血管显著扩张，压迫终止后这种扩张消失。扩张在压迫开始后30分钟达到最大值，并且可被一氧化氮合酶抑制剂NG - 单甲基 - L - 精氨酸（10微摩尔/分钟）完全阻断。从与60分钟间歇性气动压迫同时开始，持续输注NG - 单甲基 - L - 精氨酸120分钟，导致动脉直径显著减小，压迫终止后动脉直径几乎维持在同一水平。接受间歇性气动压迫和NG - 单甲基 - L - 精氨酸治疗组的直径减小幅度与单独接受NG - 单甲基 - L - 精氨酸治疗组相当。这些结果表明，一氧化氮的产生参与了间歇性气动压迫对循环的积极影响。据推测，间歇性气动压迫引起的静脉速度快速增加在血管内皮上产生强大的剪切应力，刺激一氧化氮释放增加，从而导致全身血管扩张。
