Okada A, Okuda H, Inaba R, Ariizumi M
Br J Ind Med. 1985 Oct;42(10):678-81. doi: 10.1136/oem.42.10.678.
This study was designed to obtain basic information about the mechanism of the occurrence of muscular disorders after exposure to vibration. The hind legs of rats were exposed to acute and chronic local vibration at frequencies of 30, 60, 120, 240, 480, and 960 Hz with a constant acceleration of 50 m/sec2. The exposure time was four hours for acute, and four hours a day for two weeks continuously for chronic exposure. Blood was collected after exposure to measure plasma creatine phosphokinase (CPK) activity. In both exposure groups the activity of plasma CPK was significantly higher at 30, 60, 120, 240, and 480 Hz compared with the control group and was especially high at 30 Hz; there was no significant change at 960 Hz. As a result of an analysis of the CPK isoenzymes, the increase in plasma CPK activity was shown to be due to the activity of the plasma CPK-MM fraction, originating in the skeletal muscle. Plasma CPK activity showed a tendency to decrease gradually with the increase in vibration frequency during acute exposure but showed no such tendency during chronic exposure. There was no remarkable pathohistological change in muscle preparations from the hind legs, hence it was presumed that the increase in plasma CPK activity was caused not by the morphological changes of muscle but by other mechanisms, such as an increase in the permeability of the cell membrane.
本研究旨在获取有关暴露于振动后肌肉疾病发生机制的基础信息。将大鼠的后腿暴露于频率为30、60、120、240、480和960Hz的急性和慢性局部振动,恒定加速度为50m/sec²。急性暴露时间为4小时,慢性暴露为连续两周每天4小时。暴露后采集血液以测量血浆肌酸磷酸激酶(CPK)活性。在两个暴露组中,与对照组相比,30、60、120、240和480Hz时血浆CPK活性显著更高,在30Hz时尤其高;960Hz时无显著变化。对CPK同工酶的分析结果表明,血浆CPK活性的增加是由于源自骨骼肌的血浆CPK-MM组分的活性。急性暴露期间,血浆CPK活性呈现出随振动频率增加而逐渐降低的趋势,但慢性暴露期间未呈现此趋势。后腿肌肉制剂中没有明显的病理组织学变化,因此推测血浆CPK活性的增加不是由肌肉的形态变化引起的,而是由其他机制引起的,如细胞膜通透性增加。