潛水減壓病致病機轉之研究

The Pathogenesis of Decompression Sickness

黃坤崙(Kun-Lun Huang) ； 林玉鐘(Yu-Chong Lin)

《中華職業醫學雜誌》 3卷1期 (1996/01) Pp. 30-36

摘要

潛水減壓病根本的病因是組織及血液中氣泡的生成。氣泡阻塞血管，造成組織缺血與缺氧；同時，氣泡在組織中也會引發連串之生化反應，造成二度傷害。肺部氣泡栓塞症是潛水或飛行減壓症的病症之一。透過對肺部氣泡栓塞症的致病機轉瞭解，我們可以更清楚氣泡在組織中所產生的作用，進而尋找潛水減壓病的有效防治方式。我們藉大白鼠游離肺模式，探討補體系統及中性白血球在氣泡栓塞症中所扮演之角色。結果顯示，氣泡栓塞造成肺動脈高壓及肺重增加，而不影響肺微血管壓。氣泡栓塞可經由活化補體系統、中性白血球、以及補體系統與中性球間的相互作用，造成血管通透性增加和組織水腫。預先給予indomethacin可減少氣泡栓塞所造成的血管通透性增加。而給予isoproterenol則可完全預防氣泡栓塞所造成組織傷害。透過對氣泡造成組織傷害的瞭解，一方面我們也許可以藉由測定潛水員免疫系統對氣泡活化的敏感性，來篩選較不易得急性減壓病的潛水員，以達到預防的效果。另一方面可針對氣泡引發的生化反應，給予適當的拮抗藥物，以達到輔助治療的效果。

關鍵字

氣泡栓塞症 ； 血管通透性 ； 中性白血球 ； 補體系統

並列摘要

Decompression sickness (DCS) is a consequence of bubble formation in tissues or blood circulation during acute pressure reductions in diving and aviation. In addition to the effects of vascular obstruction, air bubbles induce a number of biochemical reactions leading to tissue injury. Among the biochemical reactions, we investigated the involvement of complement system and polymorphonuclear leukocytes (PMN) in the bubble-induced tissue injury by using isolated and perfused rat lungs. Our results demonstrated that air infusion caused hypertension and lung weight gain. Air infusion increased vascular permeability activation of the complement and PMN, singly or in combinations. This suggests the involvement of complement and PMN in the pathophysiology of DCS. This also provides a possible method to select the diver by examining the sensitivity of complement or PMN activation to air bubbles. Pretreatment with indomethacin or isoproterenol reduced the lung injury caused by air infusion, suggesting that prostaglandins mediate the permeability increase induced by air infusion, which may be related to alteration of intracellular Camp level. While recompression remains the primary treatment for DCS, it may be helpful to prevent the activation of complement and PMN, to inhibit the production of prostaglandins, and to enhance the intracellular level of Camp.

並列關鍵字

Pulmonary air embolism Vascular permeability Polymorphonuclear leukocyte Complement