肺水腫とPAM

Pulmonary edema and pyridine aldoxime methiodide.

I．はじめに

　PAM（pyridine−2—aldoxime methiodide^1））は有機燐殺虫剤parathion（O，O-dietyl-O—P-nitrophenyl　thiophosphate）中毒の特効薬である。Parathionは強力なアセチールコリンエステレース（Ach E）の阻害剤であり，血中コリンエステレース（Ch E）活性を低下せしめ，アセチールコリン（Ach）蓄積によるneuro—muscular depolarizing blockを発生する^2）3）が，その一症状としての顕著な肺水腫がPAMによって改善されることが知られている。

　一方，肺剔除・アノキシア・輸液を負荷した肺水腫犬で血清Ch E活性値の低下を実証し^4），PAM投与により活性値の回復と同期して病態の改善をみとめた報告^5）があり，ともに急性肺水腫発生機序にAchの関与を考察し，肺毛細血管透過性にたいするその直接作用を想定している。

Pulmonary edema and induced by cholines-terase inhibitors are known to be counterac-ted by pyridine aldoxime methiodide (PAM). Previously we have reported the dramatic effect of PAM on pulmonary edema of surgical origin.

Present study was undertaken to elucidate the role of cholinesterase inducing surgical pulmonary edema. Adenosine triphosphatase which is known to interact active electrolyte transport is also examined histochemically.

Intracellular cholinesterase did not show significant changes by histochemical exami-nations, although plasma cholinesterase acti-vities were decreased during pulmonary ede ma. It was demonstrated that the ATPase was inhibited during pulmonary edema. Furthermore, the activity was returned to-ward control after PAM administration.

Alkaline phosphatase activities were incre-ased during pulmonary edema. This activities are seen in alveolar large epithelial cells, and seems to have some correlation with surfactant synthesis.

The necessities of biochemical approach to the pathophysiology of pulmonary edema are discussed.