Immunohistochemical Localization of the Water Channels AQP4 and AQP5 in the Rat Pituitary Gland

The pituitary gland is composed of the adenohypophysis and neurohypophysis. The adenohypophysis contains endocrine cells, folliculo-stellate (FS) cells, and marginal layer cells, whereas the neurohypophysis mainly comprises axons and pituicytes. To understand the molecular nature of water transfer in the pituitary gland, we examined the immunohistochemical localization of the membrane water channels aquaporin-4 (AQP4) and AQP5 in rat tissue. Double immunofluorescence analysis of AQP4 and S100 protein, a known marker for FS cells, marginal layer cells, and pituicytes, clearly revealed that FS cells and marginal layer cells in the adenohypophysis and the pituicytes in pars nervosa are positive for AQP4. AQP5 was found to be localized at the apical membrane in some marginal layer cells surrounding the Rathke’s residual pouch, in which AQP4 was observed to be localized on the basolateral membranes. These results suggest the following possibilities: 1) FS cells especially require water for their functions and 2) transepithelial water transfer could occur between the lumen of Rathke’s residual pouch and the interstitial fluid in the adenohypophysis through the AQP4 and AQP5 channels in the marginal layer cells

広範前壁急性心筋梗塞による重症左室機能低下例でアミオダロンにより急性呼吸促迫症候群を惹起し,救命し得なかった症例

We here report a case of 71-year-old man with acute extensive anterior myocardial infarction, who was complicated with ventricular tachycardia (VT) even after successful percutaneous coronary intervention. As intravenous administration of nifekalant terminated VT , we started oral administration of amiodarone (day 1). We gave 400 mg of amiodarone a day for the first week and 200 mg a day from the second week. The patient was stable with normoxia by day 20 , in spite of pulmonary congestion-like infiltrates on chest X-ray. On day 21, he was complicated with acute respiratory distress syndrome. Immediate discontinuance of amiodarone and high-dose pulse glucocorticoid therapy with intubation slightly improved the infiltrations on chest X-ray. However, glucocorticoid therapy induced hyperglycemia with an increase in plasma osmolality, complicated with hypoalbuminemia , and gastrointestinal bleeding. Despite treatment with a large amount of saline, high-doses of catecholamines, and blood transfusion, the patient died on day 28. It is sometimes difficult to diagnose congestive heart failure or amiodarone-induced pulmonary infiltrates in patients with severe left ventricular dysfunction.71歳,男\u271生広範前壁急性心筋梗塞による心源性ショック状態で,非持続性心室頻拍が頻発していた.まず大動脈内バルーンパンピングを挿入し,血行動態を安定化させた.冠動脈造影上,左冠動脈前下行枝,回旋枝,右冠動脈の近位部が完全閉塞していたが,回旋枝および右冠動脈は側副血行路にて栄養されていた.責任病変は左冠動脈前下行枝と考え,インターベンションを施行した.インターベンション中,心室頻拍/心室細動となり,電気的除細動を繰り返した.左冠動脈前下行枝領域の虚血解除にても心室頻拍/心室細動が改善せず,シンビット点滴にて心室頻拍/心室細動は消失した.血行動態が安定し,大動脈内バルーンパンピング挿入のまま集中治療室へ入室し経過観察した.入院翌日よりアミオダロンを開始し,20病日までは酸素化も良好だったが,21病日,急性呼吸促迫症候群の所見を認め,ステロイドパルス療法を開始した.胸写上,徐々にではあるが,急性呼吸促迫症候群所見は改善傾向に向かった.しかしながら,ステロイドパルス療法による非ケトン性高浸透圧性昏睡,低アルブミン血症,消化管出血による軽度の貧血を合併し,輸血およびアルブミン投与も無効で,救命し得なかった.アミオダロンによる肺障害は重篤な合併症の1つであるが,本症例のように重症左室機能障害を有する症例では,肺うっ血と早期のアミオダロンによる肺障害の鑑別が困難なことがあり,十分に留意する必要がある

A Fatal Case of Amiodarone-Induced Acute Respiratory Distress Syndrome in a Patient with Severe Left Ventricular Dysfunction Due to Extensive Anterior Acute Myocardial Infarction

We here report a case of 71-year-old man with acute extensive anterior myocardial infarction, who was complicated with ventricular tachycardia (VT) even after successful percutaneous coronary intervention. As intravenous administration of nifekalant terminated VT , we started oral administration of amiodarone (day 1). We gave 400 mg of amiodarone a day for the first week and 200 mg a day from the second week. The patient was stable with normoxia by day 20 , in spite of pulmonary congestion-like infiltrates on chest X-ray. On day 21, he was complicated with acute respiratory distress syndrome. Immediate discontinuance of amiodarone and high-dose pulse glucocorticoid therapy with intubation slightly improved the infiltrations on chest X-ray. However, glucocorticoid therapy induced hyperglycemia with an increase in plasma osmolality, complicated with hypoalbuminemia , and gastrointestinal bleeding. Despite treatment with a large amount of saline, high-doses of catecholamines, and blood transfusion, the patient died on day 28. It is sometimes difficult to diagnose congestive heart failure or amiodarone-induced pulmonary infiltrates in patients with severe left ventricular dysfunction.71歳,男'1生広範前壁急性心筋梗塞による心源性ショック状態で,非持続性心室頻拍が頻発していた.まず大動脈内バルーンパンピングを挿入し,血行動態を安定化させた.冠動脈造影上,左冠動脈前下行枝,回旋枝,右冠動脈の近位部が完全閉塞していたが,回旋枝および右冠動脈は側副血行路にて栄養されていた.責任病変は左冠動脈前下行枝と考え,インターベンションを施行した.インターベンション中,心室頻拍/心室細動となり,電気的除細動を繰り返した.左冠動脈前下行枝領域の虚血解除にても心室頻拍/心室細動が改善せず,シンビット点滴にて心室頻拍/心室細動は消失した.血行動態が安定し,大動脈内バルーンパンピング挿入のまま集中治療室へ入室し経過観察した.入院翌日よりアミオダロンを開始し,20病日までは酸素化も良好だったが,21病日,急性呼吸促迫症候群の所見を認め,ステロイドパルス療法を開始した.胸写上,徐々にではあるが,急性呼吸促迫症候群所見は改善傾向に向かった.しかしながら,ステロイドパルス療法による非ケトン性高浸透圧性昏睡,低アルブミン血症,消化管出血による軽度の貧血を合併し,輸血およびアルブミン投与も無効で,救命し得なかった.アミオダロンによる肺障害は重篤な合併症の1つであるが,本症例のように重症左室機能障害を有する症例では,肺うっ血と早期のアミオダロンによる肺障害の鑑別が困難なことがあり,十分に留意する必要がある