• 作者： A.E. Taylor
• 作者服務機構： 美國南阿拉巴馬大學醫學院生理學科
• 中文摘要： 本論文簡略回顧討論在各種不同動物（鼠、兔及狗等）肺臟防止肺水腫（主要為肺泡積水）發生之各種因素，
  注重於正常微血管內皮細胞屏壁與因為缺血／再灌流引起內皮細胞損傷後，這些防止水腫安全因素之異同。在正常
  情況下，提高毛細管壓力之後，組織壓、血漿膠性滲透壓及淋巴流量之增加足以防止肺水腫之產生，因此在毛細管
  壓提高至30mm Hg之內並無明顯之肺泡水腫發生。當內皮細胞之屏壁發生損傷之後，血漿蛋白質大量溢出毛細管之
  外，減少了毛細管壁內外膠性滲透壓差距之效果，因此在較低之毛細管壓力下即可造成肺水腫，但是淋巴流量之大
  量增加仍是一有效的安全因素，毛細管壓在20-25mm Hg之內仍無明顯之肺泡積水發生。另外本文討論肺臟缺血／再
  灌流造成內皮細胞損傷之機轉，在缺血∕再灌流肺損傷中氧游離基清除劑、白血球清除及改變與內皮細胞粘連之效
  應，同時也提供初步之實驗結果顯示增加細胞環狀單磷腺?可防止肺臟內皮細胞損傷的作用。
• 英文摘要： A review of the factors that oppose pulmonary edema formation (alveolar flooding) when capillarypressure is elevated are presented for a normal capillary endothelial barrier and for damaged endotheliumassociated with ischemia/reperfusion in rabbit, rat, and dog lungs. Normally, tissue pressure, the plasmaprotein osmotic pressure gradient acting across the capillary wall and lymph flow (Edema Safety Factors)increase to prevent the build-up of fluid in the lung's interstitium when capillary pressure increases. Nomeasureable alveolar edema fluid accumulates until capillary pressure exceeds 30 mmHg. When the capillarywall has been damaged, interstitial edema develops at lower capillary pressures because the plasma proteinosmotic pressure will not change greatly to oppose capillary filtration, but lymph flow increases to very highlevels to remove the increased filtrate and the result is that capillary pressures can increase to 20-25 mmHgbefore alveolar flooding results. In addition, the mechanisms responsible for producing pulmonaryendothelial damage with ischemia/reperfusion are reviewed and the effects of radical scavengers,neutrophil depletion or altering their adherence to the endothelium, and increasing cAMP on reversing thedamage to the pulmonary endothelium is presented．
• 中文關鍵字： pulmonary edema; edema safety factor; ischemia/reperfusion injury; oxygen radical; cAMP elevation; pulmonary vascular resistance.
• 英文關鍵字： --