高浓度二氧化碳致大鼠全身性水肿的机理研究

目的　探讨高碳酸血症时大鼠全身性水肿发生的机理。方法　给大鼠呼吸高浓度二氧化碳气体（８ ％ Ｃ Ｏ２ 、２１ ％ Ｏ２ ，７１ ％ Ｎ２） ，每天７ 小时，连续４ 周。观察高碳酸血症大鼠各项指标的变化，并设对照组。结果　对照组平均肺动脉压（ｍ Ｐ Ａ Ｐ） 为（１９４ ±０２８） ｋ Ｐａ， Ｐａ Ｃ Ｏ２ 为（４６ ±０９） ｋ Ｐａ 。大鼠循环血中１２５ Ｉ牛血清白蛋白半排出时间（ Ｔ１／２） 为（２３８ ±３０） ｍｉｎ ；血浆过氧化脂质（ Ｌ Ｐ Ｏ） 为（３０ ±０６）ｎｍｏｌ／ｍｌ，红细胞超氧化物歧化酶（ Ｓ Ｏ Ｄ） 活性为（１ ０４２ ±１３５） Ｕ／ｇ Ｈｂ 。肺组织中水含量为（７６２ ±１０） ％ ，肌组织为（７４１ ±２８） ％ 。高碳酸血症组ｍ Ｐ Ａ Ｐ 为（２０ ±０４） ｋ Ｐａ 、 Ｐａ Ｃ Ｏ２ 为（７４ ±０４） ｋ Ｐａ 、 Ｔ１／２ 为（１５０ ±２３） ｍｉｎ 、 Ｌ Ｐ Ｏ 为（８８ ±２０） ｎｍｏｌ／ｍｌ、 Ｓ Ｏ Ｄ 为（６８２ ±３４１） Ｕ／ｇ Ｈｂ 、肺组织中水含量为（７８８±１８） ％ 、肌组织为（７６０ ±１０） ％ 。两组比较ｍ Ｐ Ａ Ｐ 差异无显著意义（ Ｐ＞ ００５） ； Ｐａ Ｃ Ｏ２ 、

Anasarcous mechanism induced by hypercapnia in rats

OBJECTIVE: To study anasarcous pathogenesis during hypercapnia. METHODS: The mixed gases of highly concentrated carbon dioxide (8% CO2, 21% O2, 71% N2) were given to Wistar rats 7 hours a day for four weeks. The various indexes were comparatively observed between control group and hypercapnia group. RESULTS: Pulmonary arterial pressure (mPAP) in control group was (1.94 +/- 0.28) kPa and PaCO2 (4.6 +/- 0.9) kPa. T1/2 of 125I-BSA in the blood was (238 +/- 30) min, plasma lipid peroxide (LPO) level (3.08 +/- 0.69) nmol/ml, erythrocytic superoxide dismutase (SOD) activity (1,042 +/- 135) CU/g Hb. Water content was (76.2 +/- 1.0)% in lung and (74.1 +/- 2.8)% in muscular tissues. mPAP in hypercapnia group was (2.0 +/- 0.4) kPa, PaCO2 (7.4 +/- 0.4) kPa, T1/2 (150 +/- 23) min, LPO (8.8 +/- 2.0) nmol/ml, SOD (682 +/- 341) U/g Hb1 and water content was (78.8 +/- 1.8)% in lung and (76.04 +/- 1.07)% in muscular tissues. No significant differences were found in mPAP (P > 0.05). There were significant differences in PaCO2 (P < 0.01), T1/2 (P < 0.01), LPO (P < 0.001), SOD (P < 0.01), water content in lung (P < 0.01), and water content in muscular tissues (P < 0.05). CONCLUSIONS: Rat hypercapnic model can be reproduced with 8% CO2 mixed gases. Systemic water and natrium retention (edema) might occur in the model. Microvascular endothelial cell damage and its highly increased permeability induced by lipid peroxidation is the direct cause of edema. The pulmonary cause per se can produce anasarca.