Related Experiment Videos
[Anasarcous mechanism induced by hypercapnia in rats]
1Department of Respiratory Disease, Beijing Red Cross Chaoyang Hospital, Beijing 100020.
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.