The dynamic changes of the functions and the weight index of the 2 ventricles and the density of ?-adrenoceptors in the myocardium were observed and the correlation between the changes of ?-adrenoceptors of the myocardium and.the peripheral lymphocytes was investigated during and after intermittent chronic hypbxia in rabbits.The fingings were as follows.(1)Chronic hypoxia resulted in an increase of systolic pressure,dp/dtmas and weight index of the right ventricle.25 days after the restoration of normal oxygen supply,systolic pressure and dp/dtomas of the right ventricle became normal but its weight index remained increased.(2)The density of ?-adrenoceptors of the 2 ventricles was reduced on the 7th,15th and 30th day of hypoxia as compared with that of the control.25 days after the restoration of oxygen supply,the density of ?-adrenoceptors became normal in the left ventricle but remained decreased in the right ventricle.(3)There was a positive correlation between the changes of ?-adrenoceptors in the 2 ventricles and peripheral lymphocytes.The findings suggest that hypoxia-induced hypertrophy of the right ventricle is usually accompanied with a decreased density of its ?-adrenoceptors and thedensity of ?-adrenoceptors of peripheral lymphocytes can reflect the changes of ?-adrenoceptors in the myocardium.

AIM: The purpose of this study was to evaluate the mechanism of high altitude pulmonary edema (HAPE) and high altitude acute response (HAAR). METHODS: Pulmonary function and partial oxygen pressure were measured in 10 patients with HAAR and 6 patients with HAPE before and after bronchoalveolar lavage (BAL),10 high altitude healthy volunteers were served as control subjects. RESULTS: The partial oxygen pressure of HAAR and HAPE significantly decreased before BAL compared with control; DLCO%, DLCO/VA%, PaO_2 of HAPE increased significantly [from 76.01%?6.29%, 150.30%?15.20%, (31.73?3.01) mmHg before BAL to 103.31%?9.23%, 176.04%?16.10%, (45.31?3.56) mmHg after BAL]. The above parameters were also changed in HAAR and controls, but had no statistical significance. CONCLUSION: High concentration of proteins and cells in BAL fluid for HAPE, gas exchange impairment and PaO_2 increase after BAL suggest accumulation of protein-rich fluid and cells in the alveolar space plays a crucial role in the development of HAPE.

AIM: To explore the pathogenic mechanism of high altitude pulmonary edema(HAPE). METHODS: Haemodynamic changes and effects of 100 percent oxygen breathing were measured by Swan-Ganz thermistor catheters, high altitude healthy volunteers were served as controls. RESULTS: The important features of haemodynamic changes in HAPE: (1)Pulmonary arterial pressure was raised; (2)Pulmonary arterial resistance and cardiac output were raised; (3)Pulmonary artery wedge pressures and right atrial pressure were normal; (4)Pulmonary arterial pressure and resistance were induced by oxygen breathing. CONCLUSIONS: The normal pulmonary artery wedge pressures with a high cardiac output indicated that HAPE was recognized as a form of noncardiogenic pulmonary edema. The pulmonary hypertension may play an important role in the development of HAPE.

AIM: To evaluate the prophylactic effect of aminophylline on the pulmonary hypertension rebound reaction to exposure to NO in the hypoxic pigs. METHODS: The 10 pigs undergone Swan-Ganz catheter, the mPAP was measured with a Physio-recording instrument and PaO 2 was measured with a blood gas analyzer, when breathing NO for 30 minutes and suddenly stopping breathing NO, administing aminophylline 0.25 g, followed by 30 minutes with room air. The respiratory rate and heart rate were also monitorried with a Hewlett-Packard portable monitor. RESULTS: The mPAP of the acute hypoxic pig was induced significantly after breathing 10 -5 NO. When suddenly stopping breathing NO, the induced mPAP became more and more high, the level of the mPAP in 5 minutes was similar to the values before absorbing NO, the mPAP in 10 minutes was higher than values before absorbing NO, while the level of PaO 2 was lower than the values before absorbing NO; but suddenly stopping breathing NO, administing aminophylline, although the induced mPAP became high, the speed was slower than the controls, the level of the mPAP in 30 minutes still was lower than the values before absorbing NO. CONCLUSION: Aminophylline has preventive effects on the pulmonary hypertension rebound reaction to exposure to NO in the hypoxic pigs.