Changes of pulmonary ?_1-and ?-adrenergic receptor (?_1-AR and ?-AR)during endotoxin-induced acute lung injury in rates were oberved to find out the rela-tionship between them and the mechanism of change. Results showed that there was amarked decrease of B_max of both ?_1-AR and ?-AR by 35% and 43% respectively, dur-ing acute lung injury. The down regulation of ?-AR might be one of causes of acutelung injury while that of ?_1-AR seems to be a protective response. Active oxygen playedan important role in endotoxin-induced down regulation of AR in the rat lungs. The increa-sed level of norepinephrine and epinephrine was not the main factor that initiate the downregulation of AR. Intravenous injection of tumor necrosis factor (5?10~6U/kg ) exerts noiafluence on the changes of pulmonary AR in rats.

To explore the effects of lipopolysaccharide (LPS), TNF ? and IL 1? on cyclooxygenase 2 (COX 2) expression and prostaglandins (PGs) in rat polymorphonuclear (PMN), measured COX 2 mRNA was determined by reverse transcription polymerase chain reaction and changes in PGs after stimulation of PMN with LPS, TNF ? and IL 1? for 24 hours were observed. The resting PMN were found to express COX 2 mRNA weakly, while it was significantly up regulated after the stimulation of LPS,TNF ?and IL 1?. The level of PGs was increased markedly at the same time. These results suggested that COX 2 might play an important role during inflammatory process involving PMN.

To investigate the expression of TNF ?, IL 1?, IL 6 and IL 8 mRNA in the lung,and the levels of TNF ?, IL 1, IL 6 and IL 8 in serum of rats with sepsis induced acute lung injury(ALI), and to examine the effect of pentoxifylline on the production of these cytokines. The expressions of TNF ?, IL 1?, IL 6 and IL 8 mRNA were detected with dot blot.The levels of TNF ?, IL 1?, IL 6 and IL 8 were examined with ELISA. Compared to the sham operation group, TNF ?, IL 1?, IL 6 and IL 8 mRNA expression in sepsis group were increased evidently( P

AIM: To explore the mechanism of lipopolysaccharide (LPS) on vascular endothelial cell(VEC) damage. METHODS: By using cytometry techniques, we studied the effects of LPS on apoptosis of human umbilical vein endothelial cells (HUVECs) in vitro . RESULTS: LPS was able to induce apoptosis of HUVECs in a time-dose-dependent fashion.CONCLUSION:Apoptosis might play a role in LPS-induced damage of vascular endothelial cells.

0.05). VIP, however, could inhibit the Con A-induced proliferation of T-cells from control subjects more significantly than that from asthmatics (P0.05). The cAMP level in T-cells, however, increased more significantly in the control group than that in the asthmatic group after the treatment of VIP or NaF (P0.05). CONCLUSION: Inhibition effect of VIP on Con A-induced proliferation of T-cells was less in asthmatics than in control subjects, which may be related to insufficiency of Gs ? coupled VIP receptor on T-lymphocytes in asthmatics.

Homogenous fat extract was injected through the femoral vein to induce respiratory distress syndrome in 15 dogs. It was found that the changes of blood gases, chest x-ray films, and lung pathology of the dogs were similar to those of adult respiratory distress syndrome.The pathogenesis was extensive pulmonary fat embolism with complement activation and free radicals formation. Vitamin E was consumed during antiperoxidation. It is believed that this model serves better for the study of respiratory distress syndrome.

The changes of the number of beta-adrenergic receptors, the activity of cAMP-PDE and the level of cAMP were observed in the guinea pigs with allergic asthma with radioligand assay, radioenzyme assay and radioimu-noassay respectively. It was found that there were a 25% decrease of the number of beta-adrenergic receptors on the lung membrane, a 36% decrease of the level of cAMP in the lung tissue, and a 35% increase of cAMP-PDE activity in the asthmatic animals as compared with those of the control. A close positive correlation was observed between the number of beta-adrenergic receptors and cAMP level,but a negative correlation between cAMP-PDE activity and cAMP level in the asthmatic group.

The changes of erythrocytic membrane band 3 protein and intraery-throcytic and extrar rythrccytic gases and electrolytes were studied in 69 cases of cor pulmonale and 50 normal subjects.It was found that in the patients of cor pulmonale accompanied with type Ⅱ respiratory failure,the relative low level of erythrocytic membrane band 3 protein and the restriction of HCO-3/Cl-exchange were the factors to aggravate CO2 retention and respiratory acidosis,relative intraerythrocytic alkalosis resulted from the relative increase of intra-erythrocytic HCO-3([HCO-3]),and prompt adminstration of oxygen to cor pulmonale patients with hypoxemia could not only improve extraerythrocytic acid-base imbalance but also increase intraerythcocytic P5O2 and the tissue capacity to store oxygen.

The therapeutic effects of prostaglandin E1 on respiratory distress syndrome induced with homogeneous fat extraction were observed in dogs.It was found that prostaglandin E1 could alleviate hypoxemia,reduce pulmonary capillary permeability,and attenuste pulmonary edema.The mechanism of the therapeutic efficiency of prostaglandin E1 on pulmonary damages is that prostaglandin E1 can inhibit the adherence of polymorphonuclear netttrophils and the genesis of oxygen free radicals,and protect the pneumocyte type Ⅱ.

Twenty-five mongrel dogs were randomized into 3 groups;the animals of group Ⅰ were traumatized with bone marrow extract,those of group Ⅱ were similarily traumatized and then treated with anisodamine,and those of group Ⅲ received saline only and served as control.The specimens of arterial and venous blood were collected and bronchoalveolar lavage fluid (BALF) and lung homogenate were obtained after the animal was killed.The activity of superoxide dismutase (SOD) and the concentration of lipid peroxides (LPO) were determined.Meanwhile,the clinical manifestations,blood gas analysis.chest radiography,and pathological examinations were performed or observed.It was found there were following findings:(1)In group I,SOD activity and LPO level in the lung homogenate and BALF were markedly elevated immediately after injury,which suggests that there had been a rapid production of active oxygen.As a result.various degrees of lung damages were pricipitated.(2)In group Ⅱ,an increase of SOD activity and LPO level in the blood,lung homogenate and BALF:The elevation was more marked than that in group Ⅲ but less marked than that in group Ⅰ.which indicates that there was a relatively of less amount of active oxygen production by the interference anisodamine.(3)In group Ⅱ,no significant changes of SOD activity and LPO livel were found.Our findings suggest that active oxygen is likely to play a very important role in the pathogenesis of acute lung damages in respiratory distress syndrome.