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Objective To explore the effect of isoflurane on Na-K-ATPase activity in cultured primary alveolar type Ⅱ(ATⅡ) cells with or without being injured by H 2O 2.Methods ATⅡcells were isolated from adult rat lungs and incubated for 24h and divided into six groups. Group 1 served as control and received no treatment. Group 2 and 3 ATⅡ cells were exposed to 0.28 or 2.8mmol/L isoflurane. In group 4 cells were exposed to 75?mol/L H 2O 2. In group 5 and 6 cells were exposed to both 75?mol/L H 2O 2 + 0.28 or 2.8mmol/L isoflurane. Each group was incubated for another 2h after the addition of isoflurane and /or H 2O 2. The Na-K-ATPase activity of ATⅡcells ,the LDH activity and the MDA concentration of fluid culture medium were measured by biochemical methods.Results Isoflurane markedly decreased Na-K-ATPase activity in normal ATⅡ cells, but aggravated the decrease in Na-K-ATPase activity induced by H 2O 2. Isoflurane had no effect on LHD activity and MDA concentration of fluid culture medium of normal ATⅡ cells ,but significantly increased LHD activity and the MDA concentration of of fluid culture medium of ATⅡ cells injured by H 2O 2.Conclusions Isoflurane can inhibit Na-K-ATPase activity of ATⅡ cells in vitro, and aggravate the damage of ATⅡ cells caused by oxidants.
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Objective To explore the change of alveolar epithelial liquid clearance capacity in lung edema following acute lung injury induced by oleic acid.Methods Forty-eight Wistar rats were randomly divided into 6 groups: the control(C), injury(I), amiloride(A), ouabain(O),amiloride plus ouabain(AO), and terbutaline(T) groups. Acute lung injury was induced with intravenous oleic acid 0.25 mlkg -1. 24h after injury, 5% albumin solution (5 ml?kg -1) was delivered into both lungs via the trachea in C and I groups. In A, O, AO and T groups, amiloride (2?10 -3 mol/L),ouabain (5?10 -4 mol/L), amiloride (2?10 -3mol/L) and ouabain (5?10 -4 mol/L)mixture and terbutaline(10 -4 mol/L),added respectively to the albumine solution,at 5ml.kg -1 were administered intratracheally to both lungs separately. One hour later, the alveolar liquid clearance rate(ALC), total lung water content(TLW), extravascular lung water content(EVLW) and arterial blood gases were measured.Results As compared with those in C group, severe hypoxemia, hypercapnia and acidosis appeared, ALC was reduced by 49.2% ,TLW and EVLW markedly increased in I group(P
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The experiment was done to explore the effect of sodium Tanshinone Ⅱ_A, sulfonat (STS) on myocardial reperfusion injury. Myocardial ischemia was induced with the occlusion of left anterior descending coronary artery lasting 30 minutes, and postischemic reperfusion persisted 30 minutes also. Fifty rabbits were randomly divided in to five groups: operative control group (group Ⅰ, n=10), myocardial ischemia group (group Ⅱ, n=10), myocardial ischemia and reperfusion group (group Ⅲ, n=10), receiving intravenous STS 5mg?kg~(_1) 5 mins before the reperfusion (group Ⅳ, n=10) and receiving intravenous STS 5mg?kg~(_1) 10 mins before the ischemia and 5 mins before the reperfusion respectively (group Ⅴ, n=10). As compared with those of group Ⅰ, the amount of myocardial malondialdehyde (MDA) increased significantly in group Ⅱ and Ⅲ (P0.05); the activity of myocardial superoxide dismutase (SOD) decreased in group Ⅲ(P0.05); the serum creatine kinase (CK) activity rose markedly in group Ⅱ, Ⅲ and Ⅳ (P0.05). In comparison with those of group Ⅲ, the amount of MDA reduced and activity of SOD increased in group Ⅳ and Ⅴ (P
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AIM To determine the effect of isoflurane(Iso) on pulmonary surfactant(PS) synthesis in cultured primary ATⅡ cells. METHODS ATⅡ cells were isolated from adult rat lungs and used for the experiments after 32 h in primary culture. Iso 0.28 and 2 8 mmol?L -1 was added into the media of normal and H 2O 2 (75 ?mol?L -1 )-treated cells, and the cells were further incubated for 2 h. The cell proliferation was measured with MTT method and PS synthesis with 3H-choline chloride incorporation. RESULTS Iso had no effect on the proliferation of ATⅡ cells, but markedly decreased PS synthesis in normal alveolar type Ⅱ cells, and aggravated the decrease of PS synthesis induced by H 2O 2. CONCLUSION Iso may decrease PS synthesis of alveolar type Ⅱ cells in vitro , and aggravate the damage of the cells under peroxidation condition.