| ObjectiveTo explore the effects and the relationship between H2S and NO. To observe theeffects of exogenous H2S, H2S inhibitors and inducible NO synthase on H2S and NOin rats with acute lung injury induced by paraquat poisoning. Thus deduced themechanism of H2S and NO in acute lung injury induced by paraquat poisoning.Methods60male SD rats were divided into10group including the control group（20rats）and experimental group (40rats). Then the control group were divided into5group with0.5ml/kg saline by injection. Experimental group were divided into5group with100mg/kg paraquat at by fed at3,6,12,24,48h. The endogenous H2Sand NO in blood were detected at3,6,12,24,48h. The rats were killed and lungtissue specimens were collected to perform the pathology score of lung tissuedamaged.50male SD rats were randomly divided into5group including the blankcontrol group（C group）with0.5ml/Kg NS by fed and2ml/Kg NS by injection,exposure group（N group）with100mg/kg paraquat by fed and2ml/Kg NS byinjection, exogenous H2S group（H group）with100mg/kg paraquat by fed and2ml/Kg NaHS by injection, H2S inhibitor group（P group）with100mg/kg paraquatby fed and2ml/Kg PPG by injection, inducible NO synthase inhibitor group（AGgroup）with2ml/Kg AG by injection. After12h, the rats were killed and lung tissuespecimens were collected to perform the pathology score of lung tissue damaged. ResultsExperiment1:1. Pathological changes of lung tissue(1) substantially visually observation:Lung tissue of N group is pale pink, smooth surface, no bleeding and bruising,no blisters, good elasticity. Lung tissue of PQ3and PQ6group were a little congestion,mild edema, the appearance of red, no large bleeding lesions, poor flexibility. Lungtissue of PQ12and PQ24group group were congestion significantly, the appearanceof pale red, edema, poor flexibility. Lung tissue of PQ48group was the most seriousinjury, the appearance of dark red, large bruising and bleeding lesions, severecongestion and edema, very poor flexibility.(2) microscopic observation:Alveolar structure of N group was structured, no edema. Interstitial lung wasno widening and fibrosis. Pulmonary capillary was no congestion, no thrombusprecipitation. Alveolar and interstitial lung had no red blood cells and inflammatorycells. Alveolar structure of PQ3group was still intact, slightly edema. Interstitial lungwas no widening and fibrosis. Pulmonary microvascular was no congestion, nothrombus precipitation. Alveolar and interstitial lung had red blood cells andinflammatory cells. Alveolar structure of PQ6group was still intact, slight edema.Pulmonary interstitial was not widened and fibrosis. pulmonary capillary was littlecongestion, no thrombus precipitation. Alveolar and interstitial lung had a trace of redblood cells and inflammatory cells. Alveolar structure of PQ12group was lesscomplete structure, alveolar edema. Alveolar and interstitial lung had little visible redblood cells and inflammatory cells. Pulmonary microvascular had obvious thrombosisprecipitated. Interstitial lung was mild interstitial fibrosis. Among PQ12group,Alveolar structure of PQ24group was not complete, alveolar edema. Alveolar andinterstitial lung had red blood cells and inflammatory cells. Pulmonary microvascularwas congestion and micro-thrombosis obvious. Interstitial lung was slightly thickenedand lung tissue was obvious fibrosis. Among PQ24group, lveolar structure of PQ48group was disorganized, incomplete, destroyed obviously. Alveolar was edema, hyaline membrane formation. Lung interstitium and alveoli had a large number of redblood cells and granule cell for invasion occurs. Pulmonary capillary were congestionand micro-thrombosis obviously. Interstitial lung were markedly thickened. interstitialpulmonary fibrosis were evident and lung was atelectasis.2.The relationship of endogenous H2S and NO in serumCompared with the N group, the serum concentration of endogenous H2S andNO were significantly different at3,6,12,24,48h after paraquat exposure (P <0.01).The serum concentration of endogenous H2S and NO were significantlydifferent among3,6,12,24,48h (P <0.01).Experiment2:1. Pathological changes of lung tissue(1) the general eye view:Lung tissue of control group were complete, pink, surface gloss, smoothness, nobleeding and bruising, no blisters, good elasticity. Lung tissue of lung tissue exposedgroup were the appearance of dark red, no smooth, dark, visible bleeding and bruising,edema, poor flexibility. Lung tissue of exogenous H2S group were light red, mildedema, tension blisters, less smooth surface, a little dark red dot hemorrhage andflexibility is acceptable. Lung tissue of H2S lung tissue inhibitor group wereobviously dark red, extensive edema, visible large flake dark red bleeding lesions,poor flexibility. Lung tissue of lung tissue selective inhibitor of inducible NOsynthase group were dark red, mild edema, less smooth, dark red spots visiblehemorrhage, poor flexibility.(2)Microscopic view:Alveolar of blank control group was complete and no edema and fibrosis.Endothelial cell wall is complete. Alveolar and interstitial lung had no red blood cellsand inflammatory cell infiltration. Interstitial lung were no widening and lung tissuewere no fibrosis. Alveolar of exposure group was less complete, alveolar and interstitial lung edema. Endothelial cell wall were less complete. Alveolar andinterstitial lung had red blood cells and inflammatory cells. Interstitial pulmonaryfibrosis were widened a little. Alveolar of exogenous H2S group and selectiveinhibitor of inducible NO synthase group were still intact, slightly alveolar edema.Endothelial cell wall were still intact. Interstitial lung were no widening and lungtissue were no fibrosis. Alveolar and interstitial lung had a little red blood cells andinflammatory cell infiltration. Pulmonary fibrosis were obvious. Lung injury score ofN group, H group, AG group and the control group were increased. Alveolar of H2Sinhibitor group were disordered, incomplete, destroy obvious. Alveolar edema wereextensive, transparent film.Alveolar and interstitial lung had a large number of redblood cells and inflammatory cells appear widespread invasion. Interstitial lung weremarkedly thickened. Interstitial pulmonary fibrosis were visible and lung were visibleatelectasis. Compared with the control group, acute lung injury of P group was mostsevere degree.2. The relationship of endogenous H2S and NO in serumCompared with the C group, the serum concentration of endogenous H2S andNO in N, H, AG, P groups ere significantly different after paraquat exposure (P<0.01).Conclusions:1. Reduced endogenous H2S was negatively correlated with increased NO whenparaquat poisoning inducing acute lung injury in SD rats；2. Elevated H2S and increased NO could alleviate the degree of acute lung injuryafter paraquat poisoning by exogenous H2S (NaHS), PPG and selective inhibitor ofinducible NO synthase (iNOS). These results showed that paraquat caused lung injuryby inhibiting the generation of endogenous H2S and promoting the release of NO. |
PDF Full Text Request