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Objective To investigate the serum and placental expressions of asymmetric dimethylarginine (ADMA) and nitric oxide(NO) in fetal growth restriction (FGR),and explore the biological role and mechanisms of ADMA in FGR.Methods Fifty patients with FGR (FGR group)and 50 normal term pregnant women (control group) were detected for the levels of ADMA in maternal sera and placentas with enzyme linked immunosorbent assay (ELISA).The level of NO in maternal sera was analyzed with nitrate reductase method,and the placental tissue sections were analyzed with pathological morphologly.Results For FGR group,the main pathological changes were growth retardation of villi,increased syncytiotrophoblast nodules,and the lack terminal villi;and the incidence rate of pathological change of placental tissue was significantly higher than that in control group [64.0％ (32/50) vs 12.0％ (6/50),x2 =7.90,P ＜ 0.01].For the placental pathological change group,the concentrations of ADMA in the placentas and sera were significantly higher than the normal group [placenta ADMA:(2.21 ± 0.72) μmol/L vs (1.69 ± 0.77) μmol/L,t =3.33,P ＜ 0.01;serum ADMA:(2.01 ± 0.70) μmoL/L vs (1.18 ± 0.54) μmol/L,t =6.66,P ＜0.01].The expression of ADMA was up-regulated in maternal sera and placentas from FGR group compared to normal pregnancy [placenta ADMA (2.24 ± 0.81) μmol/L vs (1.53 ± 0.59) μmol/L,t =5.00,P ＜0.01;serum ADMA (1.89 ±0.75) μmol/L vs (1.10 ±0.43) μ mol/L,t =6.45,P ＜ 0.O1].The NO was extremely lower expressed in maternal sera with FGR than normal pregnancy [(39.59 ± 9.15) μmol/L vs (58.02 ± 15.45) μmol/L t =-7.26,P ＜ 0.01)].For FGR group,a significant negative correlation was observed between ADMA and NO expressions in sera (r =-0.693,P ＜ 0.01).Conelusions ADMA was associated with the occurrence and development of the FGR,and its mechanism maybe inhibits NO synthesis to result in placental malperfusion.
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Objective To explore influence of hypertriglyceridemia on serum NO ET-1 and the grade of the pathology severity in rats with severe acute pancreatitis. Methods 36 SD rats were randomly divided into 2 groups, group A (HLSAP group) , group B (SAP group). Severe acute pancreatitis was constructed by retrograde injection of 5% na-taurocholate. Blood samples were taken from all subjects to measure triglyceride, ET-1 and NO, pancreatic tissue samples were taken from head of pancreas and stained with H. E. , the degree of pancreatic damage was observed according to the point score of Schmidt and Pozsar's methods. Results In group A, the concentration of ET-1 increased more obviously than that in group B at 4 hour and 8 hour period(P ＜0. 05). The concentration of NO declined both in group A and group B at 12 hours period,but it had a great decline in group A. Animals with hyperlipidemia and severe acute pancreatitis developed significantly higher(P ＜0. 05) ET-1 than the animals of the non-hyperlipamic severe acute pancreatit group in 4 hours and 8 hours period. NO declined in group A and group B at 12 hours period, group A have significantly higher(P ＜0. 05) decline than group B in NO. The histological degree of pancreatic damage were significantly higher in group A than that in the group B at all times. Conclusions Mircrocirculation disorder had existed disorder in the early of SAP. Hypertriglyceridemia could incrase ET-1 and NO earlier and higher in severe acute pancreatitis, and then decline in the late stage. Hypertriglyceridemia intensified the pathologichistological degree of pancreatic damage.
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Objective To investigate the long-term excessive drinking semen nitric oxide (NO) content in their sperm quality and spermatogenic cell apoptosis and infertility. Methods Nitrate reductase method was used to specific reduce the NO metabolites nitrate (NO3-) to nitrite (NO2-), which was used on behalf of the total NO level. Terminal deoxynucleotidyl transferase (TdT) and mediated nick end labeling (TUNEL) method and binocular optical microscope were used to detect and observe the rate of apoptosis of spermatogenic cells and the morphological structure. The SQA-V sperm quality automatic analyzer was used to measure sperm quality. Results In not drinking semen fertility group, NO content was (54.81±11.45)μmol / L, the rate of spermatogenic cell apoptosis was (4.52±1.23)%, sperm motility was (80.24±0.17)%, energy a+b (78.32±0.12)%, deformity rate (5.30±0.13)%, and long-term excessive alcohol infertility C group was [(128.83±22.73)μmol/L,(17.34±2.53)%,(51.18±0.58)%,(21.45±0.26)%,(21.12±3.24)%] respectively. Compared to a very significant difference (t＝10.04,17.38,6.69,15.59,17.02,P＜0.01) . In long-term excessive drinking group, the levels of NO and spermatogenesis cell apoptosis rate was significantly positive correlated (r＝0.93,P＜0.01).Apoptosis of spermatogenic cell nucleus chromatin was condensed in the formation of crescent-shaped perinuclear, nuclear was cleavaged to form apoptotic bodies. Conclusions In the long-term excessive drinking semen, NO content and spermatogenic cell apoptosis rate was increased, the sperm had poor quality. The results showed that the long-term excessive drinking can cause germ cell apoptosis in male infertility and promote the body to overproduce NO, whichmay be one of the reasons for male infertility.
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Objective To investigate the changing of endothelial progenitor cells and nitric oxide in patients with pulmonary arterial hypertension secondary to chronic obstructive pulmonary disease.Method Mononuclear cells from 20 healthy persons (the control group, n = 20) , COPD patients without PAH (COPD non-PAH group, n =30) and patients with PAH secondary to COPD (COPD and PAH group, n=30) were investigated. Total mononuclear cells were isolated from peripheral blood by Ficoll density gradient centrifugation. EPC number and migration were assayed by colony forming unit-EPCs (CFU-EPCs) assay and modified Boyden chamber assay , respectively. EPC adhesion assay was performed by replanting those on fibronectin-coated dishes , then adherent cells were counted. The concentration of NO was measured with method of nitrate reductase.Result The numbers of CFU and migration, adhesion activity of circulating EPCs in COPD[ (21.9±3. 9)CFU-EPC] and PAH group[ (14. 2 ±3. 5)CFU-EPC] were significantly lower than that in non-COPD group and COPD non-PAH group [ ( 24.9 ±4.1) CFU-EPC ]. It was also observed that a strong negative correlation between the levels of PAH and the numbers of CFU and adhesion, migration activity of circulating EPCs. The NO level in the PAH group [ (43. 6 ±4. 8)ng/ml] was significantly lower than that in control group [ ( 67. 17±4.9 ) ng/ml ] ( P < 0.01). The NO level was positively correlated with number and migration ability of EPCs( r =0. 77,0.71, P <0.01) , but not correlated with adhesion ability.Conclusion The number of CFU and migratory, adhesive activity of EPC in patients withPAH secondary to COPD was significantly decreased. These changes may be associated with low level of plasma NO.
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Objective To explore the effect of nitroglycerin on ET/NO, TXA2/PGI2 and pancreas pathomorphology changes in severe acute pancreatitis (SAP) rats. Methods Sixty SD rats were random divided into five groups, including control group (A group, n = 12) and experimental group(B,C,D and E group, n = 12). The SAP was induced by injection of 5% sodium taurocholate through retrograde common biliopancreatic ducts via duodenal papilla with epidural catheter. Group C, D and E were intravenously injected with nitroglycerin 0.5μg/kg/min,1μg/kg/min and 2μg/min in 30 min respectively, and group A and B was injected with Sodium Chloride 0.5ml. The indexes of changed pathomorphology and ET/NO, TXB2/6-keto-PGF1a, were determined at the 6th and 12th hour after operations, respectively. Results The specimen data of the 6th and 12th hour displayed that the indexes of changed pathomorphology, ET, ET/NO, TXB2, and TXB2/6-keto-PGF1a of the group C,D and E degraded respectively, compared to group B(P < 0.05). Conclusion The nitroglycerin could degrade ET, ET/NO,TXA2 and TXA2/PGI2, improve the microcirculation of pancreas, and delay the pathological inflammation change in SAP rats.