Effect of fluvastatin on left ventricular remodeling after myocardial infarction in rats

AIM: To clarify the protective effect of long-term administration of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor fluvastatin on ventricular remodeling after myocardial infarction (MI) in rats and its mechanisms. METHODS: Myocardial infarction were established by ligated left coronary anterior artery in SD rats, 24 hours after the operation, the survival rats were treated by gavage fluvastatin (20 mg·kg^-1·d^-1) or distilled water for 8 weeks. Doppler echocardiography, homodynamic and cardiac histomorphometry were used to assess the ventricular remodeling and cardiac function. The plasma levels of total cholesterol (Tch), creatinine (Cr), glutamic-oxal (o) acetic transaminase (AST), lipid peroxidation (LPO), glutathione perioxidase (GSH-PX), nitrogen monoxide (NO₂^-/NO₃^-) were detected. RESULTS: The Tch, Cr and AST were not significant difference in groups. Left ventricular end-diastole pressure, right relative weight, left ventricular posterior wall thickness, collagen volume fraction and the lung weight were decreased in AMI+fluvastatin group compared to AMI group (P＜0.05, P<0.01); The levels of LPO, NO₂^-+NO₃^- in plasma and LPO in myocardium decreased, but plasma GSH-PX level increased in AMI+fluvastatin group (P＜0.05). CONCLUSION: Fluvastatin ameliorates the ventricular structural remodeling in a rat model of infarction, and delays the development of heart failure. The anti-oxidation mechanism of fluvastatin may take part in this process.     

Inhibitory effect of fructose-1, 6-diphosphate on adriamycin-induced cardiomyocyte apoptosis in rats

AIM:To study the effect of fructose-1, 6-diphosphate (FDP) on adriamycin(ADM)-induced cardiomyocyte apoptosis in rats. METHODS:Twenty-four Wistar rats were randomly divided into three groups: control group, ADM treated group and FDP intervention group. The contents of malondialdehyde (MDA) and NO₂^-/NO₃^-, the activities of glutathione peroxidase (GPx) and superoxide dismutase (SOD) were determined by colorimetric method in myocardial tissue, and the cardiomyocyte apoptosis was detected by TUNEL method in myocardial tissue, and the expression of inducible nitric oxide synthase (iNOS) mRNA, Bcl-2 mRNA and Bax mRNA in myocardial tissue were detected by in situ hybridization. RESULTS:The contents of NO₂^-/NO₃^- and MDA in myocardial tissue, the expressive levels of iNOS mRNA and Bax mRNA in cardiomyocyes and its apoptotic amounts in FDP intervention group were significantly lower than those in ADM treated group (P＜0.01). However, the activities of SOD and GPx in myocardial tissue, the expressive level of Bcl-2 mRNA of cardiomyocytes in FDP intervention group were significantly higher than those in ADM treated group (P＜0.01). CONCLUSION:FDP antagonized the reduced expression of Bcl-2 mRNA and increased expression of Bax mRNA in myocardial tissue induced by ADM, and in turn inhibited ADM-induced cardiomyocyte apoptosis.     

The inhibition of nitric oxide synthase for long time up-regulates vascular angiotensin Ⅱ receptor

AIM:To observe the effects of aortal angiotensin Ⅱ(AngⅡ)levels and AngⅡ receptor in the hypertensive rat models. METHODS: Intraperinoneal injection of L-N^ω-nitro-arginine(L-NNA) into rats induced hypertensive model, the binding of aortal AngⅡ receptor and the contents of aortal tissue AngⅡ and plasma NO₂^-+NO₃^-(NOx) were determined.RESULTS:Compared with the control group, the blood pressure of the rats treated with L-NNA was significantly increased by 142%(P＜0.01),the plasma NOx levels were decreased by 48%. However, in the rats treated for 4 weeks the ratio of cardial index was increased by 128%(P＜0.01),the plasma AngⅡ levels weren't significantly changed, the contents of vascular tissue AngⅡ were increased by 612%(P＜0.01) and the Bmax of [¹²⁵I]-AngⅡ was increased by six times (P＜0.01),the affinity was doubled respectively.CONCLUSIONS:Nitric oxide synthase (NOS) inhibition mostly influes the reninangiotensin system in regional tissue. The inhibition for long time up-regulates vascular AngⅡ and AngⅡ receptor, which can support the hypothesis "NOS inhibition can induce AngⅡ-depended hypertension".     

The kinetic alteration of nitric oxide formation in the lungs in the development of pulmonary fibrosis of rats

AIM: To observe the kinetic alteration of nitric oxide formation in the lungs in the development of pulmonary fibrosis in the rat. METHODS: The contents of hydroxyproline in the lungs, NO₂^-/NO₃^- (nitrite/nitrate) in out-flowing and in-flowing pulmonary blood (OPB, IPB) were assayed on the day 7, 14, 21, 30 and 70 after intratracheal administration of bleomycin A₅ . The content of NO₂^-/NO₃^- in supernatants of culture of the alveolar macrophages (AMs) and the amount of iNOS positive stain cells in lung tissue section were also observed in the rat on 14th day after-bleomycin A₅ administration. RESULTS: The content of lung hydroxyproline had no change on the 7th day, increased on the 14th day (P＜0.05), increased significantly on the 21th day, 30th day and 70th day post-bleomycin A₅ compared with control rats. On the 7th day and 14th day, the content of NO^- ₂ /NO₃^- increased in OPB and decreased in IPB (P＜0.01). On the 21th day, the content of NO₂^-/NO₃^- abated in OPB (P＞0.05) but still decreased in IPB (P＜0.01). On the 30th day and the 70th day, the NO₂^-/NO₃^- level recovered both in OPB and IPB. AMs from rats on the 14th day post-bleomycin A₅ showed significant elevation (P＜0.01) in NO₂^-/NO₃^- level. The amount of iNOS positive stain cells increased in rats on the 14th day post-bleomycin A₅. CONCLUSION: The amount of NO in the lungs was high in the initial phase of fibroproliferative reaction induced by bleomycin A₅ ,and these might be associated with the enhanced ability of AMs to release NO and the increased amount of iNOS.     

Effect of Xin-Tong capsule on nitric oxide production and cGMP content of ventricular myocardium in rats with experimental myocardial ischemia

AIM:To study the effect of xin-tong capsule on nitric oxide production and cGMP content of ventricular myocardium in rats with experimental myocardial ischemia. METHODS:Rat model of acute myocardial ischemia induced by pituitrin was used in this study, and the lift of ST segment in ECG was used as the index of myocardial ischemia. The NO₂^-/NO₃^- and cGMP contents of ventricular myocardium in rats with myocardial ischemia were determined.RESULTS: NO₂^-/NO₃^- and cGMP contents in ventricular myocardium of myocardial ischemia were (486±59) nmol/g protein and (0.38±0.08) nmol/g protein, respectively, and markedly lower than those of control (P＜0.01). After administration of Xin-Tong capsule, contents of NO₂^-/NO₃^- and cGMP in ventricular myocardium of rats with myocardial ischemia were obviously elevated . In comparison with control, ST segment of ECG in rats with myocardial ischemia was lifted, and the lift peak of ST segment occur in 45 min after myocardial ischemia (P＜0.01). Pretreatment of Xin-Tong capsule can improve conditions of myocardial ischemia . CONCLUSION:Xin-Tong capsule can elevate the contents of nitric oxide and cGMP, and attenuate myocardial ischemia injury in rats.     

Changes of nitric oxide synthase and nitric oxide in lung of smoking rats

AIM:To observe the changes of iNOS and eNOS in lung tissue and NO in bronchoalveolar lavage fluid (BALF) in smoking rats.METHODS:80 Wistar rats were divided into control, smoking group, L-NIL group and L-NAME group (rats were exposed to smoke and injected (i.p.) with selective iNOS inhibitor L-NIL or NOS inhibitor L-NAME). iNOS and eNOS protein levels in whole lung were detected by immunohistochemical staining, and NOS mRNA was quantified using RT-PCR. In addition, NO₂^-/NO₃^- was determined using Griess assay.RESULTS:The expression of iNOS mRNA and protein in smoking rats increased, the expression of eNOS mRNA and eNOS protein decreased, and the total cell count and the level of NO₂^-/NO₃^-in BALF increased(P＜0.05). In vivo, L-NIL reduced the total cell count and NO₂^-/NO₃^- in BALF (P＜0.05), while L-NAME had no effect on them.CONCLUSION:Cigarette smoke increased expression of iNOS mRNA and protein and decreased expression of eNOS mRNA and protein. The large amount of NO generated by iNOS may amplify inflammation in lung tissue.     

Effect of ligustrazine on pulmonary arterial pressure and pulmonary arterial wall collagen of chronic hypoxic hypercapnic rats

AIM:To study the effect of ligustrazine on pulmonary hypertensive rats induced by hypoxic hypercapnia. METHODS:Thirty rats were randomly divided into three groups:control group(A),hypoxic hypercapnic group(B), hypoxic hypercapnia+ligustrazine(lig.) group(C). RESULTS: (1) Mean pulmonary arterial pressure(mPAP)of group B was significantly higher than that of group A and mPAP of group C was significantly lower than that of group B(P＜0.01),differences of mean carotid pressure(mCAP) were not significant among three groups (P＞0.05); (2)Electron microscopy and immunohistochemistry showed ligustrazine could inhibit the diposition of collagenous fiber(collagen typeⅠ)in pulmonary arterioles induced by hypoxic hypercapnia; (3) Plasma endothelin level of group C was significantly lower than that of group B (P＜0.01), serum (NO ₂^-/NO₃^-) of group C was significantly higher than that of group B (P＜0.01). CONCLUSION:Ligustrazine can inhibit pulmonary hypertension and the diposition of collagen type Ⅰ in pulmonary arterial wall induced by hypoxic hypercapnia.     

Changes in endogenous nitric oxide and effects of inhaled nitric oxide on pulmonary artery hypertension in chronically hypoxic rats

AIM: To investigate the role of nitric oxide (NO)in the development of chronically hypoxic pulmonary artery hypertension (PAH) and the hemodynamic effects of inhaled NO on pulmonary circulation. METHODS: 67 male adult SD rats were randomly divided into 7 groups: (1) control (n=9);(2) chronically intermitent hypoxia (CIH, 6 h/d, 7 d/w) 1 week(n=7); (3) CIH 2 weeks (n=11); (4) CIH 3 weeks (n=11); (5) CIH 1 week+L-NAME (NO synthase inhibitor, 30 mg/kg, by gavage, n=10); (6)CIH 3 weeks+L-Arg (NO precursor, 10 mg/kg, by gavage, n=9); (7) CIH 3 weeks+inhaled NO (0.0004% for 20 min, n=10) to determine the mean pulmonary artery pressure (MPAP), weigh the right ventricle (R) and ventricular segment plus left ventricle (S+L), and calculate R/(S+L) (g/g) and R/Wt (Wt: body weight, g/kg). RESULTS: 1.MPAP increased compared with control when CIH 1 week, reaching the highest when CIH 2 weeks; R/(S+L) and R/Wt also increased notably when CIH 1 week (P＜0.01); 2. The level of plasma NO₂^-/NO₃^- elevated significantly when CIH 2 weeks, but fell when CIH 3 weeks; the content of plasma ET-1(endothelin-1) also increased significantly. The level of plasma ET-1 correlated with R/(S+L) and R/Wt, r=0.43 and 0.46, respectively, both P＜0.01; 3. The level of plasma NO₂^-/NO₃^- droped 33.2 % (P＜0.01) after treatment with L-NAME, with R/(S+L) increasing 15.2 % (P＜0.05); 4. L-Arg decreased the MPAP 17.8 %(P＜0.01). CONCLUSION: The endogenous NO release increases at early stage (1-2 weeks) of chronic hypoxia, but falls at the prolonged stage; the elevated level of plasma ET-1 possibly plays an important role in remodeling of chronically hypoxic pulmonary vessels and ventricle; inhaled NO significantly decreases the chronically hypoxic PAH.     

Effects of nitric oxide on mitochondrial damage caused by exogenous calcium

AIM: To study the effects of nitric oxide (NO) on mitochondrial damage caused by exogenous calcium. METHODS: Normal myocardial mitochondria were divided into three groups; L-arginine control group (CG), Ca^2＋-damaged group (DG) and L-NAME-preserved group (PG). Mitochondria of all groups were incubated at 30 ℃ with reaction medium containing 20 μmol/L EDTA, 100 μmol/L CaCl₂ and 1 μmol/L L-NAME with 100 μmol/L CaCl₂ respectively. Then the NO₂^-/NO₃^- contents, mitochondrial viability and membrane potential were investigated. RESULTS: The NO₂^-/NO₃^- contents of DG was obviously higher than that of CG and PG, meanwhile, there was no obvious difference between CG and PG. Mitochondrial viability and membrane potential of DG were significantly lower than that of CG and PG, and negatively related to NO^-₂/NO^-₃ contents (r=-0.5297, P＜0.01; r=-0.6041, P＜0.01). But, the mitochondrial viability and membrane potential of PG were still lower than that of CG. CONCLUSION: Exogenous calcium could activate mitochondrial nitric oxide synthase resulting in NO production and the latter play an important role in decreasing mitochondrial viability and membrane potential.     

Changes in L-arginine/nitric oxide pathway of the aorta in septic shock rats

AIM:To observe the change of nitric oxide (NO) generation system in the vascular adventitia, media and intima in septic shock rats.METHODS:The septic shock model was made in rats by caecal ligation and puncture. The intima, media and adventitia of the rat aorta were separated. NO production (NO₂^-), nitric oxide synthase(NOS) activity and L-arginine (L-Arg) transport were measured, separately. Inducible NOS (iNOS) distribution was detected by immunohistochemistry.RESULTS:Both in early and late stage of septic shock, NO₂^- from the intima was decreased by 66.1% and 78.9%(P<0.01), while NO₂^- from the media was increased by 1.1 and 2.2 folds(P＜0.01), and the adventitia 9.6 and 18.6-fold (P＜0.01), as compared with the sham group, respectively. The changes of NOS activity and the L-arginine transport in the intima, the media layer and the adventitia of the aorta in the septic shock rat paralleled with that of NO₂^- in these tissues. The results of iNOS immunohistochemistry showed that there were obviously positive staining in the media layer and adventitia, especially the adventitia of the rat aortas in septic shock, as compared with that in the sham control.CONCLUSIONS:During septic shock, NO production in the aortic intima was progressively suppressed. However, it was progressively increased in the aortic medial layer and adventitia, especially the adventitia with shock processes. These changes result from different changes of L-arginine transport, NOS activity and its expression in three layers of the aorta from the septic shock rat.     

Mechanisms of nitric oxide synthesis induced by human complement C5b-9complex in glomerular mesangial cells of rats

AIM: To explore the mechanism of the nitric oxide (NO) synthesis induced by human C5b-9 complex in glomerular mesangial cells(MC) of rats. METHODS: The MC of rats were cultured and stimulated with human complement C5b-9 complex to induce TNFα and IL-1β. At the same time, several parameters related to NO synthesis were measured at 3 h, 6 h and 24 h after C5b-9 stimulation. The effects of monoclonal antibodies against TNFα and IL-1β on NO synthesis were examined in this system. RESULTS: TNFα concentration in supernatant from MC in C5b-9 group was higher than that of control group at 6, 24 h after stimulation with C5b-9 complex and reversed by adding anti-TNFα McAb. C5b-9 complex didn't stimulate the release of IL-1β in same system. In addition, the expression of iNOS mRNA in MC was observed at 3 h after stimulation with C5b-9. Levels of iNOS mRNA expression and cGMP in MC and NO₃^-/NO₂^- in supernatant from MC in C5b-9 group were higher than those in control group at 6, 24 h after C5b-9 stimulation, these changes were also reversed by adding monoclonal antibody against TNFα. CONCLUSION: C5b-9 complex could induce iNOS mRNA expression at 3 h after C5b-9 stimulation, and the synthesis of NO at 6, 24 h was related to TNFα released from cultured MC of rats by C5b-9 complex to a certain extent.     

Effects of testosterone on endothelial function and intimal proliferation after balloon injury in male rabbit abdominal aorta

AIM: To investigate the effects of testosterone on endothelial function and intimal proliferation after balloon injury in male rabbit abdominal aorta. METHODS: 24 male New Zealand white rabbits were divided randomly into three groups: control group (n=8, sham castration), hypotestosteronemia group (n=8,castration) and testosterone replacement group (n=8,castration +testosterone undecanoate intramuscular injection,14mg/kg). Abdominal aorta was injured with 3 mm PTCA balloon after testosterone undecanoate had been injected for three days. Two weeks later, blood samples were obtained for detection of plasma testosterone, lipids, metabolic product of nitric oxide (NO₂^-／NO₃^-), superoxide dismutase(SOD) and malondialdehyde (MDA),and all the abdominal aorta were excised to be analyzed by computer. RESULTS: The intimal area of hypotestosteronemia group were significantly larger than that of other two groups(P＜0.01). plasma NO₂^-／NO₃^- and SOD levels were significantly decreased, while the total cholesterol(TC),triglycerides(TG), low density lipoprotein(LDL) and plasma MDA were significantly increased. No difference was observed between control group and testosterone replacement group in all parameters. CONCLUSION: Testosterone, at physiological level,had the effects of inhibiting the intimal proliferation and of protecting the endothelial function after balloon injury in male rabbit abdominal aorta.     

Protective effects of multi-enzyme Ⅱ on vascular endothelial cell injury induced by hyperlipidemia serum

AIM and METHODS: The protective effects of multi-enzyme Ⅱ was studied on cultured endothelial cells which was injuried by hyperlipidemia serum. RESULTS: Hyperlipidemia serum increased ICAM-1 expression on the surface of endothelial cells, and decreased NO₂^- release significantly (P＜0.01). ICAM-1 expression could be reduced and NO₂^- release could be enhanced markedly by multi-enzyme Ⅱ (P＜0.01). CONCLUSION: Multi-enzyme Ⅱ had an obvious protective effect on vascular endothelial cells which was injuried by hyperlipidemia seurm. Multi-enzyme Ⅱ could clean out oxide free radicals effectively because it had the acitive structure of both SOD and CAT.     

Phenytoin inhibited changes in nitric oxide of rat hippocampus induced by stress

AIM: To investigate the changes in nNOS and iNOS expression of hippocampal CA3 pyramidal neurons and NO₂^-/NO₃^- level of hippocampal homogenate of rats induced by stress, and to explore the effect of phenytoin on them. METHODS: Rats were subjected to forced-swimming stress, phenytoin was administered(ip) at 30 min before stress. Using the immunohistochemistry and the computerized image technique, the expression levels of nNOS and iNOS of rat hippocampal CA3 pyramidal neurons were assayed quantitatively, and the NO₂^-/NO₃^- level of hippocampal homogenate was also measured using nitric acid deoxidize enzyme method. RESULTS: The nNOS average grey degree of hippocampal CA3 pyramidal neurons was significantly lower in stress group (155.42±3.77)than that in control group(164.54±4.62)and in stress plus phenytoin group(164.27±2.55)(P<0.01); The iNOS relative sectional area proportion of hippocampal CA3 pyramidal neuron was significantly larger in stress group(5.87%±2.90%) than that in control group (0.90％±0.89%) and in strers plus phenytoin groups (0.90%±0.88%)(P<0.01); The NO₂^-/NO₃^- level of hippocampal homogenate was significantly higher in stress group(42.75 umol/L±14.49 umol/L)than that in control group(21.23 umol/L±6.99 umol/L)and in stress plus phenytoin group(18.40 umol/L±8.11 umol/L)(P<0.01). CONCLUSION: It is suggested that the stress could induce nNOS and iNOS expression in CA3 pyramidal neurons and excessive production of NO in hippocampus of rats, which could be inhibited by phenytoin.     

The renal L-arginine/nitric oxide pathway and erythrocyte L-arginine transport in spontaneously hypertensive rats

AIM: To investigate the changes of the renal L-arginine /nitric oxide pathway and the relationship of L-arginine transport between kidney and erythrocytes in spontaneously hypertensive rat (SHR). METHODS: Sixteen week old SHR, 16 week old SHR with captopril (CAP) treated for four weeks and 16 week old WKY rats were used in the experiment. L-arginine transport, NO synthase(NOS) activity, nitrite and cyclic GMP (cGMP) content were measured in renal tissue or erythrocytes. RESULTS: In the renal tissue, compared with that of WKY group, the Vmax of high-or low-affinity L-arginine transporter, NOS activity, NO₂^- and cGMP content of SHR group were significantly decreased (P＜0.01 or P＜0.05). The Vmax of high-affinity L-arginine transporter and NOS activity of CAP group were significantly enhanced as compared with SHR group (+90%, P＜0.01; +58.6%, P＜0.05). The NOS activity had significant positive correlation with the Vmax of high-affinity L-arginine transporter (r=0.585, P＜0.05). The changes of erythrocyte L-arginine transport were the same as that of kidney. The Vmax of SHR group was lower than that of WKY group (-30%, P＜0.01), and the Vmax of CAP group was higher than that of SHR group (+26.5%, P＜0.01). Km was not significantly changed. There is a positive correlation between the Vmax of L-arginine transport in erythrocyte and the Vmax of high- or low-affinity L-arginine transporter in renal tissue, (r=0.8434, P＜0.01, high-affinity; r=0.5255, P＜0.05, low-affinity). CONCLUSION: There existed a functional inhibition in L-arginine/nitric oxide pathway in the kidney of SHR. It can be recovered obviously by captopril treatment. The changes of L-arginine transport in kidney coincide with that in erythrocyte.     

Detection of serum MDA,NO and INOS in patients with SARS andits clinical significance

AIM: To observe free radicals (MDA, NO) and iNOS of patients with severe acute respiratory syndrome (SARS) and to explore its significance. METHODS: MDA, NO₂^-/NO₃^- and iNOS were determined in SARS patients during the early, recovery and follow-up stage, front doctors and nurses (contact group) and health people (health control). RESULTS: The level of MDA during first stage was higher than that of recovery stage and the MDA level of recovery stage was higher than that of follow-up stage, contact group, and health control group (P<0.01). The content of NO₂^-/NO₃^- during early stage was higher than that of other groups, and the NO₂^-/NO₃^- contents of recovery stage, follow-up stage were higher than that of contact group and health control group (P<0.01), respectively. The mean of iNOS during early stage was highest than that of other stages (P<0.01) and the mean of recovery stage was higher than that of contact group (P<0.05), there were no difference in iNOS activity among any other groups (P>0.05). CONCLUSION: The pathological injury in pathogenesis of SARS is related to free radicals.     

The effect of glucocorticoid receptor on level of inflammatory media in rats after critical scald

AIM:To further elaborate the effect of glucocorticoid receptor(GR) decrease on level of inflammatory media in rats after critical scald.METHOD:The changes of phospholipase A₂(PLA₂) activity and concentrations of tumor necrosis factoralpha (TNFα) and malondialdehyde (MDA), the product of lipid peroxidation metabolism in plasma and tissue homogenate have been studied in scalded rats with or without GR blockade by RU38486.RESULTS:The PLA₂ activity and the concentrations of TNFα and MDA in plasma and homogenate of pulmonary and renal tissue in scalded rats were significantly higher than those in the controls(P＜0.01) and further increased in scalded rats accompanied with GR blockade (P＜0.01 or P＜0.05).CONCLUSION: Blockade of GR might aggravate the increase of inflammatory mediator caused by scalding. It suggested that GR might potentiate anti-inflammation in scald.     

Effects of nitric oxide on hepatic encephalopathy in cirrhotic rats induced by LPS

AIM: To investigate the effects of nitric oxide (NO) on hepatic encephalopathy in cirrhotic rats induced by LPS. METHODS: The cirrhotic model of rats was established by complex pathogeny. Since the end of the 8 th week, the rats were intragastrically-infused with 0.9% salt, L-arginine(L-arg) and LNNA respectively for 2 weeks.The hepatic encephalopathy in cirrhotic rats were induced by 3 mg/kg LPS (ip) 4 hours before the rats were sacrificed. RESULTS: The normal behaviors and electroencephalograph were appeared in L-arg group. LNNA group showed hepatic encephalopathy. The content of NO₂^-/NO₃^- of brain tissue was markedly higher in L-arg group than LNNA group(P<0.05), but the content of histamine in brain tissue was lower in L-arg group than LNNA group(P<0.05). There was a negative correlation between the content of histamine in brain tissue and the content of NO₂^-/NO₃^- of brain tissue. CONCLUSION: NO can prevent hepatic encephalopathy in cirrhotic rats induced by LPS.     

Relationship between levels of IL-2, TNF-α and nitric oxide in aqueous humor after intraocular lens implantation

AIM: To investigate the relationship between the level of interleukin-2 (IL-2), tumour necrosis factor-α (TNF-α) and nitric oxide (NO) in aqueous humor after intraocular lens implantation. METHODS: New Zealand rabbits were divided randomly into three groups: (1) control group; (2) extracapsular cataract extraction group (ECCE); (3) extracapsular cataract extraction and posterior chamber intraocular lens implantation group (ECCE+IOL). The inflammation in all experimental rabbit eyes was observed via zoom-photo slit-lamp microscope on 1, 3, 7, 14 d and 30 d postoperation. Meanwhile, aqueous humor was drawn for white blood cell (WBC) counting and classifying and for determining IL-2, TNF-α and NO₂^-/NO₃^- contents. RESULTS: (1) The level of IL-2 and TNF-α and NO₂^-/ NO₃^- in aqueous humor of ECCE+IOL group were higher than that in ECCE and control at 1 to 14 days postoperation, respectively, it increased to peak value at 3 to 7 days postoperation and decreased gradually two weeks postoperation; (2) The changes in IL-2, TNF-α and NO₂^-/NO₃^- in each group were basically similer; (3) The changes of IL-2 and TNF-α level were closely related with NO content in aqueous humor (r=0.69, P<0.01 and r=0.98, P<0.01). CONCLUSION: IL-2, TNF-α and NO play an important role in intraocular inflammation intraocular lens implantation.     

Role of endogenous nitric oxide in apoptosis of alveolar epithelial cells in the development of pulmonary fibrosis in rats

AIM: To study the role of high level of endogenous nitric oxide (NO) in apoptosis of alveolar epithelial cells in the development of pulmonary fibrosis in rats. METHODS: The content of nitrite/nitrate (NO₂^-/NO₃^-) in out-flowing pulmonary blood (OPB) was assayed by nitric acid reduction method. The apoptosis of alveolar epithelial cells was observed by TdT-mediated dUTP nick-end labeling (TUNEL) and electron microscopy, respectively. The above indices were observed on the day 14 and the day 30 after intratracheal administration of BLMA₅ alone or along with blockade of iNOS by aminoguanidine (AG) in rats. RESULTS: (1) Both the content of NO₂^-/NO₃^- in OPB and the number of apoptotic alveolar epithelial cells in lung were increased in BLMA₅ 14 d group, compared with normal control group and BLMA₅ 30 d group, respectively (P<0.05). The high level of NO₂^-/NO₃^- in OPB and the apoptosis of alveolar epithelial cells were ameliorated by AG. CONCLUSION: The apoptosis of alveolar epithelial cell is induced by high level of endogenous NO in the development of pulmonary fibrosis.