Objectives: Considering NITRIC OXIDE ((NO)) as one of important molecular regulators in genital organs, we examined its effects on histo-morphologic changes in the rat ovary.Methods: 40 rats were divided in 5 groups of 8 upon observing vaginal plaque that has been considered as day zero of pregnancy. Control group, (NO)rmal saline, L-NAME, L-Arginine and L-NAME + L-Arginine groups. Except the control group the remaining groups received (NO)rmal saline (2 ml / kg / ip), L-NAME (20 mg / kg / ip), LArginine (200 mg / kg / ip) and a mixture of the same doses of L NAME + L- Arginine, respectively on the 3rd, 4th and 5th days of pregnancy. On the 18th day of pregnancy the rats were anesthetized by diethyl ether and then paralyzed by cutting the spinal cord.After laparotomy the ovaries were fixed in 10% formalin and after tissue sample preparation, general (H + E) and specific (PAS) staining was performed. The histo-morphological changes were observed by optical microscopy and the necessary photographs were taken.Results: Degenerative changes and dissemination were observed in most parts of ovaries of L- Arginine group as well as reduction in growth and weight of the rats. Ovarian volume and number of corpus Luteum were also reduced in this group.Conclusion: It seems that (NO) induces inhibition of cell growth in the pregnancy period and can interfere with (NO)rmal functions of the ovary.

Background: Abdominal colic, constipation and delay in gastric emptying are symptoms of lead poisoning, but there is scant information about the effect of lead on gastric motility. In the present study, we investigated the effect of lead acetate on gastric motility in rats.Methods: Animals were divided into nine groups (n=8); four groups were exposed to lead acetate solution (1%) for 1, 2, 3, and 4 weeks (Pb1, Pb2, Pb3, and Pb4 groups, respectively). Sodium acetate solution was given to a(NO)ther four groups for 1, 2, 3, and 4 weeks (Na1, Na2, Na3, and Na4 groups, respectively) and the control group had free access to tap water. Gastric motility was measured in the basal and acetylcholine (Ach) -stimulated states using a physiograph instrument. NITRIC OXIDE metabolite of gastric tissue was determined by Griess micro-assay.Results: There were (NO) significant differences between basal and Ach-stimulated gastric motility in Pb1, Pb2, Na1, and Na2 groups. However, it was significantly greater in Pb3 and Pb4 groups when compared with Na3 and Na4 groups in both basal and Ach-stimulated states (P<0.05).In addition, NITRIC OXIDE metabolite of gastric tissue was more in all Pb groups in comparison with their Na counterparts (P<0.05).Conclusion: We found that lead exposure could affect gastric motility via the NITRIC OXIDE pathway.

Sub chronic exposure to lead in rats slows gastric emptying, but little is k(NO)wn about the effects of lead on gastric secretion. This study was designed to investigate the effects of lead on gastric acid secretion and its possible mechanisms in rats. Lead acetate was dissolved in drinking water in a concentration of 1%. Sodium acetate-containing water with a molar concentration similar to lead was also prepared. We had nine groups of animals (n=8), four of them were exposed to lead for 1, 2, 3, and 4 weeks (Pb1, Pb2, Pb3 and Pb4 groups, respectively). Sodium acetate solution was given to a(NO)ther four groups for 1, 2, 3, and 4 weeks (Na1, Na2, Na3 and Na4 groups, respectively). Gastric secretion was collected by washout technique and its acid output was measured in the basal (Basal Acid Output, BAO), vogotomy (Vagotomized Acid Output, VAO), and vagally stimulated (Vagally Stimulated Acid Output, VSAO) states using titrator instrument. NITRIC OXIDE ((NO)) metabolite of gastric tissue was determined by Griess micro assay method to evaluate the possible mechanism of lead effect on gastric secretion. VSAO was significantly less in Pb1 and Pb2 groups than Na1 and Na2 ones respectively (1.75 ± 0.17, 2.10 ± 0.30 vs.5.79 ± 0.20, 6.18 ± 0.27 mmol/15min) (P=0.001, P=0.001). BAO was significantly more in Pb3 and Pb4 groups than Na3 and Na4 ones respectively (2.77 ± 0.37, 2.80 ± 0.31 vs.1.73 ± 0.16, 1.79 ± 0.34 mmol/15min) (P=0.01, P=0.02), but it was the same after vagotomy. VSAO was more in Pb3 and Pb4 groups than their Na counterparts (P=0.001, P=0.0001). (NO) metabolite of gastric tissue was more in all Pb groups in comparison to their Na counterparts (P=0.0001). In this study, it seems that lead exposure, via (NO) mechanism, has different effects on acid secretion. NITRIC OXIDE in small and large amounts decrease and increase gastric acid secretion, respectively.

Background and objectives: The importance of NITRIC OXIDE ((NO)) and Asymmetric dimethyllargininie (ADMA) in pathophysiology of Sickle cell disease (SCD) is being increasingly clarified. Since very few of the studies have been conducted in the word and (NO) study has been carried out in Iran, especially in Khuzestan province where is the main center of Sickle Cell disorder (SCD) in Iran, We decided to conduct the present study.Material and Methods: EDTA anticoagulated plasma samples were obtained from 35 healthy controls (Hb AA), 35 heterozygous (HB AS) and 35 homozygous (HB SS) sickle cell anemia patients. Plasma concentration of (NO) was measured by Colorimetric and Griess reaction and the concentration of ADMA by employing ELISA method. Then the results were analyzed by tstudent test and OneWay A(NO)VA.Results: There is a positive significance correlation between Hemoglobin (Hb) and (NO) in SS (r=0.703) and AS (r=0.366) groups. Also, a negative correlation between Hb and ADMA in SS (r=-0.786) and AS (r=-0.478) groups is seen. (NO) correlation is found between these parameters in AA group.Conclusion: The prevention of Hb concentration decrease and prescription of (NO) do(NO)rs and (or) ADMA disintegrators can be helpful for improving clinical signs of sickle cell patients.

Backgrounds and Objectives: Mutations in endothelial NITRIC OXIDE synthase (e(NO)s) gene can reduced (NO) production. It is an endothelial relaxing factor and its decrease accelerates the process of atherosclerosis. This study was designed to measure serum level of (NO) and the frequency of T-786C polymorphism in a group of patients with Coronary Artery Disease (CAD) in comparision with control.Materials and Methods: Sixty patients with angiographically diag(NO)sed CAD and 60 age and sex matched CAD-free subjects were studied as control. NITRIC OXIDE was measured by Griess Method. The ge(NO)type studies were carried out using allel specific PCR.Results: Serum levels of (NO) in patient groups were significantly lower than the controls (P<0.05). Significantly higher frequency of e(NO)s -786C ge(NO)type was found in CAD patients than controls (P<0.05), the differences reflected an increase in CC ge(NO)type at position -786 of (NO) synthesis gene. Mean blood pressure was significantly higher in patient compared with controls (P<0.05).Conclusion: The low levels of (NO) and high blood pressure in patient group may be related to high frequency of T-786C polymorphism in patient group and conversely T-786C polymorphism may be a risk factor for coronary artery disease.

Introduction. NITRIC OXIDE ((NO)) is a neuromodulator and an intercellular messenger that mediate several functions in the CNS. Possible involvement of  (NO)  in anxiety like behavior induced by ovarian hormones was studied in ovarectomized female rats.Materials and Methods.12 groups of rats were ovarectomized bilateraly and 14 days after surgery they received estradiol benzoate (10µg/kg, sc) and or progesterone (25 mg/kg, sc) or corn oil (0.2 ml/rat, sc) and L-Name (60 mg/kg, i.p) or L-Aarginine (100 mg/kg, i.p) or (NO)rmal saline (0.5 ml/rat, i.p). The behavioral tests began 6 hours after progesterone  and  3 hours after estradiol administeration. Behavioural test consisted measurment of exploratory activities on elevated plus maze test.Results. There was increased exploration of open arms under progesterone administeration alone or with L-Name, and decreased under estradiol administeration alone or with L-Arginine. The anxiolytic-like effect of progesterone abolished when L-Arginine administerated, and anxiogenic-like effect of estradiol was inhibited  when L-Name injected.Conclusion. These data indicate involvement of (NO) in the mediation of the effects of ovarian steroid hormones on anxiety process.

Introduction: Sildenafil is a selective inhibitor of c-GMP specific phosphodiesterase type 5 (PDE5). It increases (NO) production of endothelial cells. There is (NO) available data on sildenafil effect on endometrial epithelial cells. The aim of present work is to investigate sildenafil effect on (NO) secretion by human endometrial epithelial cells in in-vitro culture.Materials and Methods: Endometrial biopsies (n=10) were washed in PBS and digested with Collagenase I (2 mg/ml in DMEM/F12 medium) at 37oC for 90 minute. Epithelial glands were collected by sequential filtration through nylon meshes (70 and 40 μm pores) respectively. Epithelial glands were treated by trypsin to obtain individual cells. The cells were counted and divided to four groups: control and different sildenafil dose (1, 10, and 20 mM). Cultures were done for 15 days at 37oC, 5% CO2 and media were changed every 3 days and their supernatant were collected for (NO) assy. (NO) were measured by standard Griess methods. Data were analyzed by one way A(NO)VA.Results: There is (NO) significant difference between groups in (NO) secretion, but it increased slightly in cases groups. Epithelial cell morphology changed into long spindle cells in cases groups.Conclusion: Sildenafil didn’t change (NO) secretion by human endometrial epithelial cells.