Effect of L-NAME on pulmonary arterial pressure,plasma nitric oxide and pulmonary hypertension syndrome morbidity in broilers

1. Experiments were conducted to evaluate the effect of a synthetic inhibitor of nitric oxide (NO) synthase (L-NAME) on pulmonary arterial pressure (PAP) and pulmonary hypertension syndrome (PHS) morbidity in broilers. 2. In Experiment 1, broilers were infused intravenously with L-NAME, and the mean pulmonary arterial pressure (mean PAP) and plasma NO were measured at 0, 1, 2 and 4 h after the start of infusion. The mean PAP increased and plasma NO was reduced at 1 to 2 h in broilers treated with L-NAME. 3. In Experiment 2, 180 Arbor Acres broilers were evenly divided into three groups: a control group (group C), and two groups exposed to low environmental temperatures and fed a 3, 3, 5-triiodothyronine (T3) supplemented diet alone (group A) or also including 100 ppm L-NAME (group B). 4. The PHS morbidity of group A was higher than for group C but lower than for group B. Plasma endothelin-1 was higher in broilers in groups A and B than in group C. Plasma NO was not significantly lower in broilers of group B when compared with those in group A. 5. The right/total ventricular weight ratio (RV/TV) and mean PAP were higher in groups A and B than in group C, and the RV/TV ratio increased one week earlier in group B than in group A. 6. These results suggest that L-NAME increases broiler PAP by inhibiting the endogenous synthesis of NO, leading to pulmonary hypertension, right ventricular hypertrophy and the increased morbidity of PHS in broilers.     

N-carbamylglutamate restores nitric oxide synthesis and attenuates high altitudeinduced pulmonary hypertension in Holstein heifers ascended to high altitude

Background: High-altitude pulmonary hypertension(HAPH) is a life-threating condition for animals in high altitude,and disturbance of endothelial nitric oxide(NO) synthesis contributes to its pathogenesis. N-carbamylglutamate(NCG), which enhances arginine synthesis, promotes endogenous synthesis of NO. In this study, we determined the effects of NCG on alleviating HAPH in Holstein heifers that ascended to Tibet(Lhasa, 3,658 m).Methods: Exp. 1, 2,000 Holstein heifers were transported from low elevation(1,027 m) to Lhasa. After being exposed to hypoxia for 1 yr, Holstein heifers were assigned to a healthy group(Control, n = 6) with mean pulmonary hypertension(mPAP) 41 mmHg, and an HAPH affected group(HAPH, n = 6) with mPAP 49 mmHg.Lung tissues were collected to evaluate histopathological changes and the expression of endothelial nitric oxide synthase(eNOS). Exp. 2, ten healthy heifers and 10 HAPH affected heifers were supplemented with NCG(20 g/d per heifer) for 4 wk. Physiological parameters were determined and blood samples were collected on d-1 and d 28 of the feeding trial.Results: Expression of e NOS in small pulmonary arteriole intima was higher in the healthy than HAPH group(P = 0.006), whereas HAPH group had significantly thicker media and adventitia than healthy group(all P 0.05). The mRNA of eNOS and protein level of eNOS were higher in the lungs of heifers in the healthy group than in the HAPH group(both P 0.001), whereas endothelin-1 protein levels were higher in HAPH group than in the healthy group(P = 0.025). NCG supplementation decreased mPAP and ammonia(both P = 0.001), whereas it increased the expression of eNOS, arginine, and plasma NO(all P 0.05).Conclusions: The expression of eNOS was decreased in Holstein heifers with HAPH. NCG supplementation decreased m PAP through the restoration of eNOS and endogenous NO synthesis.     

Evaluation of six-lead electrocardiograms obtained from dogs in a sitting position or sternal recumbency

OBJECTIVE: To compare 6-lead ECG traces in clinically normal conscious dogs in a sitting position and sternal recumbency to that of right lateral recumbency. ANIMALS: 31 healthy dogs with no history of cardiac disease. PROCEDURE: Six-lead ECGs were recorded for dogs in right lateral recumbency, a sitting position, and sternal recumbency. Q-, R-, and S-wave amplitudes as well as QRS-complex duration were measured in all leads. Additionally, P-wave amplitude and duration, PR interval, ST-segment elevation or depression, and OT interval were measured in lead II. RESULTS: Compared with measurements in right lateral recumbency, the sitting position resulted in increased Q-wave amplitude (lead III), increased R-wave amplitude (leads I and aVL), decreased R-wave amplitude (leads III and aVF), increased S-wave amplitude (lead aVR), decreased S-wave amplitude (lead aVL), increased P-wave amplitude (lead II), and a leftward shift in the mean electrical axis. Compared with measurements in right lateral recumbency, sternal recumbency resulted in decreased Q-wave amplitude (leads I, II, and aVF), increased R-wave amplitude (leads 11, III, and aVF), decreased R-wave amplitude (lead aVR), increased S-wave amplitude (lead aVR), increased P-wave amplitude (lead II), and decreased ST-segment depression (lead II). Compared with right lateral recumbency, the sitting position or sternal recumbency did not result in significant differences in PR interval, QT interval, or QRS-complex duration. CONCLUSIONS AND CLINICAL RELEVANCE: Significant changes are found in ECG measurements in the sitting position and sternal recumbency, compared with right lateral recumbency. In dogs, many ECG reference range values for right lateral recumbency are not valid for ECGs obtained in the sitting position or sternal recumbency.     

The influence of nitric oxide on the contractile activity of the isolated porcine ovarian and uterine arteries

The aim of the present study was to investigate the influence of nitric oxide (NO) on the contractile activity of the isolated porcine ovarian and uterine arteries. Segments of the vessels, obtained from the pigs on days 1-5, 8-13 and 17-20 of the oestrous cycle, were mounted in the organ bath with Krebs-Ringer solution and contractile activity changes of the vessels were measured using isometric transducers. In Experiment I the arteries pretreated with norepinephrine (NE; 10(-7) M) were treated with sodium nitroprusside (SNP, 10(-8)-10(-4) M), a NO donor. In Experiment II administration of NE (10(-7) M) was preceded by treatment with Nomega-nitro-L-arginine methyl ester (L-NAME, 10(-8)-10(-6) M), an inhibitor of NO synthase. Donor of NO at doses of 10(-8)-10(-7) M did not affect (P>0.05) the contractility, while at doses of 10(-5)-10(-4) M caused a dose-dependent relaxation (P<0.05) of both ovarian and uterine arteries in all periods examined. Moreover, SNP at doses of 10(-6)-10(-4) M it caused significantly higher (P<0.05) relaxation of the ovarian arteries collected on days 8-13 as compared to the vessels from days 1-5 of the cycle. Pretreatment of the vessels with L-NAME caused a dose-dependent, significant (P<0.05) increase in the vasocontractile action of NE in both the ovarian and uterine arteries as compared to contractile activity of NE administered alone. Moreover, L-NAME pretreatment at a dose of 10(-6) M caused significantly higher (P<0.05) intensification of NE action in ovarian and uterine arteries collected on days 8-13 as compared to the vessels from days 1-5 (P<0.05) and 17-20 (P<0.05) of the oestrous cycle. Obtained results indicate that NO plays an important role in the regulation of the contractile activity of the isolated porcine ovarian and uterine arteries. Our data suggest that this action may be, at least in a part, dependent on the hormonal status of the organism.     

Effect of body position on the 6-lead ECG of dogs

ECGs recorded from dogs show characteristic morphology and changes in morphology with various disease states. These changes are determined by comparing individual recordings to reference ranges established from recordings obtained from normal dogs in right lateral (RL) recumbency. Using these reference ranges for ECGs recorded from dogs in other positions may not be valid. We compared ECG complexes from 39 normal dogs obtained in RL, left lateral (LL), and standing (ST) body positions. ECGs from dogs in ST position showed increased Q-wave and R-wave amplitudes in leads I and II, increased R-wave and S-wave amplitudes in leads aVR and aVL, and decreased R-wave and S-wave amplitudes in lead III when compared with recordings obtained in RL position. ECGs from dogs in LL position showed increased R-wave amplitude in leads II, III, and aVF and S-wave amplitude in lead aVL but decreased R-wave amplitude in lead aVR when compared with recordings obtained in RL position. The mean electrical axis (MEA) shifted to the left in ST position but remained within the normal range in LL position. We determined that both a change in the relative position of the recording electrodes with respect to the heart as well as a change in intrathoracic cardiac position contributed to these changes. P-wave amplitude, P-R and S-T intervals, and QRS complex durations remained unaltered by changes in body position. Our findings indicate that ECGs of dogs recorded in RL, LL, and ST positions yield dramatically different results, and investigators should use position-specific reference ranges to minimize potential misinterpretation of ECG results.     

Effects of nitric oxide donor and nitric oxide synthase inhibitor on ruminal contractions in conscious sheep

The present study was planned to evaluate a role of nitric oxide (NO) in the regulation of regular ruminal contractions in conscious sheep. Intravenous infusion of S-nitroso-acetyl-DL-penicillamine (SNAP) at doses of 3-30 nmol kg(-1) min(-1)for 30 minutes inhibited both the amplitude and frequency of ruminal contractions in a dose-dependent manner. However, intravenous infusion of Nomega-nitro-L-arginine-methyl ester (L-NAME) at doses of 0.3-3.0 micromol kg(-1) min(-1)did not alter the basal tone of intraruminal pressure and the amplitude of ruminal contractions. The frequency of contractions was slightly inhibited by L-NAME infusion at 1.0 micromol kg(-1)min(-1). The effects of L-NAME were abolished by simultaneous infusion of L -arginine at 30 micromol kg(-1) min(-1). These results suggest that exogenous NO can diminish the ruminal contractions, while endogenous NO is not involved in the regulatory mechanism of basal tone and regular phasic contractions of the rumen in healthy sheep.     

Influence of nitric oxide on in vitro growth, survival, steroidogenesis, and apoptosis of follicle stimulating hormone stimulated buffalo (Bubalus bubalis) preantral follicles

Effect of sodium nitroprusside (SNP), a nitric oxide (NO) donor, on in vitro survival, growth, steroidogenesis, and apoptosis of buffalo preantral follicles (PFs) was investigated. PFs (200~250 µm) were isolated by micro-dissection and cultured in 0 (control), 10^-3, 10^-5, 10^-7, and 10^-9 M SNP. To examine the reversible effect of SNP, PFs were cultured with 10^-5 M SNP + 1 mM N^ω-nitro-L-arginine methyl ester (L-NAME) or 1.0 µg hemoglobin (Hb). The results showed that greater concentrations of SNP (10^-3, 10^-5, 10^-7 M) inhibited (p < 0.05) FSH-induced survival, growth, antrum formation, estradiol production, and oocyte apoptosis in a dose-dependent manner. However, a lower dose of SNP (10^-9 M) significantly stimulated (p < 0.05) the survival, growth, antrum formation, follicular oocyte maturation, and stimulated progesterone secretion compared to the control. A combination of SNP + L-NAME promoted the inhibitor effect of SNP while a SNP + Hb combination reversed this effect. Nitrate and nitrite concentrations in the culture medium increased (p < 0.05) in a dose-dependent manner according to SNP concentration in the culture medium. At higher concentrations, SNP had a cytotoxic effect leading to follicular oocyte apoptosis whereas lower concentrations have stimulatory effects. In conclusion, NO exerts a dual effect on its development of buffalo PFs depending on the concentration in the culture medium.     

Inhibition of endogenous nitric oxide production influences ovine hindlimb metabolism independently of insulin concentrations

The hindlimb arteriovenous difference (AVD) model was used to determine whether 30 mg/ kg of the nitric oxide synthase (NOS) inhibitor L-NGnitroarginine methyl ester (hydrochloride; L-NAME) inhibited ovine NO synthesis and influenced muscle metabolism. Eight Border Leicester x Merino cross lambs (50 to 55 kg BW) were infused with saline (control) or saline containing L-NAME via an indwelling jugular vein catheter in a balanced randomized crossover design with 3 d between treatments. The abdominal aorta and deep femoral vein were catheterized for assessment of AVD of hind limb metabolism. Arterial hematocrit and insulin concentration and both arterial and venous concentrations of nitrate/nitrite (NOx), glucose, lactate, NEFA, and urea were determined. Infusion of L-NAME decreased arterial NOx concentrations (P = 0.049), indicating inhibition of systemic NO synthesis. Treatment had no effect on arterial (3.5 vs. 3.6 +/- 0.19 mmol/L for control and L-NAME lambs, respectively; P = 0.39) or venous (3.3 vs. 3.4 +/- 0.16 mmol/L, P = 0.55) plasma glucose concentrations or on glucose AVD (0.19 vs. 0.27 +/- 0.065 mmol/L, P = 0.20). There was an interaction (P = 0.038) between time and treatment, such that L-NAME initially increased the AVD of glucose (up to 180 m) divergent from control lambs. The response was then decreased before a possible inflection beyond 240 min. Infusion of L-NAME increased hindlimb venous NEFA (222 vs. 272 +/- 13.2 micromol/L, P = 0.007) and NEFA AVD (79.4 vs. -13.3 +/- 31.5 micromol/L, P = 0.018). These metabolic changes were independent of plasma insulin concentrations, which were not affected by L-NAME infusion (25.3 vs. 27.8 +/- 3.62 mU/L, P = 0.85). The increase in hindlimb lipolysis after L-NAME infusion does not seem to be due to increased lipolysis of plasma triacylglycerol because circulating arterial (155 vs. 142 +/- 20.8 micromol/L, P = 0.58), venous (154 vs. 140 +/- 20.5 micromol/L, P = 0.50), and AVD (1.0 vs. 2.9 +/- 3.17 micromol/L, P = 0.38) triacylglycerol concentrations were unaffected by L-NAME infusion. In conclusion, these data indicate that infusion of 30 mg of L-NAME/kg inhibits NO synthesis, which in turn influences fat and carbohydrate metabolism in the ovine hindlimb independently of plasma insulin concentrations.     

Role of nitric oxide in regulating the ductus arteriosus caliber in fetal rats

The role of nitric oxide (NO) on the ductus arteriosus (DA) patency was examined in fetal rats at various stages of gestation. N(G)-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg, i.p.), an NO synthase (NOS) inhibitor, or indomethacin (3 mg/kg, p.o.), a cyclooxygenase inhibitor, was administered at 3 hr before cesarean section to pregnant rats ranging from day 17 to day 21 of gestation. Dams were decapitated and the fetuses were obtained by cesarean section. The fetuses were rapidly frozen in an acetone-dry ice mixture. Using rapid-freezing and shaving methods, the calibers of the DA and pulmonary artery were measured. The constrictive effect of L-NAME on the fetal DA caliber was stronger than that of indomethacin in 19-day-old and immature fetuses. In near-term fetuses, the constrictive effects of L-NAME were reduced, while indomethacin caused marked DA constriction. We conclude that endogenous NO may play a major role in regulating the patency of the DA in earlier fetal stages, while dilator prostaglandins may play a greater role in regulating the ductal patency in the near-term fetus.     

Role of the nitric oxide-cGMP system in the regulation of ductus arteriosus patency in fetal rats

The purpose of this study was to examine the role of the nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) system in the regulation of the ductus arteriosus (DA) patency in fetal rats. Pregnant rats were administered N(G)-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg, ip), an NO synthase (NOS) inhibitor; methylene blue (30, 50 and 100 mg/kg, ip), a soluble guanylate cyclase inhibitor; or indomethacin (3 mg/kg, po), a cyclooxygenase inhibitor, at various times before cesarean section. Dams were decapitated to obtain the fetuses by cesarean section, and fetuses were rapidly frozen in an acetone-dry ice mixture. Using rapid freezing and shaving methods, the calibers of the DA, pulmonary artery (PA) and descending aorta (Ao) were measured to evaluate the effects of treatment. L-NAME reduced the DA calibers to 86% of the initial values, but recovery to the control levels occurred 6 hr after the injection. Indomethacin decreased the DA calibers to 34% of the control values and sustained the DA constriction until 24 hr after the treatment. Methylene blue caused DA constriction to almost the same degree as indomethacin, but the levels normalized within 24 hr after the treatment. We conclude that L-NAME caused a slight constriction of the DA, whereas methylene blue and indomethacin caused marked constriction of the vessels, suggesting that the NO-cGMP system as well as prostaglandins contribute to the DA patency.     

外源NO对盐胁迫下沙打旺种子萌发和幼苗生长的影响

本研究以沙打旺(Astragalus adsurgens)种子为材料,硝普钠(sodium nitroprusside,SNP)为外源NO供体,测定不同浓度(30、60、90、120、150、200、300μmol·L~(-1))SNP处理盐胁迫(0.3%)下沙打旺的种子萌发和幼苗生长,以此探讨NaCl胁迫下外源NO在沙打旺种子萌发和幼苗生长过程中的生理调节功能。结果表明,沙打旺种子和幼苗经SNP处理后,除300μmol·L~(-1) SNP处理对盐胁迫下沙打旺种子萌发和幼苗生长起到一定的抑制作用外,其余SNP处理组均能不同程度地减缓盐胁迫造成的损伤;60μmol·L~(-1)SNP能显著降低盐胁迫对沙打旺种子造成的伤害(P0.05),该处理下沙打旺种子的发芽势、发芽率、发芽指数、活力指数、胚根长较单盐对照分别提高了54.5%、22.6%、58.2%、112.0%、43.7%,并且接近或略高于空白对照;120μmol·L~(-1)SNP明显减轻了盐对沙打旺幼苗的胁迫(P0.05),沙打旺幼苗叶片叶绿素含量、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和过氧化物酶(POD)的活性分别较单盐对照提高了208.91%、117.565%、40.24%和89.95%,丙二醛含量降低了32.55%。综上所述,适宜浓度的外源NO能够提高盐胁迫下沙打旺种子的萌发,促进幼苗叶绿素的合成,降低丙二醛含量,减少膜脂过氧化产物,保护叶绿体膜的完整性,提高SOD、CAT和POD活性,抑制过氧化物和自由基的积累,加快幼苗生长,从而缓解盐胁迫对沙打旺幼苗的伤害。     

静脉注射L-氨基胍对肉鸡肺动脉压及其相关指标的影响

按常规饲养条件饲养AA雄性肉鸡120羽，30日龄时随机分为试验组（T组）和对照组（C组）。T组肉鸡静脉注射L-AG（40mg／kg），C组肉鸡静脉注射生理盐水。分别在注射L-AG和生理盐水1、2、4h后测定平均肺动脉压（mPAP）、诱导型一氧化氮合酶（iNOS）活性、原生型一氧化氮舍酶（cNOS）活性、一氧化氮（NO）含量、红细胞压积（PCV）、电解质浓度、pH、超氧化物歧化酶（SOD）活性、过氧化氢酶（CAT）活性和丙二醛（MDA）含量。结果显示：（1）试验组mPAP、NO含量和iNOS活性均显著或极显著低于对照组（P〈0．05或P〈0．01）；（2）PCV和Ca^2＋在给药后2h和4h与对照组差异显著（P〈0．05）；（3）K^＋浓度在给药1h和2h后显著或极显著低于时照组（P〈0．05或P〈0．01）。结果表明，L-AG通过抑制iNOS活性，引起肉鸡肺动脉压的升高，从而推测iNOS具有调节肉鸡体内mPAP的作用并与肉鸡肺动脉高压综合征发生有着密切的联系。     

Effect of inhaled nitric oxide on experimentally induced pulmonary hypertension in neonatal foals

OBJECTIVE: To evaluate the efficacy of inhaled nitric oxide (NO) in anesthetized healthy newborn foals with experimentally induced pulmonary hypertension. ANIMALS: Five 1- to 3-day-old foals. PROCEDURE: Anesthesia was induced and maintained with propofol, and foals were intubated and mechanically ventilated. Systemic pressure and pulmonary arterial pressure (P(PA)) were recorded every 30 seconds. Hypertension was induced via a hypoxic gas mixture or chemical vasoconstriction, using the thromboxane mimetic U46619. Nitric oxide was added at a concentration of 80 parts per million (ppm) for 6 minutes under baseline conditions and during pulmonary hypertension-induced alveolar hypoxia (inspired oxygen concentration = 0.08). Nitric oxide (20, 40, 80, and 160 ppm) was evaluated during U46619-induced hypertension. Samples for determination of arterial blood gas tensions were collected before and after each NO treatment. RESULTS: Inhaled NO (approx 80 ppm) did not have an effect on baseline variables. Infusion of U46619 (0.35 +/- 0.04 microg/kg of body weight/min) or alveolar hypoxia resulted in increased P(PA) and decreased arterial oxygenation (PaO2) and hemoglobin saturation (HbSat). The increase in P(PA) was attenuated, in a dose-dependent manner, by NO during U46619 infusion and reversed by NO during induced hypoxemia. The PaO2 and HbSat were significantly improved at all NO doses during U44619 infusion but not during alveolar hypoxia. For all inhaled NO concentrations, nitrogen dioxide and methoglobin values were < 5 ppm and 3%, respectively. CONCLUSIONS AND CLINICAL RELEVANCE: Nitric oxide is a potent, selective vasodilator of the pulmonary circulation in healthy newborn foals. Inhaled NO may have value as a therapeutic agent in foals with pulmonary hypertension.     

Effects of nitric oxide and tumor necrosis factor-alpha on production of prostaglandin F2alpha and E2 in bovine endometrial cells

The purpose of this study was to determine whether nitric oxide (NO) mediates tumor necrosis factor (TNF)alpha influence on the bovine endometrium. TNFalpha influence on the bovine endometrium is limited to the stromal cells. Therefore, it was interesting to find out whether NO production by the stromal cells, stimulated by TNFalpha might influence the endometrial epithelium. Moreover, we investigated the intracellular mechanisms of TNFalpha- and NO-regulated prostaglandin (PG) F(2alpha) and PGE(2) synthesis. Epithelial and stromal cells from the bovine endometrium (Days 2-5 of the oestrous cycle) were separated by means of enzymatic dispersion and cultured for 6-7 days in 48-well plates. The confluent endometrial cells were exposed to a NO donor (S-NAP; 1-1000 microM) for 24 h. S-NAP strongly stimulated PGE(2) production in both bovine endometrial cell types (P<0.001). The effect of SNAP on PGF(2alpha) production was limited only to the stromal cells (P<0.05). To study the intracellular mechanisms of TNFalpha and NO action, stromal cells were incubated for 24 h with TNFalpha or S-NAP and with NO synthase (NOS) inhibitor (L-NAME; 10 microM) or an inhibitor of phosphodiesterase (IBMX; 10 microM). When the cells were exposed to TNFalpha in combination with NOS inhibitor (L-NAME), TNFalpha-stimulated PGs production was reduced (P<0.05). The inhibition of enzymatic degradation of cGMP by IBMX augmented the actions of S-NAP and TNFalpha on PGs production (P<0.05). The overall results suggest that TNFalpha augments PGs production by bovine endometrial stromal cells partially via induction of NOS with subsequent stimulation of NO-cGMP formation. NO also stimulates PGE(2) production in epithelial cells.     

The effect of intravenous insulin infusion on renal blood flow in conscious sheep is partially mediated by nitric oxide but not by prostaglandins

To test the effect of insulin on renal perfusion and the participation of NO and PG as mediators of this response, renal blood flow (RBF) was measured in sheep (n = 8) implanted with ultrasonic flow probes around renal arteries and with a systemic arterial pressure (SAP, n = 4) telemetry device. Three protocols were performed: 1) RBF and SAP were recorded (0800 to 1800 h) in fed and fasted sheep, with the latter receiving intravenous (i.v.) infusions (0.5 mL/min) of insulin at 2 or 6 mU/(kg·min); 2) fasted sheep received i.v. infusions of either an inhibitor of NO synthesis (N(G)-nitro-L-arginine methyl ester, L-NAME) alone [0.22 mg/(kg·min), 1000 to 1200 h] or L-NAME (1000 to 1200 h) + insulin during the second hour (6 mU/(kg·min), 1100 to 1200 h); and 3) the same protocol was followed as in protocol 2, substituting L-NAME with ketoprofen [0.2 mg/(kg·min)], a cyclooxygenase inhibitor. In all protocols, plasma insulin and glucose were determined. During insulin administration, euglycemia was maintained and hypokalemia was prevented by infusing glucose and KCl solutions. After the onset of meals, a long-lasting 18% increase in RBF and a 48% insulin increase were observed (P < 0.05), without changes in SAP. Low- and high-dose insulin infusions increased RBF by 19 and 40%, respectively (P < 0.05). As after meals, the increases in RBF lasted longer than the insulin increase (P < 0.05). The L-NAME infusion decreased RBF by 15% (P < 0.05); when insulin was added, RBF increased to preinfusion values. Ketoprofen decreased RBF by 9% (P < 0.05); when insulin was added, RBF increased to 13% above preinfusion values (P < 0.05). In no case was a modification in SAP or glucose noted during the RBF changes. In conclusion, insulin infusion mimics the meal-dependent increase in RBF, independent of SAP, and lasts longer than the blood insulin plateau. The RBF increase induced by insulin was only partially prevented by L-NAME. Ketoprofen failed to prevent the insulin-dependent RBF increase. Both facts suggested that complementary vasodilatatory agents accounted for the insulin effect on sheep renal hemodynamics.     

Mechanical stretch-induced activation of skeletal muscle satellite cells is dependent on nitric oxide production in vitro

Mechanical stretch induces activation of cultured quiescent satellite cells and the activation response is owing to rapid release of hepatocyte growth factor (HGF) from its extracellular association with satellite cells and its subsequent presentation to the c-met receptor. We provide new evidence that the stretch activation is dependent on nitric oxide (NO) production. Stretch activation could be abolished by the addition of N ^G-nitro- L -arginine methyl ester (L-NAME), a competitive inhibitor of NO synthesis, but not by N ^G-nitro- D -arginine methyl ester hydrochloride, a less active enantiomer of L-NAME. Adding HGF to the L-NAME culture restored the activation response, indicating that L-NAME does not directly inhibit satellite cell activation, but acts upstream from the HGF release. In addition, immunoblots of satellite cell lysate revealed the presence of nitric oxide synthase. These experiments suggest that NO is involved in linking mechanical perturbation of satellite cells to chemical signaling responsible for HGF release from its sequestration in vitro .     

Effects of prostaglandin F(2alpha) and nitric oxide on the secretory function of bovine luteal cells

The objective of the present study was to investigate the influence of prostaglandin F(2alpha) (PGF (2alpha)) and nitric oxide (NO) on production of steroids and PGs by culturing bovine luteal cells obtained from ovaries on days 8-12 of the estrous cycle with a nitric oxide (NO) donor (Spermine NONOate), and a NO synthase inhibitor (N(G)-nitro-L-arginine methyl ester dihydrochloride: L-NAME). When the cells were exposed for 24 h to PGF(2alpha) (10(-7)-10(-5) M), production of progesterone (P(4)) increased significantly at all doses used (P<0.05). Moreover, PGF(2alpha) stimulated PGF(2alpha) production (P<0.01), depressed testosterone (T) production (P<0.05), but did not affect synthesis of prostaglandin E(2) (PGE(2)). Spermine NONOate decreased P(4) production to 66%, 47% and 34% of the control concentration after treatment with 10(-5) M, 10(-4) M and 10(-3) M, respectively, but did not affect T production, and increased PGF(2alpha) synthesis (P<0.05) and PGE(2) (P<0.01) at all doses used. L-NAME increased production of P(4) (P<0.01) but did not affect (P>0.05) secretion of T, PGF(2alpha) and PGE(2). Estradiol-17beta (E(2)) was detectable on the level of sensitivity of assay and was not significantly altered by any treatments. The overall results suggest that PGF(2alpha) and NO produced locally in bovine CL play roles in the regulation of the secretory function of the bovine CL as auto/paracrine factors.     

外源NO对NaCl胁迫下燕麦幼苗氧化损伤的缓解效应

以加燕2号为试验材料,用一氧化氮（NO）供体硝普钠（SNP）、NO清除剂牛血红蛋白（Hb）及SNP类似物亚铁氰化钠处理燕麦植株,研究NO对NaCl胁迫下燕麦幼苗生长和氧化损伤的缓解效应。结果表明,NaCl胁迫下添加外源NO提高了燕麦幼苗的株高,提高了SOD、POD、CAT和APX活性,降低自由基含量和膜脂过氧化程度,表明外源NO能缓解NaCl胁迫诱导的氧化损伤,增强植株的耐盐性。NO供体SNP的类似物亚铁氰化钠（不产生NO）对NaCl胁迫燕麦植株的株高和氧化伤害无缓解效应;施用Hb提高了自由基含量,降低了抗氧化酶活性,而添加外源NO能缓解Hb对燕麦生长的抑制,表明内源NO也可能参与燕麦幼苗耐盐性的调节。     

外源NO对NaCl胁迫下燕麦幼苗氧化损伤的保护作用

用不同浓度的外源一氧化氮(NO)供体SNP处理100 mmol/L NaCl胁迫下一年生燕麦草幼苗,研究了外源NO对NaCl胁迫下燕麦幼苗氧化损伤的影响.结果表明,外源NO可缓解NaCl胁迫造成的燕麦幼苗膜质过氧化产物丙二醛(MDA)含量的升高,促进脯氨酸(Pro)积累,提高超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和过氧化物酶(POD)活性,并能缓解叶绿素含量的降解,提高可溶性糖的含量.而且NO的这种作用存在明显的剂量效应,其中以0.2 mmol/L SNP处理效果最为显著.     

Year-round breeding of crossbred Dorset or Finnish landrace ewes using a synthetic light regimen

A group of crossbred Dorset or Finnish Landrace ewes maintained under a synthetic light regimen (Light Treatment, 4 mo long days - 16 h light, 4 mo short days - 8 h light) and exposed to rams every 8 mo (January 1, September 1, May 1) was compared for lamb production over a period of 4.5 yr with two other comparable groups under natural daylight conditions, one exposed to rams once a year in the fall (Control I) and the other every 8 mo (Control II). Conception rates across breed type of ewe were 92% for Control I, 66% for Control II and 83% for Light Treatment ewes. Conception rates for May breedings only were 16% in Control II and 88% in Light Treatment ewes. Prolificacies of crossbred Finn ewes were higher (P less than .05) than those in crossbred Dorset ewes of Control I (258 vs 193%), Control II (187 vs 165%) and Light Treatment (238 vs 163%). The annual production at lambing from the crossbred Finn and Dorset ewes in Control I was 251 and 206 lambs/100 ewes exposed to rams, respectively. Corresponding productions were 231 and 178 for Control II and 296 and 211 for Light Treatment ewes. Mortality of lambs from the crossbred Finn ewes (27%) was higher (P less than .01) than that from the crossbred Dorset ewes (12%). Annual attrition of the crossbred Dorset ewes in Control I, Control II and Light Treatment groups was 5.2, 5.4 and 5.4%, respectively. Corresponding percentages of the crossbred Finn ewes were 7.0, 8.8 and 11.2.(ABSTRACT TRUNCATED AT 250 WORDS)