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Exposure to combustion-derived air pollution is associated with an early (1-2 h) and sustained (24 h) rise in cardiovascular morbidity and mortality. We have previously demonstrated that inhalation of diesel exhaust causes an immediate (within 2 h) impairment of vascular and endothelial function in humans. To investigate the vascular and systemic effects of diesel exhaust in humans 24 hours after inhalation. Fifteen healthy men were exposed to diesel exhaust (particulate concentration, 300 microg/m(3)) or filtered air for 1 hour in a double-blind, randomized, crossover study. Twenty-four hours after exposure, bilateral forearm blood flow, and inflammatory and fibrinolytic markers were measured before and during unilateral intrabrachial bradykinin (100-1,000 pmol/min), acetylcholine (5-20 microg/min), sodium nitroprusside (2-8 microg/min), and verapamil (10-100 microg/min) infusions. Resting forearm blood flow, blood pressure, and basal fibrinolytic markers were similar 24 hours after either exposure. Diesel exhaust increased plasma cytokine concentrations (tumor necrosis factor-alpha and interleukin-6, p < 0.05 for both) but appeared to reduce acetylcholine (p = 0.01), and bradykinin (p = 0.08) induced forearm vasodilatation. In contrast, there were no differences in either endothelium-independent (sodium nitroprusside and verapamil) vasodilatation or bradykinin-induced acute plasma tissue plasminogen activator release. Twenty-four hours after diesel exposure, there is a selective and persistent impairment of endothelium-dependent vasodilatation that occurs in the presence of mild systemic inflammation. These findings suggest that combustion-derived air pollution may have important systemic and adverse vascular effects for at least 24 hours after exposure.

Background The development of long-term vascular disease can be linked to the intrauterine environment, and maternal nutrition during gestation plays a critical role in the future vascular health of offspring. The purpose of this investigation was to test the hypothesis that a high-energy (HE) gestational diet, HE post-weaning diet, or their combination will lead to endothelial dysfunction in offspring. Methods Duroc × Landrace gilts (n = 16) were assigned to either a HE (10,144 Kcal/day, n = 8) or normal energy (NE: 6721 Kcal/day, n = 8) diet throughout pregnancy. Piglets were placed on either a NE or HE diet during the growth phase. At 3 months of age femoral arteries were harvested from offspring (n = 47). Endothelial-dependent and -independent vasorelaxation was measured utilizing wire-myography and increasing concentrations of bradykinin (BK) and sodium nitroprusside (SNP), respectively. Results BK and SNP induced vasorelaxation were significantly reduced in the femoral arteries of gestational HE offspring. However, no effect for the post-weaning diet on BK and SNP induced vasorelaxation was seen. This investigation demonstrates that a HE diet prenatally diminishes both BK and SNP induced vasorelaxation in swine. Conclusions These findings suggest that a HE gestational diet can play a critical role in the development of offspring’s vascular function, predisposing them to endothelial dysfunction. This dysfunction may lead to atherosclerotic disease development later in life.

Salinity is among the major abiotic stresses negatively affecting the growth and productivity of crop plants. Sodium nitroprusside (SNP) -an external nitric oxide (NO) donor- has been found effective to impart salinity tolerance to plants. Soybean ( Glycine max L.) is widely cultivated around the world; however, salinity stress hampers its growth and productivity. Therefore, the current study evaluated the role of SNP in improving morphological, physiological and biochemical attributes of soybean under salinity stress. Data relating to biomass, chlorophyll and malondialdehyde (MDA) contents, activities of various antioxidant enzymes, ion content and ultrastructural analysis were collected. The SNP application ameliorated the negative effects of salinity stress to significant extent by regulating antioxidant mechanism. Root and shoot length, fresh and dry weight, chlorophyll contents, activities of various antioxidant enzymes, i.e., catalase (CAT), superoxide dismutase (SOD), peroxidase (POD) and ascorbate peroxidase (APX) were improved with SNP application under salinity stress compared to control treatment. Similarly, plants treated with SNP observed less damage to cell organelles of roots and leaves under salinity stress. The results revealed pivotal functions of SNP in salinity tolerance of soybean, including cell wall repair, sequestration of sodium ion in the vacuole and maintenance of normal chloroplasts with no swelling of thylakoids. Minor distortions of cell membrane and large number of starch grains indicates an increase in the photosynthetic activity. Therefore, SNP can be used as a regulator to improve the salinity tolerance of soybean in salt affected soils.

Cold temperatures harm tropical crops, but understanding how molecular signals help plants cope could aid in climate change adaptation. This study tested if sodium nitroprusside (SNP), a nitric oxide (NO) donor, could improve potato tolerance to cold. Potato seedlings, treated or non-treated (0.5 mM) with SNP, were exposed to cold stress (0 and ‒2 °C) for 6 h. The study was conducted in a completely randomized design, incorporating three factors in three replications. Results showed that cold stress reduced physiological and biochemical parameters in all seedlings, but less so in those treated with SNP. SNP treatment boosted physio-biochemical activity and increased levels of soluble sugars and enzymatic and non-enzymatic antioxidants. Seedlings treated with SNP and exposed to cold stress had lower levels of H 2 O 2 and malondialdehyde, suggesting that NO may alleviate the harmful effects of cold. The analysis conducted using PCA demonstrated correlations between variables and treatment groups. Notably, the first two principal components (PC1 and PC2) accounted for 77.6% and 78.1% of total variance, respectively, under both 0 and − 2 °C temperatures. Under temperatures below 0 °C, the results of the factor analysis (FA) revealed that PC1 exhibited the highest distribution of data, containing the most prominent variation in Squared cosine values (SCV) values at 0.79. Among the variables, Electrolyte leakage (EL) had the best representation in PC1, with the corresponding maximum SCV values at 0.78 under − 2 °C. This result highlights the potential use of SNP in manipulating cold tolerance in potato plants.

Background Glasswort ( Salicornia persica ) is identified as a halophyte plant, which is one of the most tolerant plants to salt conditions. The seed oil of the plant contains about 33% oil. In the present study, the effects of sodium nitroprusside (SNP; 0, 0.1, 0.2, and 0.4 mM) and potassium nitrate (KNO 3 ; 0, 0.5, and 1%) were evaluated on several characteristics of glasswort under salinity stress (0, 10, 20, and 40 dS/m). Results morphological features, phenological traits, and yield parameters such as plant height, number of days to flowering, seed oil, biological yield, and seed yield significantly decreased in response to severe salt stress. However, the plants needed an optimal salinity concentration (20 dS/m NaCl) to obtain high amounts of seed oil and seed yield. The results also showed that a high level of salinity (40 dS/m NaCl) caused a decrease in plant oil and yield. In addition, by increasing the exogenous application of SNP and KNO 3 , the seed oil and seed yield increased. Conclusions The application of SNP and KNO 3 were effective in protecting S. persica plants from the deleterious effects of severe salt stress (40 dS/m NaCl), thereby restoring the activity of antioxidant enzymes, increasing the proline content, and maintaining cell membrane stability. It seems that both factors, i.e. SNP and KNO 3 , can be applied as mitigators of salt stress in plants.

Recent studies suggested intrathecal vasodilator administration as a therapy to mitigate post-ischemic cerebral hypoperfusion following cardiac arrest. We examined the effects of two commonly used intrathecal vasodilators, sodium nitroprusside (SNP) and nicardipine, on cerebral pial microcirculation, cortical tissue oxygen tension (PctO 2 ), and electrocortical activity in the early post-resuscitation period using a porcine model of cardiac arrest. Thirty pigs were resuscitated after 14 min of untreated cardiac arrest. At 30 min after resuscitation from cardiac arrest, 30 pigs randomly received 4 mg of SNP, 4 mg of nicardipine, or saline placebo via subdural intracranial catheters and were observed for 5 h. Group effect and group-time interaction were assessed using linear mixed-effects models. The mean arterial pressure was lower in the nicardipine group (coefficient [95% confidence interval CI], -15.824 [-24.082 to -7.566]) and higher in the SNP group (coefficient [95%CI], 11.232 [2.974–19.490]) compared to the saline group. The percentage of pial arteriole diameter relative to the pre-arrest baseline value (coefficient [95% CI], 48.970 [13.884–84.057]), microvascular flow index (coefficient [95% CI], 0.296 [0.071–0.521]), and PctO 2 (coefficient [95% CI], 26.926 [12.404–41.449]) were higher in the SNP group but not in the nicardipine group compared to the saline group. Amplitude-integrated electroencephalography amplitude recovery was faster in the SNP group (coefficient [95% CI], 1.149 [0.468–1.829]) but not in the nicardipine group compared to the saline group. In conclusion, intrathecal SNP but not nicardipine was effective in treating post-ischemic cerebral hypoperfusion after cardiac arrest.

Objective Chondrocyte apoptosis plays a vital role in osteoarthritis (OA) progression. Angelica sinensis polysaccharide (ASP), a traditional Chinese medicine, possesses anti-inflammatory and anti-apoptotic properties in chondrocytes. This study aimed to determine the protective role of ASP on sodium nitroprusside (SNP)-induced chondrocyte apoptosis, and explore the underlying mechanism. Method Human primary chondrocytes isolated from the articular cartilage of OA patients were treated with SNP alone or in combination with different doses of ASP. Cell viability and apoptosis were assessed, and apoptosis-related proteins including Bcl-2 and Bax were detected. Autophagy levels were evaluated by light chain 3 (LC3) II immunofluorescence staining, mRFP-GFP-LC3 fluorescence localization, and western blot (LC3II, p62, Beclin-1, Atg5). Meanwhile, activation of the ERK 1/2 pathway was determined by western blot. The autophagy inhibitors, 3-methyladenine (3-MA), chloroquine (CQ), and a specific inhibitor of ERK1/2, SCH772984, were used to confirm the autophagic effect of ASP. Results The results showed that SNP-induced chondrocyte apoptosis was significantly rescued by ASP, whereas ASP alone promoted chondrocyte proliferation. The anti-apoptotic effect of ASP was related to the enhanced autophagy and depended on the activation of the ERK1/2 pathway. Conclusion ASP markedly rescued SNP-induced apoptosis by activating ERK1/2-dependent autophagy in chondrocytes, and it made ASP as a potential therapeutic supplementation for OA treatment.

Cadmium (Cd) is a heavy metal that is highly toxic to plants and animals and can accumulate in the environment as a result of industrial activities and agricultural application of some types of phosphate fertilizer. This study aimed to assess the role of sodium nitroprusside (SNP), as a source of nitric oxide (NO) in alleviating Cd stress in maize plants. Maize plants were kept in soil saturated with 40%-strength nutrient solution in a greenhouse, and cadmium nitrate, Cd(NO 3 ) 2 , was applied at different concentrations, (0, 10, and 50 µM). Sodium nitroprusside, [Fe(CN) 5 NO]·2H 2 O, at concentrations of 0.05, 0.1, and 0.2 µM. Growth, leaf gas exchange, and leaf anatomy analyses were performed. The experimental design was completely randomized in a 3 × 3 factorial arrangement with five replicates. The highest concentrations of Cd and SNP reduced the total dry mass and leaf and stem dry mass but increased the allocation of biomass to the roots and stem, but the leaf allocation did not change. The application of Cd and SNP promoted an increase in gas exchange and leaf area, in addition to an increase in leaf tissue thickness and stomatal density. The presence of SNP at low concentrations reduces the toxicity of Cd, but at high concentrations, this compound can generate negative effects and even toxicity in maize plants.

Schizophrenia is a chronic persistent disease with high recurrence rate and high disability rate in the field of psychiatry. Sodium nitroprusside is a nitric oxide (NO) donor and considered a promising new compound for the treatment of schizophrenia. New high-quality clinical trials of sodium nitroprusside in the treatment of schizophrenia have been published in recent years. It is necessary to re-conduct the meta-analysis after the inclusion of these new clinical trials. Our study will conduct a systematic review and meta-analysis of the relevant literature in this field, so as to lay an evidence-based medicine foundation for the efficacy of sodium nitroprusside in the treatment of schizophrenia. Randomized controlled trials (RCTs) of sodium nitroprusside in the treatment of schizophrenia were searched through English databases (PubMed, Web of Science, Embase, and Cochrane Library) and Chinese databases (China Biology Medicine disc, VIP, WanFang Data, and CNKI). The extracted data will be inputted into Review Manager 5.3 for Meta-analysis. The included literature will be assessed for bias risk according to the bias risk assessment tools in the Cochrane Handbook for Systematic Reviews of Interventions. Funnel plots will be used to assess possible publication bias. Heterogeneity is tested by I2 and χ2 tests, and the existence of heterogeneity is defined as I2 ≥50% and P ≤0.1. If heterogeneity exists, the random-effect model will be used, and sensitivity analysis or subgroup analysis will be performed to further determine the source of heterogeneity. CRD42022341681.

Abstract Background Arteries from boys with hypospadias demonstrate hypercontractility and impaired vasorelaxation. The role of sex hormones in these responses in unclear. Aims We compared effects of sex steroids on vascular reactivity in healthy boys and boys with hypospadias. Methods Excess foreskin tissue was obtained from 11 boys undergoing hypospadias repair (cases) and 12 undergoing routine circumcision (controls) (median age [range], 1.5 [1.2-2.7] years) and small resistance arteries were isolated. Vessels were mounted on wire myographs and vascular reactivity was assessed in the absence/presence of 17β-estradiol, dihydrotestosterone (DHT), and testosterone. Results In controls, testosterone and 17β-estradiol increased contraction (percent of maximum contraction [Emax]: 83.74 basal vs 125.4 after testosterone, P < .0002; and 83.74 vs 110.2 after estradiol, P = .02). 17β-estradiol reduced vasorelaxation in arteries from controls (Emax: 10.6 vs 15.6 to acetylcholine, P < .0001; and Emax: 14.6 vs 20.5 to sodium nitroprusside, P < .0001). In hypospadias, testosterone (Emax: 137.9 vs 107.2, P = .01) and 17β-estradiol (Emax: 156.9 vs 23.6, P < .0001) reduced contraction. Androgens, but not 17β-estradiol, increased endothelium-dependent and endothelium-independent vasorelaxation in cases (Emax: 77.3 vs 51.7 with testosterone, P = .02; and vs 48.2 with DHT to acetylcholine, P = .0001; Emax: 43.0 vs 39.5 with testosterone, P = .02; and 39.6 vs 37.5 with DHT to sodium nitroprusside, P = .04). Conclusion In healthy boys, testosterone and 17β-estradiol promote a vasoconstrictor phenotype, whereas in boys with hypospadias, these sex hormones reduce vasoconstriction, with androgens promoting vasorelaxation. Differences in baseline artery function may therefore be sex hormone-independent and the impact of early-life variations in androgen exposure on vascular function needs further study.