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Query: UMLS:C0476273 (respiratory distress)
 19,632 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate drought-associated increases in concentrations of nitrate and cyanide in animal forage, we compared forage nitrate and cyanide in 1986-87 (annual rainfall 33 in) to nitrate and cyanide in a drought (1988 and 1989; annual rainfall 20 and 27 in, respectively). Fifteen to 20% of the nitrate and cyanide samples from 1986-1987 had sufficiently high concentrations to be of concern (3000 ppm nitrate, 20 ppm cyanide as submitted). Only 4-6% of the 1986-1987 samples had concentrations sufficiently high to produce acute respiratory distress (13,000 ppm nitrate, 50 ppm cyanide as submitted). During 1988 sample numbers had more than doubled, suggesting increased concern for the possibility of nitrate or cyanide intoxication and yielding parallel increases in the number of samples with elevated nitrates or cyanides. By 1989, 25-33% of the samples had concentrations of health concern with respect to either nitrate or cyanide, while 14-19% had concentrations sufficiently high to produce acute respiratory signs. Shortages of forage caused by a 2-y drought were further exacerbated by nitrate and cyanide increases in that feed. Future efforts should concentrate on controlling groundwater nitrate and delivery of nitrate to the plant root-systems.
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PMID:Drought increases forage nitrate and cyanide. 185 4

A 2 yo male child ingested approximately 15 ml of a Gun Blue solution containing selenious acid, nitric acid and copper nitrate. He was immediately given milk and vomited spontaneously blood-stained food with a garlic smell. He was admitted to our Centre less than 3 hr following ingestion. An esophago-gastroscopy showed a second degree burn of both esophagus and stomach. He became comatose and had to be ventilated mechanically. Metabolic acidosis, leucocytosis, hyperglycemia and hemoconcentration were also observed. During the following day he developed a severe intestinal distension, a cardiomyopathy (CPK = 1,302, cardiac arrhythmia), and moderate hepatic, renal and pulmonary dysfunctions. Plasma selenium concentration was 285 micrograms/L and the maximum urinary concentration was 28,459 micrograms/L. After 4 days, his condition had improved considerably and he was about to be extubated when he suddenly developed acute respiratory distress. A similar episode occurred 24 hr later. His lung function progressively deteriorated; later he required the use of an extracorporeal membrane lung. Legionella dumofii was found the causative agent. He died 17 d after ingestion despite aggressive treatment. Acute selenious acid poisoning and its relation to Legionnaire's disease is discussed.
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PMID:Acute poisoning by selenious acid. 408 70

Hyperoxia is commonly used in the treatment of newborn respiratory distress. Although essential and life saving, oxygen therapy can result in the development of lung injury. Oxygen toxicity is associated with the production of reactive oxidant species. Nitric oxide (NO) is an oxidant formed by the catalysis of L-arginine when acted upon by the enzyme nitric oxide synthase (NOS). We studied the differential effects of prolonged normobaric hyperoxia (FIO2 = .95, for 3, 4, and 5 days) on the two major NOS enzymes, constitutive endothelial cell NOS (ecNOS) and inducible NOS (iNOS). Hyperoxia led to a significant lung injury, as measured by pulmonary compliance studies. Hyperoxia did not increase serum NO production, measured as the concentration of nitrite and nitrate. However, hyperoxia did result in a small but significant increase in NO production in the bronchoalveolar lavage fluid, as measured by the products of nitrite and nitrate concentration. This increase in NO was not associated with an induction of whole lung iNOS, as measured by the conversion of L-[3H]arginine to L-[3H]citrulline or by Northern blot analysis. Hyperoxia significantly decreased ecNOS activity as measured by the conversion of L-[3H]arginine to L-[3H]citrulline. In addition, administration of the NOS inhibitor NG-nitro-L-arginine methyl ester worsened the injury, as measured by lung compliance and survival. Further studies need to be performed to determine whether this decrease in ecNOS activity during hyperoxia plays a role in the pathogenesis of hyperoxia-related lung injury.
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PMID:Differential effects of hyperoxia on the inducible and constitutive isoforms of nitric oxide synthase in the lung. 916 69

We measured the urinary nitrite and nitrate (NOx-) excretion, an index of endogenous nitric oxide formation, in term and preterm newborns on the 1st and 4th days of age. In the infants of both groups, the urinary NOx- excretion significantly increased from the 1st to the 4th day. The urinary NOx- excretion in preterm infants was significantly higher as compared with term babies on both days. Furthermore, the urinary NOx- excretion was significantly elevated in preterm infants with respiratory distress syndrome as compared with those without cardiopulmonary complications on the 4th day. These changes of urinary NOx- excretion in newborns strongly suggest the presence of an active physiological role for nitric oxide in the circulatory adaptation to extrauterine life.
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PMID:Assessment of endogenous nitric oxide formation in newborns: measurement of urinary nitrite and nitrate concentrations. 939 43

We present for the first time direct continuous assay of NO concentration (porphyrinic sensor) in the lung parenchyma of Sprague-Dawley rats in vivo during endotoxemia. Intravenous infusion of lipopolysaccharide (LPS, 2 mg x kg(-1) x min(-1) for 10 minutes) stimulated an acute burst of NO from constitutive NO synthase (NOS) that peaked 10 to 15 minutes after the start of LPS infusion, mirroring a coincident peak drop in arterial pressure. NO concentration declined over the next hour to twice above pre-LPS infusion NO levels, where it remained until the rats died, 5 to 6 hours after LPS infusion. The chronic drop in arterial pressure observed from 70 minutes to 6 hours after the start of LPS infusion was not convincingly mirrored by a chronic increase in NO concentration, even though indirect NO assay (Griess method, assaying NO decay products NO2-/NO3-) showed that NO production was increasing as a result of continuous NO release by inducible NOS. A NOS inhibitor, N(omega)-nitro-L-arginine (L-NNA, 10 mg/kg i.v.) injected 45 minutes before LPS infusion, resulted in sudden death accompanied by macroscopically/microscopically diagnosed symptoms similar to acute respiratory distress syndrome <25 minutes after the start of LPS infusion. Pharmacological analysis of this L-NNA+LPS model by replacing L-NNA with 1-amino-2-hydroxy-guanidine (selective inhibitor of inducible NOS) or by pretreatment with S-nitroso-N-acetyl-penicillamine (NO donor), camonagrel (thromboxane synthase inhibitor), or WEB2170 (platelet-activating factor receptor antagonist) indicated that in the early acute phase of endotoxemia, LPS stimulated the production of cytoprotective NO, cytotoxic thromboxane A2, and platelet-activating factor.
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PMID:Protective role of pulmonary nitric oxide in the acute phase of endotoxemia in rats. 956 42

Recently, a second pathway for the generation of potential oxidants with the reactivity of the hydroxyl radical without the need for metal catalysis has been described. In response to various inflammatory stimuli, lung endothelial, alveolar, and airway epithelial cells, as well as activated alveolar macrophages, produce both nitric oxide (.NO) and superoxide anion radicals (O2.-). .NO regulates pulmonary vascular and airway tone and plays an important role in lung host defense against various bacteria. However, .NO may be cytotoxic by inhibiting critical enzymes such as mitochondrial aconitase and ribonucleotide reductase, by S-nitrosolation of thiol groups, or by binding to their iron-sulfur centers. In addition, .NO reacts with O2.- at a near diffusion-limited rate to form the strong oxidant peroxynitrite (ONOO-), which can nitrate and oxidize key amino acids in various lung proteins such as surfactant protein A, and inhibit their functions. The presence of ONOO- in the lungs of patients with acute respiratory distress syndrome has been demonstrated by measuring levels of nitrotyrosine, the stable product of tyrosine nitration. Various studies have shown that inhalation or intratracheal instillation of various respirable mineral dusts or asbestos fibers increased levels of inducible nitric oxide synthase mRNA. In this presentation, we review the evidence for the upregulation of .NO in the lungs of animals exposed to mineral particulates and assess the contribution of reactive nitrogen species in the pathogenesis of the resultant lung injury.
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PMID:Contribution of reactive oxygen and nitrogen species to particulate-induced lung injury. 978 91

Exhaled nitric oxide (NO) is increased in some inflammatory airway disorders but not in others such as cystic fibrosis and acute respiratory distress syndrome. NO can combine with superoxide (O-2) to form peroxynitrite, which can decompose into nitrate. Activated polymorphonuclear neutrophils (PMNs) releasing O-2 could account for a reduction in exhaled NO in disorders such as cystic fibrosis. To test this hypothesis in vitro, we stimulated confluent cultures of LA-4 cells, a murine lung epithelial cell line, to produce NO. Subsequently, human PMNs stimulated to produce O-2 were added to the LA-4 cells. A gradual increase in NO in the headspace above the cultures was observed and was markedly reduced by the addition of PMNs. An increase in nitrate in the culture supernatant fluids was measured, but no increase in nitrite was detected. Superoxide dismutase attenuated the PMN effect, and xanthine/xanthine oxidase reproduced the effect. No changes in epithelial cell inducible NO synthase protein or mRNA were observed. These data demonstrate that O-2 released from PMNs can decrease NO by conversion to nitrate and suggest a potential mechanism for modulation of NO levels in vivo.
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PMID:Superoxide released from neutrophils causes a reduction in nitric oxide gas. 984 49

When an infant presents severe cyanosis which is not associated with respiratory distress, methaemoglobinemia should always be suspected. In children its main inducers are contaminated water or vegetable broths with high nitrate levels (especially spinach and carrots) used to prepare powdered formula or soups. Children affected with methaemoglobinemia have a peculiar lavender colour. Blood from the heel sticks is chocolate-brown and does not become pink when exposed to room air. Diagnosis can be confirmed by excluding other causes of cyanosis and by spectrophotometric analysis of blood for methaemoglobin. When methaemoglobin's levels reach 60% or more, the patient will collapse and become comatose and may die. Therapy with methylene blue results in prompt relief. In this article we report a case of methaemoglobinemia due to the administration of powdered formula mixed with vegetable broths to a newborn aged 16 days. Furthermore we will present a short review of literature regarding methaemoglobinemia caused by toxic agents over the last 10 years.
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PMID:[Acquired methemoglobinemia: a case report]. 1033 42

We investigated the effects of dexamethasone on nitric oxide synthase activity, nitrate/nitrite concentration, and cGMP concentration in the lungs of premature and full-term neonate rats. Dexamethasone or vehicle alone was administered to the mother (1 mg/kg/d, s.c., 2 d), and the neonate was killed 24 h after birth. Ca2+-dependent nitric oxide synthase activity and nitrate/nitrite and cGMP concentrations in lungs of dexamethasone-treated neonates, both premature and full-term, were significantly higher than those in the lungs of the control rats. Ca2+-dependent nitric oxide synthase activity, nitrate/nitrite concentration, and cGMP concentration in the lungs of control rats showed developmentally associated increases during late gestation and in the early postnatal period. The activation of the nitric oxide synthasenitric oxide-cGMP system by antenatal dexamethasone treatment may be related to the improvement of pulmonary function by antenatal glucocorticoid therapy to minimize respiratory distress syndrome.
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PMID:Effect of antenatal dexamethasone treatment on Ca2+-dependent nitric oxide synthase activity in rat lung. 1087 5

Septic shock is characterized by a decrease in systemic vascular resistance. Nevertheless, regional increases in vascular resistance can occur that may predispose mammals to organ dysfunction, including the acute respiratory distress syndrome. In the host infected by endotoxin (lipopolysaccharide, LPS), the expression and release of proinflammatory tumor necrosis factor-alpha (TNFalpha) rapidly increases, and this cytokine production is regulated by agents elevating cyclic AMP. In this report, we present evidence that terbutaline, a beta2-agonist, inhibits TNFalpha production and enhances interleukin-10 (IL-10) release in the anesthetized rat treated with LPS. In addition, an overproduction of nitric oxide (NO, examined by its metabolites nitrite/nitrate) by inducible NO synthase (iNOS, examined by western blot analysis) is attenuated by pretreatment of LPS rats with terbutaline. Overall, pretreatment of rats with terbutaline attenuates the delayed hypotension and prevents vascular hyporeactivity to norepinephrine. In addition, pretreatment of mice with terbutaline also improves the survival in a model of severe endotoxemia. The infiltration of polymorphonuclear neutrophils into organs (e.g., lung and liver) from the surviving LPS mice treated with terbutaline was reduced almost to that seen in the normal controls. These findings suggest that the inhibition of TNFalpha and NO (via iNOS) production as well as the increment of IL-10 production contribute to the beneficial effect of terbutaline in animals with endotoxic shock.
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PMID:Terbutaline prevents circulatory failure and mitigates mortality in rodents with endotoxemia. 1090 95


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