Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476273 (respiratory distress)
 19,632 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platinum-metal oxidation catalysts are to be introduced in exhaust systems of many 1975 model-year automobiles in the U.S. to meet Clean Air Act standards. Small quantities of finely divided catalyst have been found issuing from prototype systems; platinum and palladium compounds may be found also. Although platinum exhibits a remarkable resistance to oxidation and chemical attack, it reacts chemically under some conditions producing coordination complex compounds. Palladium reacts more readily than platinum. Some platinum-metal complexes interact with biological systems as bacteriostatic, bacteriocidal, viricidal, and immunosuppressive agents. Workers chronically exposed to platinum complexes often develop asthma-like respiratory distress and skin reactions called platinosis. Platinum complexes used alone and in combination therapy with other drugs have recently emerged as effective agents in cancer chemotherapy. Understanding toxic and favorable interactions of metal species with living organisms requires basic information on quantities and chemical characteristics of complexes at trace concentrations in biological materials. Some basic chemical kinetic and thermodynamic data are presented to characterize the chemical behavior of the complex cis-[Pt(NH3)2Cl2] used therapeutically. A brief discussion of platinum at manogram levels in biological tissue is discussed.
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PMID:Interactions of platinum metals and their complexes in biological systems. 5 Sep 43

We report on five preterm infants (34 to 36 weeks' gestation) in whom an overwhelming illness developed within the first 48 hours of life. Each had mild respiratory distress that progressed within 48 hours to deep coma requiring ventilatory assistance. Ammonia concentrations in the plasma ranged from 844 to 7640 microgram per deciliter. Four received exchange transfusion and peritoneal dialysis; ammonia values returned to the normal range (less than 150 mug per deciliter) within 72 hours and remained there even after protein challenge. These four subsequently fed and developed normally. The fifth infant died without an attempt to lower plasma ammonia. In this infant (and two of the others) urea-cycle enzymes measured in liver tissue were in the normal range. Transient hyperammonemia of unknown cause may be a relatively common variety of neonatal hyperammonemia; it responds well to prompt diagnosis and aggressive therapy.
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PMID:Transient hyperammonemia of the preterm infant. 69 97

Oral administration of graded doses of paracetamol to dogs produced hepatic necrosis with some similarities to the clinical syndrome seen in man following a paracetamol overdose. Coma, with raised levels of arterial ammonia, was produced and the aspartate aminotransferase levels became markedly elevated in 2 animals who survived more than 24 h. However, the extent of the hepatic necrosis and the time of survival following paracetamol administration were too variable for this model to be of value for the testing of new methods of temporary liver support. When paracetamol was given by intraperitoneal injection many of the animals died of respiratory distress. Significant methaemoglobinaemia was detected, which was associated with a reduction in the arterial partial pressure of oxygen and was partly reversed by the administration of methylene blue.
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PMID:A dog model of fulminant hepatic failure produced by paracetamol administration. 121 24

Two autopsy cases of neonatal argininosuccinate synthetase (ASS) deficiency demonstrating the particular histological changes of the liver are presented. Case 1 was a female infant with elevated blood ammonia and citrulline. The patient died of sepsis at nineteen days after birth. Autopsy revealed hematomas in bilateral cerebral hemispheres and a yellow liver parenchyma. Histologically, the cerebrum showed diffuse astrogliosis with Alzheimer type II cell and swollen cytoplasm. Status spongiosus and gliosis were observed in the subthalamic and pontine nuclei. The liver demonstrated fatty degeneration and wide portal space with bile duct proliferation and inflammatory cell infiltration. The ASS activities in the liver and the kidneys were not detected. Case 2 was a female infant who died of respiratory distress twenty-four days after birth. Autopsy revealed hematomas in the bilateral cerebral ventricles and a liver with yellow parenchyma. Histologically, there was destruction of arrangement in the cerebrum and cerebellum together with marked decrease of nerve cells with gliosis and phagocytosis. The liver showed mild fatty degeneration and wide portal space accompanied by bile duct proliferation and inflammatory cell infiltration. The ASS activities in the liver and kidneys were not detected.
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PMID:Neonatal type of argininosuccinate synthetase deficiency. Report of two cases with autopsy findings. 407 82

A symptomatic elevation in plasma ammonium concentration, termed hyperammonemia, is associated with numerous congenital and acquired conditions (Table 11). In some cases, such as urea cycle disorders, ammonia is the principal toxin. In other instances, such as portal systemic encephalopathy, it is but one of a number of metabolic disturbances, However, in either case hyperammonemic episodes should be treated aggressively to prevent coma, subsequent brain damage, or death. This involves restricting protein intake, providing adequate calories, and giving agents that remove accumulated nitrogen. Long-term therapy relies on diagnosing the specific disease rate. This rarely requires invasive procedures such as liver biopsy. In most cases measurement of plasma amino acids and urinary organic acids will identify the defect. Treatment involving restriction of nitrogen intake, vitamin supplementation, or stimulation of alternative pathways of waste nitrogen excretion can then be instituted. Early therapy, especially in patients with neonatal-onset hyperammonemia, is imperative to avoid severe brain damage. On this basis, the plasma ammonium level should be determined in virtually every newborn with lethargy, hypotonia, poor feeding, seizures, and/or respiratory distress of unclear origin (Table 12).
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PMID:Hyperammonemia. 651 17

As part of a double-blind clinical trial of antenatal betamethasone, we studied the effects of this drug on urinary ammonia excretion in 28 premature infants. Betamethasone was administered before 34 weeks of gestation according to dosage schedules which have been shown to alter the incidence of respiratory distress syndrome. Although glucocorticoids affect renal ammoniagenesis in adults, the antenatal betamethasone trial did not augment ammonia excretion measured during the first day of postnatal life. We speculate that precocious maturation of renal ammoniagenesis cannot be triggered by glucocorticoids during the gestational period studied.
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PMID:Antenatal betamethasone and renal ammoniagenesis in the newborn. 733 21

Twenty-three preterm infants with respiratory distress syndrome (mean birth weight 1.07 kg, SD 0.24 kg) were randomly assigned to receive glucose alone or glucose with amino acids (1.5 g.kg-1.d-1) i.v. beginning on the 1st d of life. Blood ammonia and serum urea, CO2 content, sodium, potassium, chloride, and ionized calcium concentrations were normal and did not differ between treatment groups. Nitrogen balance was significantly greater in the group that received amino acids [88 (SD 54) versus -135 (SD 45) mg.kg-1.d-1]. In 12 infants (seven, glucose-only; five, glucose and amino acids), leucine kinetic studies were also performed on the 3rd d of life. These 12 infants received a 4-h primed constant infusion of L-[1-13C]leucine. Blood and breath were collected and analyzed for [1-13C]ketoisocaproate and 13CO2, respectively. Leucine turnover and oxidation were calculated. Both leucine turnover and oxidation were significantly higher in the group receiving amino acids than in the glucose-only group [241 (SD 38) versus 164 (SD 25) mumol.kg-1.h-1 and 71 (SD 22) versus 40 (SD 17) mumol.kg-1.h-1, respectively]. In addition, the calculated rate of protein synthesis was higher in the group receiving amino acids [6.9 (SD 1.1) versus 5.0 (SD 1.2) g.kg-1.d-1]. These data indicate that the i.v. administration of amino acids (1.5 g.kg-1.d-1) to ill preterm infants beginning on the 1st d of life improves whole-body protein balance as a result of increased protein synthesis.
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PMID:Effect of intravenous amino acids on protein metabolism of preterm infants during the first three days of life. 843 84

The objective of this experimental study was to determine the effects of aerial ammonia on disease development and bacterial colonization in weaned pigs inoculated with toxigenic Pasteurella multocida and Mycoplasma hyopneumoniae. Two groups of 10 pigs each were continuously exposed to 50 and 100 p.p.m. ammonia, respectively, and compared to a non-exposed control group of 20 pigs. Following aerosol inoculation with M. hyopneumoniae at day 9, all pigs were aerosol-inoculated with toxigenic P. multocida type A at days 28, 42 and 56. At day 63 they were euthanized. Clinical signs including coughing and respiratory distress were present in all groups following inoculation. No significant differences could be established in the extent or frequency of pneumonia between ammonia-exposed pigs and controls, or in the extent of conchal atrophy, the frequency of isolation of toxigenic P. multocida from conchae, tonsils, lungs and kidneys, or the average daily weight gain. The recovery of toxigenic P. multocida from nasal swabs following inoculation was significantly greater in pigs exposed to 50 p.p.m. ammonia or more as compared to the control group. In conclusion, high levels of ammonia combined with inoculations with M. hyopneumoniae and toxigenic P. multocida had no significant effect on disease development, but may have enhanced colonization by toxigenic P. multocida on the nasal turbinates.
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PMID:Lack of effect of aerial ammonia on atrophic rhinitis and pneumonia induced by Mycoplasma hyopneumoniae and toxigenic Pasteurella multocida. 1082 70

Sepsis and septic shock constitute an important cause of morbidity and mortality in critically ill children. Thus, the systemic response to infection and its management remains a major challenge in clinical medicine. Apart from antibiotic administration, the majority of available therapies are limited to supportive strategies, although considerable efforts are being undertaken to devise innovative approaches that modulate host inflammatory responses. In suspected sepsis, 2 or 3 days' empiric antibiotic therapy should begin immediately after cultures have been obtained without awaiting results. Antibiotics should be re-evaluated when the results of the cultures and susceptibility tests are available. The initial antibiotic (combination) is determined by the likely causative agent, susceptibility patterns within a specific institution, CNS penetration, toxicity, and the patient's hepatic and renal function. The likely offending micro-organism in turn depends primarily on the patient's age, coexistence of any premorbid condition leading to impaired immune response, and the presenting signs and symptoms. Close attention to cardiovascular, respiratory, fluid and electrolyte, haematological, renal and metabolic/nutritional support is essential to optimise outcome. Fluid resuscitation is of utmost importance to overcome hypovolaemia on the basis of a diffuse capillary leak. Monitoring and normalisation of the heart rate is essential. In case of nonresponse to fluid resuscitation, inotropic and vasoactive agents are commonly used to increase cardiac output, maintain adequate blood pressure and enhance oxygen delivery to the tissue. Because respiratory distress syndrome is seen in about 40% of critically ill children with septic shock, increased inspired oxygen is essential. To provide optimal relief from respiratory muscle fatigue and facilitate the provision of positive airway pressure, early intubation and mechanical ventilation should be considered. Renal support is essential to avoid prolonged renal shutdown in hypoperfusion states. Haematological support comprises replacement therapy of clotting factors to overcome disseminated intravascular coagulation. Metabolic support may include glucose support, extraction of ammonia from the body and recognition of liver dysfunction. Nutritional support may modify the inflammatory host response, and early enteral feeding can improve outcome in critical illness. To date, glucocorticoid and non-glucocorticoid anti-inflammatory agents have not shown significant benefit in septic patients.
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PMID:Management of sepsis and septic shock in infants and children. 1122 Apr 6

A limited field study of covered facilities used for raising dairy calves suggested that respiratory disorders and death rates were highest when calves were continuously housed on bedding composed of wood shavings, where ventilation was poor and where automatic feeders were installed. High concentrations of ammonia were found in the urine-soaked bedding following overnight incubation. A prolific growth of mixed micro-organisms isolated from the shavings rapidly colonised plates of selective urea medium. Death rates of 10% and 13.5% were observed on two properties. Respiratory distress was common and lung disease was intractable to treatment on these farms. A histopathological diagnosis of subacute purulent pneumonia with distal necrotising bronchiolitis was made, similar to lung lesions produced experimentally in cats, guinea pigs and rabbits exposed to ammonia gas.
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PMID:Some preliminary observations on the possible relationship between ammonia production from soiled bedding in calf rearing sheds and calf illness. 1603 1


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