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)

Diseases which manifest with the respiratory distress in the newborn include 1) respiratory diseases-IRDS, type II RDS, neonatal asphyxia, and MAS etc. 2) anemia, CHD 3) CNS and 4) metabolic diseases. Among these, IRDS has high mortality rate because of the lack of the pulmonary surfactant and immaturity of respiratory center, and has many difficult problems in terms of its prevention and respiratory management. The points of its respiratory management are as follows: 1) Estimation of the level of arterial oxygen ation-this is the most important point. It has become possible, these days, to monitor continuous oxygenation using a transcutaneous oxygen electrode. 2) Knowledge of the physiology & management of apnea, and monitoring of heart rate and respiration. 3) Correction of acidosis & anemia and the nutritional supply by the intraveonous fluid administration. 4) Airway maintenance. 5) Oxygen administration to main PaO2 or tc PO2 of 60--80 mmHg. 6) Artificial ventilation by CPAP or IMV and 7) The specific drug therapy includes indomethacin for PDA associated with IRDS, Tolazoline for the fetal circulation syndrome, and Xanthine derivatives for primary apnea. 8) However, improvement by exchange transfusion has been contro-versial. On the other hand, in the type II RDS which has a relatively good prognosis, the intact survival can be expected by means of the proper management of general condition and respiration. In MAS, pneumothorax, pneumomediastinum and severe asphyxia, the proper resuscitation, oxygen administration should be given according to several conditions, especially the degree of hypoxia. The peritoneal dialysis can be lifesaving in case of severe renal impairment with RD. As the respiratory distress in the newborn is very frequent in its occurrence and death rate, its proper management is expected to result in the decrease in the newborn death rate in Hokkaido (8.1--6.6 per 1,000 live births) and the increase in the survival rate without any handicap, particularly if hospitals in each Hokkaido district give the newborn medical care more intensively than at present.
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PMID:[Respiratory distress in the newborn (author's transl)]. 39 87

The use of hypoxanthine measurements for quantitative monitoring of intrauterine asphyxia is generally accepted. A high level in blood or in CSF is a consequence of tissue hypoxia. Hypoxanthine and xanthine were measured by selective high pressure liquid chromatography in mature newborns, in healthy, symptom-free preterm babies, and in preterm babies affected by idiopathic respiratory distress syndrome. The measurements were carried out from peripheral venous blood within three hours after birth and at the age of 48-72 hours. In mature newborns the mean hypoxanthine level was 11.10 mumol/l in the early determinations, and 8.45 mumol/l in the second set of measurements. In unaffected prematures there were significantly higher levels, and the highest values (44.22 +/- 15.13 mumol/l) were encountered in premature babies subsequently dying of severe hypoxia. Xanthine showed a similar course. In addition to establishing normal values for prematures we desired to clarify the changes in the levels of purine metabolites during idiopathic respiratory distress and their prognostic value. Hypoxanthine and xanthine levels were found to be informative in postnatal hypoxia, especially together with other parameters.
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PMID:Plasma hypoxanthine and xanthine levels in the early newborn period in problem-free preterm babies and those with idiopathic respiratory distress syndrome. 398 48

This study quantifies apnoea and assesses the response to xanthine derivatives amongst 172 consecutively born, surviving very low birth weight (VLBW) infants, 136 appropriate weight for gestational age (AGA), 36 small for gestational age (SGA). All babies had electronic monitoring of heart and respiratory rates and nursing staff recorded episodes of apnoea (greater than 10 s), bradycardia (less than 100) and cyanosis. Only 42 (24.2%) babies had no episodes recorded. (25 AGA, 17 SGA). Sixty-four (37.2%) received active resuscitation on at least one occasion with six babies ventilated by bag and mask on more than 10 occasions. Apnoea had commenced by day 10 of life in all the babies who had apnoea and persisted beyond day 50 in only six; however four of these infants were still requiring active resuscitation. Apnoea had ceased by 37 weeks post-conceptual age in 88% and by 40 weeks in all but three babies. Risk factor analysis revealed a strong correlation (P less than 0.005) with lower gestational ages and birth weights, respiratory distress syndrome (RDS) and the problems associated with it, such as mechanical ventilation, patency of the ductus arteriosus (PDA) and chronic neonatal lung disease. A single, reversible cause for apnoea was rarely demonstrated. Care must be exercised with feeding, physiotherapy and suctioning the pharynx and trachea of 'at risk' infants. Xanthine derivatives were highly effective in decreasing the frequency of recurrent apnoea from a mean of 10.08 episodes one day before, to 1.83 two days after commencement of treatment.
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PMID:Clinical spectrum of neonatal apnoea in very low birthweight infants. 646 30

Hyperpermeability is the crux of pathogenesis of sudden lung edema in many pulmonary disorders, especially in acute lung injury and acute respiratory distress syndrome (ARDS). Using our modified method for assessment of pulmonary vascular permeability, we observed the effects of xanthine with xanthine oxidase (X-XO) perfused in rat pulmonary artery and the protection of vasoactive intestinal polypeptide (VIP) against the injury of pulmonary vascular permeability. After addition of xanthine oxidase in the perfusate reservoir containing xanthine, 125I-albumin leak index (125I-ALI) was remarkably increased while peak airway pressure (Paw) showed no significant increase, and perfusion pressure of pulmonary artery (Ppa) and lung wet/dry weight ratio (W/D) were only slightly increased. Xanthine plus xanthine oxidase also increased thromboxane B2 (TX B2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in the perfusate. Treatment with VIP obviously reduced or totally prevented all signs of injury. Simultaneously, VIP also diminished or abolished the associated generation of arachidonate products. The results indicated that VIP has potent protective activity against injury of pulmonary vascular permeability and may be a physiological modulator of inflammatory damage to vascular endothelium associated with toxic oxygen metabolites.
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PMID:[Vasoactive intestinal polypeptide prevents injury of pulmonary vascular permeability due to xanthine with xanthine oxidase]. 857 46

We have recently reported that in an anesthetized rat model, generation of oxygen free radicals (OFR) via i.v. administration of Xanthine plus Xanthine Oxidase [X + XO] resulted in death of about 90% of the animals within a 120-min observation period. Pretreatment of the rats with endogenous scavengers Superoxide Dismutase and Catalase, or with felodipine, a dihydropyridine calcium channel blocker, and/or with dopexamine, an agonist of beta 2 adrenoceptors as well as dopamine (DA-1) receptors significantly enhanced the survival rate to over 70%. The present study was designed to investigate whether lipid peroxidation and ensuing respiratory depression contributed to the lethal toxicity of the free radicals. In the control group, the death of the rats administered [X + XO] was proceeded by significant increases in the plasma lipid peroxides (PLP) and by a severe hypertensive response characteristic of an intense ischemic state, which was confirmed by the presence of hypercapnia, hypoxemia, and acidosis. Placement of the animals on the positive pressure ventilation prior to the administration of [X + XO] did not prevent increases in PLP but, prevented any adverse alterations in the respiratory markers and significantly enhanced survival rate up to 70%. In contrast, both felodipine as well as dopexamine prevented any increases in PLP, normalized blood gas profile, and significantly increased survival rate to 80 to 90%. These observations suggest that the lethal toxicity produced by oxygen free radical was due to respiratory distress. The relationship between increases in the PLP and respiratory depression and the mechanisms via which two pharmacologically distinct agents, felodipine and dopexamine, facilitated the salutary effects cannot be conclusively stated at this time. It is further suggested that although the doses of these two drugs employed in the present studies are not adequate to function as antioxidants, such a possibility cannot be entirely ruled out.
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PMID:Effect of pharmacological interventions in the prevention of lipid peroxidation and respiratory depression induced by oxygen free radicals in anesthetized rats. 890 25