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)

Endothelial release of the arachidonate derivative PGI2 may be increased in response to cyclic lung stretching. We therefore sought to determine if the stable metabolite of PGI2, 6-keto-PGF1 alpha, would be found in increased quantities in primates ventilated with conventional mechanical ventilation (CMV) compared to treatment with high frequency oscillatory ventilation (HFOV). We also sought to determine if other membrane-derived vasoactive substances such as LTC4, PAF and TXB2 would be elevated in plasma and lung tissue of animals developing hyaline membrane disease (HMD) and if the levels would correlate with the severity of the respiratory distress. Twenty prematurely delivered monkeys were treated with either CMV or HFOV from the first breath after Cesarean delivery until sacrifice at 6 h of age. We found a significant increase from birth to 5 min and from 5 min to 5 h in 6-keto-PGF1 alpha, and a significant increase from 5 min to 5 h in TXB2. We found a significant decline from cord blood to 5 min of LTC4, without further change by 5 h. PAF was present in all plasma samples but showed no upward or downward trend. There was no difference in the 5-h plasma level or in the lung homogenate level of any of the lipid mediators between the two types of assisted ventilation. There was no correlation between any lipid mediator level and severity of the HMD, as measured by gas exchange, radiographic or histologic criteria, when assessed by each ventilator group alone or with both groups combined. We conclude that the immediate postnatal increases in TXB2 and PGI2 and decrease in LTC4 are not altered substantially by use of HFOV.
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PMID:Acute changes in vasoactive lipid mediators in experimental hyaline membrane disease. 148 Aug 45

Using streptozotocin (STZ)-diabetic mice, we examined the respiratory distress induced by arachidonic acid. Male ddY mice were made diabetic by injecting STZ (170 mg/kg, i.p.) 2 weeks prior to the experiment. Control mice received the vehicle (citrate buffer, pH 4.6). The duration of respiratory distress was observed by a slow i.v.-injection of sodium arachidonic acid (AA) into the caudal vein of mice at the dose of 50 mg/kg. Aspirin was i.p.-administered 30 min before AA. OKY-046 (specific thromboxane A2 (TXA2) synthetase inhibitor), OP-41483 (stable prostacyclin analog) and 9, 11 epithia-11, 12-methano-TXA2 (STA2, stable TXA2 analog) were i.v.-administered 30 min before AA. The duration of respiratory distress induced by AA was significantly reduced in STZ-diabetic mice. Aspirin (10-50 mg/kg) and OKY-046 (25-100 mg/kg) enhanced the AA-induced respiratory distress in STZ-diabetic mice. OP-41483 (1-100 micrograms/kg) reduced the AA-induced effect in both control and STZ-diabetic mice. STA2 (10 micrograms/kg) enhanced the AA-induced effect in both control and STZ-diabetic mice. ONO-1078 (1-10 mg/kg) did not affect the AA-induced effect in both control and STZ-diabetic mice. TMK-688 (0.01-1 mg/kg) reduced the AA-induced effect in the control mice, but not in the STZ-diabetic mice. These results suggest an involvement of leukotriene in the respiratory response to AA in diabetic mice, especially when cyclooxygenase and TXA2 synthetase are inhibited.
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PMID:[Changes in arachidonic acid-induced respiratory distress in streptozotocin-diabetic mice]. 153 87

Lytic H2O2-induced injury to human umbilical vein endothelial cells provides a model for endothelial cell damage in diverse states including acute respiratory distress and septic shock. Endothelial cell lysis is an extreme result of inflammatory cell activation. Functional alterations such as responsiveness to endothelial cell agonists and eicosanoid production might be impaired by exposure to inflammatory cell products including H2O2. Soluble mediators such as thrombin or histamine cause endothelial cell activation via a signal transduction mechanism that hydrolyzes phosphatidylinositol 4,5-bisphosphate (IP), liberating inositol trisphosphate (IP3). Accordingly, pretreatment of endothelial cells with H2O2 blocked the subsequent production of IP3 in response to thrombin and histamine. H2O2 inhibition of IP3 was time- and concentration-dependent. The endothelial cells were viable by trypan blue dye exclusion and chromium release. H2O2 inhibition of signaling was completely prevented by catalase. Iron-dependent oxidant radical formation appears critical because deferoxamine (10(-4) mol/L) pretreatment of endothelial cells prevented H2O2 inhibition of IP hydrolysis. Prostacyclin and platelet activating factor production in response to thrombin have been linked to IP hydrolysis. Pretreatment of endothelial cells with H2O2 reduced prostacyclin and platelet-activating factor production by thrombin by at least 50%. It appears H2O2 can induce defects in signaling pathways with sequelae (decreased prostacyclin and platelet-activating factor) short of endothelial cell death. The possible consequences of H2O2 interaction with endothelial cells is reviewed with the aim of presenting a hypothesis to integrate these various observations.
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PMID:Hydrogen peroxide alters signal transduction in human endothelial cells. 198 9

Acute lung injury was produced by intravenous injection of oleic acid. After oleic acid injection, PaO2 was decreased, dogs were involved in respiratory distress. Histological examination indicated aggregation of leukocytes in microvasculature, interstitial and intraalveolar pulmonary edema and congestion in the lung. Using radioimmunoassay technique, changes in arterial and venous plasma levels of stable metabolite of thromboxane A2 (TXA2), thromboxane B2 (TXB2) have been observed. After oleic acid administration, plasma 6-keto-PGF1alpha level was markedly elevated with two peaks. 6-keto-PGF1alpha level in arteries was higher in concentration than in veins. It was suggested that the lung might synthesis a great quantity of prostacyclin entering the systemic circulation. TXB2 was markedly elevated in plasma, which was more in veins than in arteries. A significant arteriovenous difference suggests that there might be extrapulmonary sources contributing to the elevation of plasma TXB2 in oleic acid induced lung injury in dogs. After treatment with large dose of anisodamine (654-2), platelets and leukocytes aggregation could be inhibited as well as the synthesis of TXA2 and prostacyclin. 654-2 might play a role of cyclo-oxygenase inhibitor. It was suggested that 654-2 reduce synthesis of the precursors of TXA2 and prostacyclin, reduce pulmonary edema and might be a therapeutical effect to lung injury.
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PMID:[The study of thromboxane A2 and prostacyclin in oleic acid-induced lung injury in dogs]. 273 67

It is generally accepted that vasodilator prostaglandins are involved in the pathogenesis of persistent ductus arteriosus (PDA) in preterm infants suffering from respiratory distress syndrome (RDS). When studying the prostaglandin metabolism it became apparent that in about 80% of these infants the activity of PGI2 and/or PGE2 was increased. In parallel to weaning infants from the respirator a decrease in prostaglandin activity was observed which was associated with ductal closure. The inhibition of prostaglandin synthesis with indomethacin had the same effect. Considering the various lines of evidence that an artificially ventilated lung is releasing vasodilatory prostaglandins into the circulation we postulated the following sequence of events in the pathogenesis of PDA in preterm infants: development of RDS or other pulmonary lesions which require artificial ventilation; this mechanical intervention causes permanent shear stress and barotrauma on the pulmonary tissue; this stress causes release of arachidonic acid from phospholipids; subsequently vasodilatory prostanoids, such as PGI2 and PGE2 are released and reach the pulmonary circulation and the ductus arteriosus. As a consequence the left-to-right shunt causes pulmonary hypercirculation with further need to continue artificial ventilation. A vicious circle is established. This circle can be broken by ductus ligation, by indomethacin treatment, by less traumatic artificial ventilation or by early weaning from the respirator with theophylline.
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PMID:[New aspects on the pathogenesis of patent ductus arteriosus in premature infants]. 352 23

Measurement of 6 ketoprostaglandin F1 alpha was made by radioimmunoassay during the first 3 days of life in 33 infants with respiratory distress syndrome who were subjects in a double blind controlled trial of ethamsylate for the prevention of intraventricular haemorrhage. Levels of 6-ketoprostaglandin F1 alpha were significantly lower on the first and second days of life in babies receiving ethamsylate. There was a reduction in the incidence of intraventricular haemorrhage in the treated group. High levels of prostacyclin metabolite are found in babies who develop haemorrhage, and reduction of prostacyclin synthetase activity may be the mode of action of this drug in vivo.
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PMID:Ethamsylate reduces immunoreactive prostacyclin metabolite in low birthweight infants with respiratory distress syndrome. 354 93

Levels of the stable metabolite of prostacyclin, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were measured by radioimmunoassay during the first 48 hours of life in a group of 20 infants ventilated for the respiratory distress syndrome in whom a simultaneous record of respiratory activity was made. 6-Keto-PGF1 alpha was significantly lower when the infants were paralysed (P = 0.0004) than when they were breathing spontaneously. Elimination of the capacity for spontaneous respiration may reduce barotrauma and hence the stimulus for prostacyclin release from the lung.
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PMID:Reduction of immunoreactive prostacyclin metabolite after paralysis in ventilated preterm infants. 375 6

To determine if vascular abnormalities in preterm neonates might be related to vasoactive prostaglandins, stable prostacyclin (6-KPGF1 alpha) and thromboxane A2 (T X B2) metabolites in arterial blood were measured at less than or equal to 6 hours after birth and at 24, 48, and 72 hours using a radioimmunoassay. Neonates of less than 32 weeks gestation (N = 26) were diagnosed as having either the idiopathic respiratory distress syndrome (IRDS, N = 15) or pulmonary edema (PE, N = 11), and were also grouped according to the presence or absence of intracranial hemorrhage (ICH, N = 11) or patent ductus arteriosus (PDA, N = 10). Initial plasma 6-KPGF1 alpha was greater in neonates with ICH (0.23 +/- 0.04 ng/ml, mean +/- SE) than without ICH (0.11 +/- 0.04, p less than 0.05). Neonates with both ICH and IRDS (N = 8) had significantly elevated T X B2 at all sampling times compared to neonates with IRDS and no ICH (N = 7). Both T X B2 and 6-KPGF1 alpha increased with time in those with major ICH. Among neonates without ICH, 7 with IRDS had higher initial 6-KPGF1 alpha (0.19 +/- 0.07 ng/ml) and lower T X B2 (0.15 +/- 0.04 ng/ml) than 8 with PE (0.04 +/- 0.01 and 0.37 +/- 0.09 ng/ml, respectively). The initial 6-KPGF1 alpha (0.024 + 0.003 ng/ml), measured in neonates with PE and without PDA or ICH (N = 6), was significantly less than the corresponding value in the other neonates (0.201 +/- 0.036 ng/ml) (N = 20).
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PMID:Plasma 6-keto prostaglandin F1 alpha and thromboxane B2 in sick preterm neonates. 385 77

Hypertension in pregnancy has implications for both maternal and fetal welfare. Extrapolation from concepts of mechanisms operating in hypertension in general to pregnancy-related hypertension is not justified. In the latter, the major features are a hyper-adrenergic state, plasma volume reduction and an increased systemic resistance. A reduction in uteroplacental perfusion may result from or may activate the mechanisms that elevate blood pressure. Humoral factors (e.g. hormonal attenuation of vascular reactivity) and prostacyclin deficiency may be central to the disordered physiology. Treatment of hypertension in pregnancy should aim at avoiding the vascular damage due to blood pressure elevation but not cause a reduction in uteroplacental perfusion. Unlike earlier antihypertensive regimens using centrally acting sympatholytics, adrenergic neuron blockers or diuretics, regimens using beta-blockers or combinations of beta-blockers with alpha-blockers or vasodilating agents such as hydralazine permit effective blood pressure control, even in severe hypertension, and pregnancy can often proceed until term or until fetal maturity is secured. Adverse effects on the fetus (growth retardation, cardiorespiratory depression, hypoglycaemia, hyperbilirubinaemia) formerly attributed to beta-blockers are more likely related to poorly controlled hypertension. Specific benefits of maternal beta-adrenoceptor blockade are suggested by evidence for prevention of proteinuric deterioration and a decrease in the incidence and severity of respiratory distress in premature infants. Hypertension in pregnancy still presents a formidable therapeutic challenge and requires comprehensive management with close monitoring of fetal welfare. The presence or development of proteinuria in a hypertensive pregnant woman implies a major increase in risk to the fetus and warrants immediate admission to hospital for specialist management.
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PMID:Hypertension in pregnancy. Pathophysiology and management. 614 40

The effect of a new aspirin derivative, aspirin-isopropylantipyrine (AIA), with potent platelet anti-aggregant activity, on several experimental thromboses was evaluated and compared with that of aspirin. AIA (50 mg/kg, s.c.) as well as aspirin (50 mg/kg, s.c.) significantly inhibited thrombus formation in extracorporeal shunt model of rats. AIA (50 mg/kg, s.c.) significantly shortened the duration of apnea and respiratory distress induced by a rapid injection of adenosine 5'-diphosphate in rats, while aspirin (50 mg/kg, s.c.) did not. Inhibitory effect of AIA (50 mg/kg, s.c.) on arachidonic acid-induced mortality in mice was less than that of aspirin (50 mg/kg, s.c.). AIA and aspirin (10 mg/kg/d X 10, s.c.) had no effect on laurate-induced arterial occlusive disease in rats. AIA (200 microM) showed weak and reversible inhibition of prostaglandin I2 generation in isolated rat aorta strip, while aspirin (200 microM) showed irreversible inhibition. AIA (50 and 200 microM inhibited Ca2+-, K+- or norepinephrine-induced contraction on isolated rat aorta strip. AIA (200 microM) had no effect on malondialdehyde formation, cyclic AMP level and adenylate cyclase activity in rat platelets. AIA (100 microM) inhibited arachidonic acid-induced contraction on rat fundus strip by about 50%, while aspirin (100 microM) did not. These results strongly suggest that anti-thrombotic activity of AIA was originated at least from its anti-aggregant effect on platelets, differing from aspirin.
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PMID:Studies on aspirin derivatives with very little side effect. IV. Inhibitory effect of aspirin-isopropylantipyrine (AIA) on several experimental thromboses. 630 82


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