Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

This study was designed to investigate the effects of ketoconazole, a thromboxane synthetase inhibitor, on pulmonary and systemic hemodynamics and pulmonary function in experimental respiratory distress syndrome. Pulmonary artery infusion of oleic acid (PAIOA), 0.1 ml/kg, was used to cause lung injury. Ten dogs were randomized into two groups (Gps): Gp I (n = 5) acted as control, whereas Gp II (n = 5) were treated with IV ketoconazole (2.5 mg/kg bolus then 10 mg/kg/hour for 2.5 hours). Hemodynamics, extravascular lung water (EVLW), serum levels of PGE2, and TxB2 were obtained at baseline (BL) and at 30-minute intervals for 2.5 hours (T30-T150). After 30 minutes of PAIOA the mean arterial pressure (MAP) decreased significantly in both Gps (131 +/- 17 vs. 88 +/- 9 mmHg Gp 1, 119 +/- 9 vs. 79 +/- 8 mmHg Gp II, P less than 0.05); however, while MAP returned to BL values in Gp II, it remained significantly lower throughout the experimental interval in Gp I. Mean pulmonary artery pressure (MAP) was not significantly affected by PAIOA in either Gp, while pulmonary vascular resistance increased significantly from BL at T120 in Gp II. Pulmonary function measured by partial pressure of arterial O2 (PaO2) and extravascular lung water (EVLW) were significantly affected by PAIOA. There was a significant decrease in PaO2 (66 +/- 6 vs. 96 +/- 8 mmHg, Gp I and 60 +/- 7 vs. 100 +/- 6 mmHg, Gp II) as well as an increase in EVLW (604 +/- 61 vs. 135 +/- 9 ml, Gp I and 641 +/- 110 vs. 117 +/- 18 ml, Gp II) in both Gps.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of arachidonic acid metabolites in oleic acid induced pulmonary injury in a canine model. Effect of ketoconazole (thromboxane synthetase inhibitor). 190 Jun 83

One peculiarity of pulmonary surfactant, which is the tensioactive material physiologically present at the surface of alveoli, lies in its very quick localization at in the air-water interface. This being one of the limiting factors of artificial exogenous surfactants for the treatment of patients suffering of respiratory distress syndromes, we have studied the mechanisms which are intervening in the adsorption kinetics of a pure liquid--phase phospholipid, the dioleylphosphatidylcholine (DOPC), and of mixtures of dipalmitoylphosphatidylcholine (DPPC) and phosphatidic acid (PA) in presence of divalent cations (Ca++ and Mg++). The adsorption kinetics of liposomal suspensions of DOPC, which were studied by the Wilhelmy plate method, are determined by the existence of a barrier potential which height depends on the temperature and medium osmolarity, and on the deformability of vesicules. The study of PA-DPPC liposomes was performed with the help of a pulsating bubble surfactometer, a physicochemical instrumentation which mimics the pulmonary alveoli. To obtain performant responses with this model, high concentrations of PA and of divalent cations Ca++ and Mg++ are needed. These results, which are similar to those observed during the study of liposomal fusion, allow to propose a model, according to which adsorption of liposomes at the air-water interface is comparable to liposomal fusion and may be related to the presence of a thin aqueous film.
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PMID:[Tension activity of pulmonary surfactant: adsorption of liposomes of model phospholipids]. 192 19

LH, a 76-year-old Caucasian male, ingested 3 teaspoons (15 mL) of a homemade wine over a 1-h period and became ill. Approximately 1.5 h later, he was taken to the emergency room of a local hospital with symptoms of respiratory distress and weakness. The plant used in making the wine was Angel's trumpet (Datura suaveolens), which reportedly contains varying amounts of scopolamine and atropine. A sample of the wine was collected and analyzed for these two compounds by reversed-phase HPLC chromatography using 97% methanol-3% deionized water. The filtered wine contained an estimated 29 mg scopolamine/mL, which produced a total ingested dose of 435 mg. No atropine was detected. The scopolamine was confirmed by TLC. An oral dose of 50 mg of atropine sulfate in humans has been reported fatal, but there is no reported fatal dose for scopolamine. The alcohol content and 3.8 pH of the homemade wine may have increased the extraction of this compound from the plant material, and the wine fermentation process may have concentrated the original extract.
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PMID:Scopolamine poisoning from homemade 'moon flower' wine. 194 73

A prospective randomized trial was performed in 58 neonates comparing nasal continuous positive airway pressure (NCPAP) vs oxyhood following extubation of neonates weighing less than 1 kg. All neonates had been ventilated for the treatment of respiratory distress syndrome for at least 24 hours and weighed less than 1 kg at the time of extubation. Clinical criteria for elective extubation included improving pulmonary status, fraction of inspired oxygen (FIO2) less than or equal to 0.35, mean airway pressure less than or equal to 7 cm H2O, ventilator rate less than or equal to 20 breaths per minute, and weight at least 80% of birth weight. Informed consent was obtained and neonates were randomized to NCPAP or oxyhood following extubation. Success was defined as remaining free of additional ventilatory support for at least 5 days. Failure criteria included FIO2 greater than or equal to 0.60 to maintain pulse oximetry greater than or equal to 93%, PaCO2 greater than or equal to 60 mm Hg, pH less than or equal to 7.23, or moderate to severe apnea. Results demonstrate that 22 (76%) of 29 neonates were successfully extubated to NCPAP while only 6 (21%) of 29 were successfully extubated to oxyhood (P less than .0001). There were no differences in baseline characteristics between the two groups. Of the 23 neonates who failed oxyhood, 21 were then given a trial of NCPAP and 58% (12/21) remained extubated. Data indicate that using selected clinical criteria for elective extubation of neonates weighing less than 1 kg, NCPAP facilitates successful extubation.
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PMID:Nasal continuous positive airway pressure facilitates extubation of very low birth weight neonates. 194 42

The influence of the timing of surfactant replacement therapy for the treatment of neonatal respiratory distress syndrome was evaluated in a study of 182 neonates of less than 30 weeks' gestation who were randomly assigned prior to delivery to one of three study groups: control (dummy instillation of air given at birth), early surfactant (surfactant given at birth), or late surfactant (surfactant given at less than 6 hours of age). Subjects in the late surfactant group could avoid treatment if they had a clear chest roentgenogram and required no supplemental oxygen at a mean airway pressure of less than 7 cm of water. All treated neonates were eligible to receive up to three additional doses during the first 5 days of life. The three groups were comparable with respect to birth weight, gestational age, and other perinatal parameters with the exception of a lower cord arterial pH and 1-minute Apgar score in the early surfactant group. Of the 60 neonates randomly assigned to late treatment, 29 (48%) were deemed surfactant sufficient and thereby avoided treatment; the other 31 received their first dose at a mean age of 2.9 hours. There was a significant improvement in gas exchange during the first week of life in both surfactant groups compared with the control group, reflected by differences in fraction of inspired oxygen, arterial/alveolar PO2, and ventilation index (peak pressure x rate on the ventilator) (P less than .001). Surfactant therapy also resulted in a lower incidence of pulmonary air leak and severe chronic lung disease (defined as requirement for respiratory support beyond 36 weeks post-conceptional age). There were no differences between early and late surfactant groups in any of these parameters. The only statistically significant difference between the surfactant groups was that the early group had a higher incidence of mild chronic lung disease (respiratory support beyond 28 days of age) than the late treatment group (P less than .005). Neonates in the late treatment group were extubated earlier and had a shorter neonatal intensive care unit stay than control neonates (P less than .05), whereas those in the early group were not significantly different from control neonates in these parameters. It is concluded that replacement therapy with bovine lung surfactant extract in neonates of less than 30 weeks' gestation results in decreased oxygen and ventilatory requirements during the first week of life and a lower incidence of pulmonary air leak and severe chronic lung disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Bovine surfactant replacement therapy in neonates of less than 30 weeks' gestation: a randomized controlled trial of prophylaxis versus treatment. 200 Feb 78

A randomized, placebo-controlled trial of human surfactant given intratracheally at birth (prophylactic) versus rescue administration after the onset of severe respiratory distress syndrome (RDS) was conducted among preterm infants born at 24 to 29 weeks of gestation. Singleton fetuses were randomly assigned to receive (1) placebo (air), (2) prophylactic surfactant treatment, or (3) rescue surfactant treatment; infants of multiple births received either (1) prophylactic or (2) rescue treatment. Of 282 potentially eligible fetuses, 246 infants received treatments at birth and 200 infants had RDS. Outcomes are presented both as an intention-to-treat analysis (including infants who met exclusion criteria at or after birth) and as a full treatment protocol analysis for those infants with RDS and likely to benefit from surfactant. Preterm infants (mean 1.0 kg birth weight, 27 to 28 weeks of gestational age) randomly assigned to receive prophylactic treatment received surfactant soon after birth; those assigned to receive rescue surfactant had instillation at a mean age of 220 minutes if the lecithin-sphingomyelin ratio was less than or equal to 2.0 and no phosphatidylglycerol was detected in either amniotic fluid or initial airway aspirate, oxygen requirements were a fraction of inspired oxygen of greater than 0.5, and mean airway pressure was greater than or equal to 7 cm H2O from 2 to 12 hours after birth. Up to four treatment doses (or air) were permitted within 48 hours; approximately 60% of surfactant-treated infants required two or more doses. Surfactant-treated infants had significantly less pulmonary interstitial emphysema than placebo-treated infants (p = 0.02), but there were no other significant differences in mortality rates or morbidity. Indexes of oxygenation and ventilation were improved in surfactant recipients during the first 24 hours. An intention-to-treat analysis found no significant differences between infants given placebo and surfactant-treated infants or between prophylactic- and rescue-treated infants; an improved total mortality rate (p = 0.002) was found among surfactant-treated infants in Helsinki but not in San Diego. Among infants with RDS, the total mortality rate was significantly improved (p = 0.004) with surfactant treatment but not the proportion alive and without bronchopulmonary dysplasia at 28 days (p = 0.052), or the proportion alive and without bronchopulmonary dysplasia at 38 weeks of postconceptional age (p = 0.18) to adjust for differences in prematurity. Deaths caused by RDS or bronchopulmonary dysplasia were significantly reduced among surfactant recipients (p = 0.0001). Neither among singletons nor among multiple-birth infants was there a selective advantage to prophylactic versus rescue treatment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Randomized, placebo-controlled trial of human surfactant given at birth versus rescue administration in very low birth weight infants with lung immaturity. 200 29

We investigated the histopathologic pulmonary changes induced by mechanical pulmonary ventilation (MV) with a high peak airway pressure and a large tidal volume in healthy baby pigs. Eleven animals were mechanically ventilated at a peak inspiratory pressure (PIP) of 40 cm H2O, a respiratory rate (RR) of 20 min-1, a positive end-expiratory pressure (PEEP) of 3 to 5 cm H2O, and an FIO2 of 0.4. High airway pressure MV was terminated in 22 +/- 11 h because of severe hypoxemia in the animals. Five of the baby pigs were killed for gross and light microscope studies. The pulmonary changes consisted of alveolar hemorrhage, alveolar neutrophil infiltration, alveolar macrophage and type II pneumocyte proliferation, interstitial congestion and thickening, interstitial lymphocyte infiltration, emphysematous change, and hyaline membrane formation. Those lesions were similar to that seen in the early stage of the adult respiratory distress syndrome (ARDS). The remaining six animals were treated for 3 to 6 days with conventional respiratory care with appropriate ventilator settings. Prominent organized alveolar exudate in addition to lesions was also found in the five animals. These findings were indistinguishable from the clinical late stage of ARDS. Six control animals were mechanically ventilated at a PIP of less than 18 cm H2O, a RR of 20 min-1, a PEEP of 3 to 5 cm H2O, and an FIO2 of 0.4 for 48 h. They showed no notable changes in lung functions and histopathologic findings. Aggressive MV with a high PIP is often applied to patients with respiratory distress to attain adequate pulmonary gas exchange.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Histopathologic pulmonary changes from mechanical ventilation at high peak airway pressures. 202 23

To test the hypothesis that administration of allopurinol could modify the response to prolonged hyperoxia in premature baboons (140 days gestation) with respiratory distress syndrome, we evaluated physiological, pathological, and lung biochemical parameters in groups of premature baboons treated with mechanical ventilation and exposed to various amounts of oxygen for 6 days. Three groups of experimental animals were studied, including animals that received oxygen as needed to maintain arterial oxygen between 60 and 80 Torr [inspiratory O2 concentration- (FIO2) PRN], animals that received 100% oxygen continuously but also received allopurinol intravenously at a dose of 10 mg.kg-1.day-1 (FIO2-1.0 + allopurinol), and animals that received 100% oxygen continuously and the vehicle for allopurinol administration (FIO2-1.0). Pathological examinations of the experimental animals showed evidence of lung injury in both 100% oxygen-exposed groups, but the allopurinol-treated animals had findings more compatible with the FIO2-PRN group, with relatively few macrophages or polymorphonuclear lymphocytes being present in lung tissue. Lungs of animals treated with allopurinol were also more distensible and had a trend toward decreased lung water compared with the FIO2-1.0 group. Allopurinol-treated animals were able to induce lung glutathione concentrations and glutathione-related and antioxidant enzyme activities compared with the normoxic control (FIO2-PRN) group. Ventilator pressure requirements were also decreased in the allopurinol-treated animals compared with the FIO2-1.0 controls after 42 h. These data suggest that treatment of hyperoxia-exposed premature baboons with allopurinol for the first 6 days of life results in significant changes in lung responses and antioxidant defenses compared with vehicle-treated baboons exposed to 100% oxygen for the same time period.
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PMID:Allopurinol-induced effects in premature baboons with respiratory distress syndrome. 203 82

To demonstrate the characteristics of impaired gas exchange in acute respiratory distress syndrome (ARDS), an experimental model of lung injury was produced in 24 mongrel dogs by intravenously injecting 0.07 ml/kg of oleic acid. While allowing the animal to breathe a mixture of 0.1% CO in air, normal saline, which contained appropriate amounts of six inert gases such as SF6, ethane, cyclopropane, halothane, ether and acetone, was infused at a constant rate through a peripheral vein. After a steady state was established, the expired gas was collected and the samples of both arterial and mixed venous blood were taken simultaneously. The concentrations of the nine indicator gases (O2, CO2, CO and six inert gases) in the samples were measured in terms of a gas chromatograph, permitting analysis of the distribution of ventilation to perfusion (VA/Q) as well as the diffusing capacity to perfusion (G/Q) in injured lungs. To determine the role of hypoxic pulmonary vasoconstriction (HPV) in maintaining gas exchange in ARDS, hemodynamic and gas-exchange parameters were investigated at inspired O2 concentrations (FIO2) of either 21 or 60%. The impairment of gas exchange was examined by measuring the fractional retention (R) of the inert gases in arterial blood. Furthermore, to assess the possible contribution of vasoactive prostanoids in regulating vascular reactivity in ARDS, observations at FIO2 of 60% were repeated after administered indomethacin at a dose of 5 mg/kg. Analytical results revealed that shunt flow in experimental dogs with lung damage caused by oleic acid averaged 17%. Furthermore, widening of VA/Q distribution was found accompanied with significant contribution of extremely low VA/Q areas. In addition, most of the lung was operating in G/Q units with values ranging from 10(-3) to 10(-2) but 9.8% of total Q(QT) was received by the area with G/Q less than 10(-3), which might limit O2 exchange between the alveolar gas phase and capillary blood. Although pulmonary vascular resistance (PVR) in injured lungs observed at FIO2 of 60% was significantly smaller than the value obtained at FIO2 of 21%, QT as well as extravascular lung water did not differ in the two conditions. The R value for the indicator gas was consistently lower at FIO2 of irrespective of gas species. Administration of indomethacin caused a considerable diminution of the R value for inert gas but a rise in PVR without an appreciable change of either QT or extravascular lung water. This was followed by a significant rise in arterial PO2 from 84 to 99 Torr.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Impairment of gas exchange in acute lung injury]. 203 87

In 55 infants with respiratory distress syndrome the dynamic compliance of the respiratory system (CRS) was measured by pneumotachography during the course of the disease. Lecithin/sphingomyelin ratio (L/S) was evaluated at birth and every 10th day. Thirteen infants who developed bronchopulmonary dysplasia (BPD) had lower L/S ratios at birth than those infants without BPD (mean = 1.0 versus 3.5, p less than 0.01). During the course of disease, L/S ratios were variable and increased in all infants independently of outcome. In the first days of life CRS was low (0.30 ml/cm H2O/kg) in all infants independently of outcome. In infants with BPD who survived, CRS was significantly higher from the 30th day on than in infants who died from the disease (0.35 versus 0.23 ml/cm H2O/kg). Together with an decrease in oxygen supply at this time (less than 70%) the CRS is a reliable predictor of survival in cases of BPD.
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PMID:Lecithin/sphingomyelin ratio from tracheal aspirates and compliance of the respiratory system in infants with bronchopulmonary dysplasia. 211 8


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