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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The respiratory pathophysiology of A2 influenza infection was studied in mice treated with small-particle aerosols (SPA) of rimantadine or ribavirin. Untreated infections in mice resulted in survival rates of 15% or less and were characterized by (i) severe hypoventilation (decreased P(O2) and increased P(CO2)), (ii) compensated respiratory acidosis (increased P(CO2) and HCO(3) (-), with normal pH), (iii) pneumonia with increased ratio of wet/dry lung weight, and (iv) hypothermia. Treatment with SPA of rimantadine (21 mg/kg per day for 4 days) beginning 72 h after virus challenge significantly improved survival rate (80%) but failed to alter lung pathology from that found in infected, untreated mice. Rimantadine treatment decreased somewhat the severity of hypoventilation, respiratory acidosis, lung wet weight, hypothermia, and lung virus titers from that observed in infected, untreated mice. SPA of ribavirin (26 mg/kg per day for 4 days) initiated 6 h after SPA exposure of mice to virus significantly improved survival rate (95%) and reduced lung virus titers and lung pathology. Gas exchange and pulmonary edema in ribavirin-treated, infected mice were significantly improved over those of infected, untreated controls. The mechanisms for increased survival rates induced by SPA of rimantadine remain uncertain, since increased survival rates could not be ascribed entirely to improvements in lung functions. In contrast, however, ribavirin treatment appeared to improve survival rates by reducing major lung pathology and pulmonary dysfunction. This was probably mediated through the antiviral effects of ribavirin.
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PMID:Effects of small-particle aerosols of rimantadine and ribavirin on arterial blood pH and gas tensions and lung water content of A2 influenza-infected mice. 1 87

The effects of positive end-expiratory pressure (PEEP) at 5, 10, 15, and 20 cm H2O on the distribution of ventilation-perfusion (VA/Q) ratios was determined in four normal dogs and in ten with oleic acid-induced acute hemorrhagic pulmonary edema. Tidal volume and frequency were held constant at all times with mechanical ventilation during intravenous pentobarbital and gallamine anesthesia. Normal dogs had little or no shunt, and no areas of low (less than 0.1) or high VA/Q (greater than 10.0) at zero end-expiratory pressure (intermittent positive-pressure breathing). In these animals increasing PEEP caused progressive depression of cardiac output, associated with an increase in ventilation to both high VA/Q and unperfused regions. PEEP greater than or equal to 10 cm H2O resulted in a reduction in Pao2 and an increase in PaCO2. In dogs with pulmonary edema, PEEP's of 5 and 10 cm H2O resulted in dramatic reductions in shunt, virtual obliteration of low VA/Q regions, and market improvement in Pao2. However, at 15 and 20 cm H2O PEEP's high VA/Q and dead space ventilation with CO2 retention again developed in all but the most severely affected (shunt greater than 40%) dogs.
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PMID:Effects of positive end-expiratory pressure on gas exchange in dogs with normal and edematous lungs. 33 16

Edema transudation from extra-alveolar vessels was investigated in anesthetized, open-chested dogs. Fluid accumulation at different alveolar and extra-alveolar vascular pressures was assessed by continuous lung weighing and microscopy. The left (experimental) lung was distended with 6% CO2 and air while normal arterial blood gases were maintained by separately ventilating the right lung. Extra-alveolar vessels were isolated by compressing alveolar vessels with alveolar pressures high enough to stop blood flow. Weight increased steadily (edemogenesis) when pulmonary arterial and/or pulmonary venous pressure was 1 cmH2O below this pressure. Because some alveolar vessels at the lung base could have remained open and leaked, extra-alveolar vessels were also separated from alveolar vessels by glass bead embolization sufficient to stop perfusion. Lung weight gains followed selective pulmonary arterial or venous pressure elevations. Electron microscopy demonstrated edema in experimental lobes which was not present in control lobes with undistended extra-alveolar vessels at the same alveolar pressure. Thus pulmonary edema can be caused by fluid leaking from extra-alveolar vessels.
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PMID:Fluid leaks from extra-alveolar vessels in living dog lungs. 34 59

Hemorrhagic pulmonary edema was produced consistently in 19 of 20 anesthetized, paralyzed, ventilated cats when intracranial pressure (ICP) was raised for 30 minutes by intraventricular infusion of mock CSF to 150 mm Hg in 14, or 200 mm Hg in six. However, under identical conditions, except that ICP was raised to only 100 mm Hg, three of seven animals did not develop hemorrhagic edema of the lungs and the remaining four had spotty hemorrhage. Thirteen control animals with normal ICP had normal lungs. Gravimetric lung water analysis by Pearce's method confirmed gross and microscopic appearance of hemorrhagic pulmonary edema. Extravascular lung water (p less than 0.05) and lung blood (p less than 0.05) were significantly greater than control values when ICP was raised to or exceeded 150 mm Hg. Despite hemorrhagic edema, pulmonary gas exchange (O2, CO2) remained unaffected. This animal model allows quantitative measurement of neurogenically-mediated hemorrhagic edema of the lungs before gas exchange is impaired. The model may facilitate clarification of the pathogenesis of neurogenic pulmonary edema and, consequently, refine evaluation of therapy.
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PMID:Experimental neurogenic pulmonary edema in cats. 63 62

Methods of estimating arterial-venous O2 content difference, mixed venous CO2 content and tension, and average arterial CO2 content are presented. They are based on the continuous gas analysis of expired air during a prolonged expiration. The influence of CO2 storage in lung tissue and certain pathophysiologic conditions on the accuracy of these methods was systematically investigated with a comprehensive multi-chamber computer simulation of the lung. For normal levels of CO2 storage capacity, satisfactory estimates of arterial-venous O2 content difference are feasible for differences less than 8 volumes percent; with high levels of CO2 storage capacity, large errors can occur. Storage of CO2 in lung tissue causes large errors in the estimates of mixed venous CO2 content and tension, and average arterial CO2 content; reliable estimates do not appear to be feasible from analysis of expired gas. Simulated pathophysiologic conditions of interstitial pulmonary edema or atelectasis also introduce large errors. This analysis delineates the theoretic limitations of an estimation technique in clinical applications where acute respiratory dysfunctions occur.
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PMID:Estimation of blood gas contents from expired air under normal and pathologic conditions. 95 35

Oxygen and carbon dioxide tensions of arterial blood and subcutaneous tissue were studied in rats during 84 h of continuous exposure to oxygen. O2 and CO2 tensions in the subcutaneous tissue were measured by means of an implanted Silastic tonometer. As pulmonary edema developed after 48 h of exposure to oxygen, Pao2 started to decline and PaCO2 rose. Tissue Po2 decreased below the normal level already after 24 h of exposure, probably due to O2-induced vasoconstriction. After 84 h of oxygen exposure, the mean tissue Po2 was 29 mm Hg. In general, a distinctly hypoxic tissue microclimate was not observed. After 48 h of exposure to oxygen, the tissue PCO2 exceeded the control level. An 84-h exposure resulted in a profound retention of CO2, both in peripheral tissues and arterial blood. It is concluded that, in contrast to earlier suggestions, hypercapnia rather than hypoxia is the final factor leading to death in oxygen toxicity.
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PMID:Arterial and tissue gas tensions in rats during development of pulmonary oxygen poisoning. 115 98

Adenosine is a possible mediator of myocardial and skeletal muscle blood flow regulation. Whether adenosine plays a similar role in modulating the pulmonary pressor response to acute alveolar hypoxia is not known. Adenosine levels (nmol/g tissue) in lung in six dogs ventilated with 95% N2, and 5% CO2 for a period of 3 min increased nearly 10-fold. Inosine and hypoxanthine, adenosine enzymatic degradation products, sustained a 10- and 7-fold increase, respectively. These degradative products are mainly formed in the capillary endothelial cells that contain the degradative enzyme nucleoside phosphorylase as demonstrated by histochemical techniques. To determine the effect of ATP, ADP, AMP, and adenosine on the pulmonary circulation, the in situ left lower lobe of 10 dogs was perfused at either free flow or constant flow via its pulmonary artery. ATP and ADP increased lobar vascular resistance; AMP and adenosine decreased the resistance. During hypoxic ventilation, adenosine infusions (100 nmol/ml blood) entirely abolished the increase in vascular resistance that was due solely to hypoxia. Dipyridamole produced similar responses. These data indicate that adenosine is a pulmonary vasodilator and that it may modulate the pulmonary pressor response to acute alveolar hypoxia. The findings suggest that the use of adenosine or dipyridamole may be beneficial in patients with pathologic elevations of the pulmonary vascular resistance which are a result of an exaggerated pulmonary pressor response to hypoxia, as seen in high-altitude pulmonary edema or that following cerebral injury.
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PMID:Release of adenosine by hypoxic canine lung tissue and its possible role in pulmonary circulation. 121 95

Pulmonary edema is known to induce a rapid and shallow breathing pattern. However, its effects on the level and pattern of distribution of motor activity to the respiratory muscles is unclear. In the present study we evaluated the effect of oleic acid induced pulmonary edema on the electrical activity of the inspiratory muscles (costal and crural diaphragm and parasternal and external intercostal muscles) in the dog, and related it to the transdiaphragmatic pressure and ventilatory parameters over the course of CO2 rebreathing. Pulmonary edema, reflected by a 7.1 +/- 0.6 wet to dry ratio, decreased lung compliance by 57%, increased pulmonary shunt to 35%, and was associated with a rapid and shallow breathing pattern. When compared at equal levels of PCO2 during CO2 rebreathing before and during edema, ventilation and mean inspiratory flow were increased only at lower levels of hypercapnia and their responses to increasing levels of PCO2 were significantly diminished during edema. Transdiaphragmatic pressures were elevated during edema as compared to control values. The rate of rise of the electrical activity of all inspiratory muscles increased significantly during edema at all levels of PCO2. Peak activity, however, remained unchanged, due to shortening of the inspiratory duration. The EMG responses to progressive hypercapnia were not affected by edema. Pulmonary edema did not change the pattern of breathing and neural output to the inspiratory muscles in vagotomized dogs. We conclude that stimulation of pulmonary proprioreceptors during edema increases neural output to all inspiratory muscles. The neural response to hypercapnia is not altered by edema, and is additive to the vagal input. The ventilatory response to CO2 is blunted during severe edema, due to alterations in lung mechanics.
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PMID:Inspiratory muscle activity during pulmonary edema in anesthetized dogs. 141 Aug 42

Perfluoroisobutene (PFIB) is produced by the pyrolysis, and as a by-product during the manufacture, of polytetrafluoroethylene. When inhaled it produces a fulminating and sometimes fatal pulmonary oedema similar to that of phosgene after a latent period of 6-8 h. As part of a study to determine the retained dose and the factors that control the amount retained, this study has investigated the retention in rats of inhaled PFIB at concentrations of 10, 50 and 250 micrograms l-1 in a flow-through system combining head-only exposure and plethysmography. Uptake of PFIB was measured by gas chromatography during elevated and reduced inspired volume and respiratory rate induced by exposure to increased CO2 and injection of pentobarbitone, respectively. The percentage of PFIB retained in the upper airways and lungs was found to be 27.5, 28.1 and 23.7% of the amount inspired at the three concentrations tested. The rate of uptake (nmol min-1 kg-1) of PFIB was a power law of the amount inhaled, an n-fold increase in minute volume producing an nb-fold increase in uptake, where b varied between 0.4 and 0.85. Thus, doubling the inhaled dose produces a 1.3-1.8-fold increase in uptake with a corresponding decrease in percentage retained. The relative contribution of respiratory rate and tidal volume upon PFIB retention could not be defined.
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PMID:Retention of inhaled perfluoroisobutene in the rat. 145 72

Treatments other than descent and supplemental oxygen are discussed in this short review. Exercise gives rise to physiologic responses which may enhance acute mountain sickness (AMS), high altitude cerebral edema (HACE) and high altitude pulmonary edema (HAPE). Therefore, physical rest can be considered the principle treatment for moderate AMS and it should always accompany any treatment of severe high altitude illnesses as long as descent is not possible. Therapy with a portable fabric hyperbaric chamber has a beneficial short-term effect in subjects with AMS, HACE and HAPE. However, treatment modalities using this device which result in long-term beneficial effects need yet to be established. New technical solutions practicable under field conditions at extreme altitude are required for the removal of CO2 from the bag. Expiratory positive airway pressure (EPAP) improves arterial oxygen saturation by 10-20% in subjects with HAPE in trials of 10 min duration. Clinical studies examining longterm effects are necessary, before EPAP can be recommended as initial emergency treatment of HAPE.
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PMID:Treatment of high altitude diseases without drugs. 148 99


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