Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We tested the preventive effects of catalase, an enzymatic scavenger of hydrogen peroxide, or dimethyl sulfoxide (DMSO), a hydroxyl radical scavenger, on intravenous alloxan-induced lung edema in four groups of pentobarbital sodium-anesthetized, ventilated dogs for 3 h: saline (20 ml.kg-1.h-1) infusion alone (n = 5), alloxan (75 mg/kg) + saline infusion (n = 5), catalase (150,000 U/kg) + alloxan + saline infusion (n = 5), or DMSO (4 mg/kg) + alloxan + saline infusion (n = 5). Catalase or DMSO significantly prevented the increase in plasma thromboxane B2 and 6-keto-prostaglandin F1 alpha over 3 h after alloxan and the accumulation of extravascular lung water after 3 h [3.95 +/- 0.52 (SE) g/g with catalase, 3.06 +/- 0.42 g/g with DMSO] but not early pulmonary arterial pressor response. An electron microscopic study indicated that catalase or DMSO significantly reduced the endothelial cellular damages after alloxan. These findings strongly suggest that hydrogen peroxide and hydroxyl radical are major mediators responsible for intravenous alloxan-induced edematous lung injury in anesthetized ventilated dogs.
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PMID:Pretreatment with catalase or dimethyl sulfoxide protects alloxan-induced acute lung edema in dogs. 144 76

The effects of cardiogenic and noncardiogenic pulmonary edema on the activities of rapidly adapting receptors (RARs) and pulmonary C-fibre receptors were investigated in dogs anaesthetized with chloralose. Cardiogenic pulmonary edema was produced by elevating the mean left atrial pressure by 25 mmHg (1 mmHg = 133.32 Pa) above the control value for a period of 45 min, by partial obstruction of the mitral valve. Noncardiogenic pulmonary edema was produced by injecting alloxan (100 mg/kg) intravenously. The effect of the latter was examined on RARs alone. Cardiogenic edema activated RARs (n = 8) and the activity was greatest during the first few minutes after elevation of mean left atrial pressure. The pulmonary C-fibre receptors (n = 6) were also activated by cardiogenic edema, but these responses were variable. Noncardiogenic pulmonary edema also activated RAR (n = 6), and this response was maintained during the entire recording period (20 min). The extravascular lung water (%), measured 15 min (n = 5) and 45 min (n = 5) after the elevation of the mean left atrial pressure, was significantly elevated above control values. However, these two values were not significantly different from each other. The extravascular lung water increased significantly after the injection of alloxan also (n = 5). These results show that during pulmonary edema, there is significant stimulation of the RARs and the pulmonary C-fibre receptors. It is suggested that the reflex respiratory responses observed in pulmonary edema may be due to the activation of both the RARs and the pulmonary C-fibre receptors.
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PMID:Responses of pulmonary C-fibre and rapidly adapting receptor afferents to pulmonary congestion and edema in dogs. 158 57

Anesthetized dogs with thoracotomy were injected with Evans blue dye and were exposed acutely (5 min) to wood smoke inhalation. Thin slices from freeze-dried samples were photographed and assessed for periarterial and perivenous cuff area and for blue coloration with a score of 0 to 5. Bloodless extravascular lung water (EVLW) was also measured. The smoke-exposed animals were compared with controls and with animals exposed to alloxan or to high-pressure-induced pulmonary edema. EVLW at 2 h after smoke (6.46 +/- 0.80) was above control value (4.30 +/- 0.63) but not different from the alloxan (6.13 +/- 0.70) or high-pressure (6.88 +/- 1.30) groups. Despite the similarity in EVLW in the edematous lungs, there were marked differences in the intensity of blue color and size of cuffing around arteries and veins: the smoke, alloxan, and high-pressure groups had blue color scores of 1.0 +/- 0.1, 2.9 +/- 0.3, and 0.3 +/- 0.1, respectively. These scores indicated a large increase in microvascular permeability to proteins in the alloxan group, a moderate increase in the smoke group, and minimal change in the high-pressure group. The perivascular cuff area was largest in the alloxan group and moderate in the smoke and high-pressure groups. The cuff area was higher for arteries than for veins in all groups except the 0.5-h smoke group. We conclude that smoke inhalation causes a moderate increase in permeability and EVLW compared with alloxan. The extravascular lung water accumulates preferentially around the arteries, but the size of the perivascular cuff is not similar for all causes of pulmonary edema.
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PMID:Distribution of extravascular lung water after acute smoke inhalation. 238 21

Pulmonary edema was induced in dogs by an aerosol of detergent dioctyl sodium sulfosuccinate. The permeability of the pulmonary microvascular membrane was assessed by cannulating an afferent tracheobronchial lymphatic and comparing the lymph-to-plasma total protein concentration (CL/CP) during high lymph flows induced by increasing left atrial (LA) pressure after detergent aerosol. Base-line CL/CP of 0.69 +/- 0.02 fell to 0.55 +/- 0.03 with increased LA pressure alone. CL/CP fell to 0.47 +/- 0.02 when LA pressure was increased following detergent, 0.51 +/- 0.04 following an aerosol of the vehicle in which the detergent was dissolved, and 0.73 +/- 0.10 following intravenous alloxan. In additional animals protein concentration of the airway edema fluid was compared with that of plasma. The ration of protein concentration of airway fluid to plasma was 0.63 +/- 0.08 following detergent aerosol, 0.64 +/- 0.10 following increased LA pressure, and 0.94 +/- 0.09 following administration of alloxan. These data indicate no major increase in pulmonary microvascular permeability following detergent aerosol and support the concept that pulmonary edema is the consequence of reduced interstitial perimicrovascular hydrostatic pressure caused by increased alveolar surface tension.
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PMID:Microvascular membrane permeability in high surface tension pulmonary edema. 241 5

We aimed to study the agreement of estimates of the pulmonary blood volume by the double indicator dilution method and the direct destructive method and the fluid volume balance between the pulmonary intravascular and extravascular spaces. We employed the double indicator dilution method using heat and indocyanine green, with a single injection (into the right atrium) and double sampling technique, that is from the pulmonary artery trunk (PAT) and the aortic root (Ao). With this method, we simultaneously determined the pulmonary extravascular water volume (PEWV), defined as the extravascular lung thermal volume estimated in Ao (LTVAo), and the pulmonary blood volume (PBV) from PAT to the left atrium (LA) (PBVPAT-LA). Dogs were divided into groups: a group without intervention (n = 16), a group loaded with dextran (n = 12) and a group loaded with alloxan (n = 7). When all groups were included, PBVPAT-LA (ml/kg) = 1.02 X PBVdirect(g/kg) + 0.96, n = 35, r = 0.83 where PBVdirect means the blood contents from the pulmonary artery bifurcation to the pulmonary vein measured by the direct destructive method. We substantiated the validity of the use of the double indicator dilution method. In studying the fluid volume balance, based on the results of the direct destructive method, the pulmonary intravascular-extravascular fluid volume ratio (intra/extra) was 1.3 +/- 0.3 (mean +/- SD) in the control state, implying that the interstitium in the lung is relatively "dry". As overt pulmonary edema developed by dextran infusion, the ratio exponentially decreased to 1.0 +/- 0.1 (p less than 0.01). The behavior of the fluid volume balance in question (intra/extra), studied with the double indicator dilution method, was essentially similar to that analyzed by the direct destructive method.
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PMID:Fluid volume balance between pulmonary intravascular space and extravascular space in dogs. 243 88

We studied the incidence of electron microscopic pathological patterns of the alveolar septum observed 30 min after induction of pulmonary edema by dextran-70 infusion (6 dogs, dextran group) and by alloxan injection (6 dogs, alloxan group). For comparable amounts of extravascular lung water in both dextran and alloxan groups, which were twice as much as control group (6 dogs), we characterized the pathological changes. The incidence of the electron microscopic pathological patterns that appeared in dextran group compared with that in control group was significantly high in terms of the widening of the interstitial space, dispersion and disarray of collagen fibrils, and erythrocytes in the interstitial space. The incidence in alloxan group compared with that in control group was significantly high in terms of the swelling of epithelial cells and endothelial cells as well as the widening of the interstitial space, and dispersion and disarray of collagen fibrils. We conclude that dextran causes interstitial changes exclusively and alloxan causes cellular changes primarily coupled with secondary interstitial changes in acute pulmonary edema.
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PMID:Electron microscopic pathological patterns of alveolar septum in acute dextran-induced and alloxan-induced pulmonary edema in dogs. 248 73

Coronal proton and sodium images of control rats and rats with either increased permeability edema produced by intravenous alloxan (300 mg/kg) or increased pressure edema produced by saline infusion (2 ml/min) were obtained. Axial chest CT images were used to monitor the development of pulmonary edema. Immediately after the imaging session compartmental lung water was measured gravimetrically. The sodium and proton imagings were done sequentially in a 31-cm-bore 1.9-T magnet without moving the animal. The anatomical boundaries of the lung on the proton images were transferred to the sodium images for calculation of the average sodium signal intensity which was determined by extrapolating the mean values from five echoes to time zero. The sodium signal intensity was correlated (r = 0.7) with the total water fraction. There was poor correlation (r = 0.56) with the extravascular water due to confounding by the sodium vascular signal.
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PMID:Sodium NMR imaging of lung water in rats. 338

Intracisternal administration of veratrine (40 micrograms/kg) in the alpha-chloralose-anesthetized dog produces fulminant neurogenic pulmonary edema (NPE). To determine whether the edema resulted from increased microvascular pressure or from increased permeability, the airway fluid-to-plasma protein (A/P) concentration ratios were compared for both total proteins and endogenous protein fractions of known molecular radii (37-114 A) from dogs with edema produced by either veratrine, alloxan (permeability edema), or combined left atrial pressure and volume overload (hemodynamic edema). High A/P ratios (0.98 +/- 0.05) were observed after alloxan administration, whereas lower values (0.54 +/- 0.04) were observed in hemodynamic edema. A/P ratios were observed after veratrine administration that formed a continuum (0.48-0.84) between these extremes. Veratrine animals with high overall A/P ratios exhibited elevated A/P ratios for all protein fractions, whereas animals with lower overall A/P ratios exhibited A/P protein fraction ratios similar to those observed in the hemodynamic group. These data indicate that both hemodynamic and increased permeability mechanisms may play a role to varying degrees in the development of this form of NPE.
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PMID:Analysis of airway fluid protein concentration in neurogenic pulmonary edema. 355 6

Pulmonary edema has been proposed as a stimulus for pulmonary C-fibers. Stimulation of pulmonary C-fibers causes depression of cardiovascular function and either tachypnea or apnea. Our objective was to determine whether pulmonary edema, induced by either increasing pulmonary vascular permeability with alloxan or hydrostatic challenges, would elicit depression of cardiovascular function or changes in frequency of inspiratory activity. Utilizing a preparation in which the left pulmonary vessels and left airway were isolated, we monitored systemic blood pressure (BP), heart rate (HR), and diaphragm contractions (DC) in 13 anesthetized dogs. Injection of alloxan into the left pulmonary artery (LPA) produced transient decreases in HR, BP, and frequency of DC within 20 s of injection with no subsequent cardiorespiratory changes up to 5 min. These alloxan injections also caused coagulation necrosis. Generation of hydrostatic pulmonary edema in the left lung caused no changes in HR, BP, or in the frequency and amplitude of DC. We conclude that alloxan does stimulate reflex cardiorespiratory depression consistent with C-fiber stimulation, but these reflex responses are probably caused by alloxan's caustic effect and not by the resultant edema. We also conclude that pulmonary edema induced by increased hydrostatic pressure does not evoke any reflex cardiovascular responses or changes in frequency of inspiratory activity.
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PMID:Pulmonary edema in dogs fails to cause reflex responses. 381 22

This study determined the effects of end-expiratory pressures (EEP) and alterations in end-expiratory lung volume (EELV) on lung compliance (CL) and pulmonary resistance to gas flow (RP) in 20 cats with normal and edematous lungs. EELV was varied using EEP ranging from -8 to +10 cm H2O. Negative EEP was used to decrease EELV of the healthy lung causing CL to decrease and RP to increase. Positive EEP in the healthy lung also caused CL to decrease but did not significantly affect RP. After inducing pulmonary edema using alloxan, functional residual capacity (FRC) decreased 38%, CL decreased 66% and RP increased 106% (p less than 0.001). An EEP of 4 cm H2O returned EELV to normal FRC levels and produced maximum values for CL. Increases in EEP to 4 cm H2O also caused decreases in RP in the edematous lungs but further increase did not cause significant changes in RP. These results show that (1) relatively low levels of EEP returned EELV to normal FRC levels in alloxan-induced pulmonary edema, and (2) optimal lung mechanics were obtained when EELV was equal to or slightly above normal FRC values in both healthy and edematous lungs.
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PMID:Effects of end-expiratory lung volume on lung mechanics in normal and edematous lungs. 389 43


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