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

Clinical feature and creatinine metabolism were studied in 86 diabetic patients who had newly initiated dialysis treatment. In 32.5% of the patients, serum creatinine was below 8.0 mg/dl at the initiation of dialysis treatment. Gastrointestinal symptoms, general malaise, pulmonary edema and uremic encephalopathy were the causes which required dialysis treatment in those patients, and the frequency of pulmonary edema was significantly higher than in patients whose serum creatinine was above 8.0 mg/dl at the initiation of dialysis (p less than 0.05). There were no significant differences in serum urea nitrogen, potassium, sodium, albumin levels and hematocrit between low serum creatinine group (3.0-7.9 mg/dl) and high serum creatinine group (8.0-11.9 mg/dl) at the initiation of dialysis. Serum creatinine levels were highly correlated with creatinine generation rate (r = 0.788, p greater than 0.01). There was a significant correlation between creatinine generation rate and muscle volume (r = 0.863, p less than 0.001). Muscle volume of diabetic dialyzed patients was 29.5 +/- 7.0 cm3/cm in males and 26.9 +/- 5.0 cm3/cm in females, and those values were lower than those of non-diabetic dialyzed patients (p greater than 0.005). Frequency of the patients whose creatinine generation rate was below 1500 mg/day was 81.3% in diabetic hemodialyzed patients and this was significantly higher than in non-diabetic hemodialyzed patients (p less than 0.005). In conclusion, in patients with diabetic nephropathy who have to initiate dialysis treatment, uremic symptoms have progressed though serum creatinine levels are relatively low. This low serum creatinine levels in patients with diabetic end-stage renal disease are resulted from their low muscle volume.
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PMID:[Characteristics of the patients with diabetic nephropathy with relatively low serum creatinine at the initiation of dialysis]. 226 24

The Extra Vascular Lung Water (EVLW) was measured using the thermal sodium double indicator dilution technique in 21 patients undergoing surgery for esophageal cancer. This measurement is an important parameter in the control of the respiratory function. In the 16 cases without pulmonary complications, the preoperative EVLW was 5.3 +/- 0.2 (mean +/- SEM) ml/kg and the immediate postoperative EVLW was 4.8 +/- 0.4 ml/kg. This change was significant (p less than 0.05), but within 24 hours the EVLW returned to almost the same levels as those recorded before surgery. In only 3 cases, the EVLW were elevated beyond 7.5 ml/kg, but these high EVLW levels did not continue for more than 12 hours. Of the 5 patients with pulmonary complications, only two experienced pulmonary edema. Their preoperative EVLW levels were normal, but the immediate postoperative EVLW levels were significantly elevated beyond 10 ml/kg. These elevated levels were observed before the PaO2, the portable chest roentgenograms and the other test results changed following surgery. The high EVLW levels beyond 7.5 ml/kg continued for 72 hours after surgery. We found no correlation between the EVLW and measureable hemodynamic parameters (Cardiac Index, Pulmonary Wedge Pressure, Colloid Osmotic Pressure-Pulmonary Wedge Pressure gradient) during the observation period. In the other cases with pulmonary complications (2 cases were pneumonia, one was atelectasis with pneumonia), the changes in the EVLW levels were the same as for the cases without pulmonary complications. These results indicate that the EVLW is the optimum parameter for the control of the respiratory function and early diagnosis of pulmonary edema after surgery for esophageal cancer.
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PMID:[The measurement of extra vascular lung water using a thermal-sodium double indicator dilution technique in patients undergoing surgery for esophageal cancer]. 228 95

The role of oxygen free radicals in the mechanism of lung damage after smoke inhalation injury was investigated. 42 dogs were used and equally divided into control and treated group. In treated group, a comprehensive anti-lipid peroxidation treatment including Ginseng-ophiopgon, hydrocortisone sodium succinate, Vit. C and E were used at 5 min, 6 hr, and 12 hr postinjury. SOD activity in blood, hypoxanthine, xanthine, uric acid, MDA and SCL in plasma, C2H6 and C2H4 in exhaled breath of dogs after smoke inhalation injury were measured. In addition, blood gas analysis and EVLW were determined to evaluate the lung damage. The results demonstrated that the injured dogs suffered from lung edema and acute lung dysfunction. MDA, SCL in plasma and C2H6, C2H4 in exhaled breath increased markedly, reaching their first peaks at 30 min. and second peaks at 24-72 hours postinjury. The values revealing in first peak in treated group were lower than that in control group. The increase of SOD activity, however, was higher in treated group than in control group. Changes of oxygen free radicals and lipid peroxidation were closely related to lung damage and respiratory dysfunction. These data showed that in early postinjury period increase of oxygen free radicals and excessive lipid peroxidation existed in lungs of dogs. And in treated group, anti-lipid peroxidation activity was increased and lipid peroxidation was inhibited. Lung damage was improved obviously. It was believed that the first peak of changes in oxygen free radicals and lipid peroxidation was related to the onset of early pulmonary damage and the stress response, and the second peak to the development of pulmonary infection and lung repaired.
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PMID:[Experimental treatment of smoke inhalation injury with anti-lipid peroxidation agents]. 228 97

The objective of this study was to determine whether myocardial contractility is depressed by intense activation of the sympathetic nervous system. A massive sympathetic discharge was produced by injecting veratrine or sodium citrate into the cisterna magna of anesthetized rabbits (n = 10). Two and one-half hr later, the hearts were isolated and their left ventricular (LV) performance evaluated and compared with the LV performance of hearts isolated from control animals (n = 10). LV performance was evaluated from steady-state peak isovolumic systolic and end-diastolic pressures that were generated at various end-diastolic volumes (LV function curves). The relationship between peak LV systolic pressure (or the average peak developed LV wall stress) and LV end-diastolic volume was rotated downward (P less than 0.01) in the hearts removed from rabbits treated with veratrine or citrate. The LV end-diastolic pressure or LV end-diastolic wall stress of these hearts was not different from control at any end-diastolic volume. The diminished ability of the experimental hearts to develop systolic pressure or wall stress suggests that intense sympathetic activation depressed contractility. Severely damaged myofibers, located largely in the subendocardium, were found in these hearts. Furthermore, the depressed contractility was not related to pulmonary edema since only 2 of 10 rabbits developed edema.
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PMID:Excessive sympathetic nervous system activity decreases myocardial contractility. 230 25

The effect of positive end expiratory pressure (PEEP) on the rate of lung water accumulation with high surface tension pulmonary edema was examined. Alveolar surface tension was elevated by inhalation of 15 mg/kg of the aerosolized detergent dioctyl sodium sulfosuccinate (OT). Hemodynamic measurements, blood gases, and colloid oncotic pressures were recorded in anesthesized dogs for 2 hours after surfactant displacement and elevation of PEEP to 10 cm H2O pressure (group II; n = 10). These data were compared with those of an identical protocol that used only 5 cm H2O PEEP (group I; n = 10). Pulmonary extravascular water volume (PEWV) was measured gravimetrically at the end of the experiment. OT inhalation resulted in an immediate fall in Pao2 and rise in venous admixture (QVa/QT), with little change in colloid oncotic pressure or left atrial pressure. In group I, Pao2 and QVa/QT did not improve significantly over 2 hours, whereas both returned to near baseline in group II. PEWV was elevated in group I compared with normal PEWV (historic controls; n = 11) (6.1 +/- 0.07 - 3.6 +/- 0.01 ml/gm dry lung; p less than 0.01); however, PEWV in group II (9.1 +/- 1.0 ml/gm dry lung; p less than 0.01) was greater than in both group I and historic controls. These data indicate that high alveolar surface tension induces pulmonary edema and PEEP accelerates this edema formation.
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PMID:Positive end-expiratory pressure accelerates lung water accumulation in high surface tension edema. 240 36

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

Uncertainty persists concerning the mechanisms responsible for fluid clearance from the lungs after the air spaces become flooded in severe pulmonary edema. In this study, solute and water fluxes were investigated in an isolated, fluid-filled, perfused rabbit lung preparation. These lungs were perfused with physiologic 1.0 or 5.0 g/dl albumin solutions, and the air spaces were flushed and filled with the same solutions. Samples were obtained at intervals from the perfusate, and at the end of 1 or 2 h, fluid was pumped from the trachea into collection tubes. Concentrations of albumin (labeled with Evans blue) in the air space increased by 2.4 +/- 0.7% (SEM) at 1 h and by 7.0 +/- 0.8% at 2 h. Approximately half of the increase at 2 h could be attributed to dehydration (as judged by increases in perfusate and air-space Na+ concentration). Because previous studies have indicated that the movement of labeled protein between these compartments is very slow in this preparation, it can be concluded that fluid is being reabsorbed from the air spaces. However, reabsorption appears to be slower in rabbits than in rats and it is not stimulated by terbutaline, an effect observed in other species. Under control conditions, potassium concentrations in the air-space fluid fell from 4.01 +/- 0.05 (SEM) mEq/L to 3.37 +/- 0.14 mEq/L at 1 h. Concentrations of K+ in the perfusate rose during this interval from 3.95 +/- 0.05 mEq/L to 4.39 +/- 0.08 mEq/L.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reabsorption of solutes and water from fluid-filled rabbit lungs. 244 49

Experiments were performed to determine the effects of conventional mechanical ventilation (CMV) and high-frequency oscillation (HFO) on the clearance of technetium-99m-labeled diethylenetriamine pentaacetate (99mTc-DTPA) from lungs with altered surface tension properties. A submicronic aerosol of 99mTc-DTPA was insufflated into the lungs of anesthetized, tracheotomized rabbits before and 1 h after the administration of the aerosolized detergent dioctyl sodium sulfosuccinate (OT). Rabbits were ventilated by one of four methods: 1) spontaneous breathing; 2) CMV at 12 cmH2O mean airway pressure (MAP); 3) HFO at 12 cmH2O MAP; 4) HFO at 16 cmH2O MAP. Administration of OT resulted in decreased arterial PO2 (PaO2), increased lung wet-to-dry weight ratios, and abnormal lung pressure-volume relationships, compatible with increased surface tension. 99mTc-DTPA clearance was accelerated after OT in all groups. The post-OT rate of clearance (k) was significantly faster (P less than 0.05) in the CMV at 12 cmH2O MAP [k = 7.57 +/- 0.71%/min (SE)] and HFO at 16 cmH2O MAP (k = 6.92 +/- 0.61%/min) groups than in the spontaneously breathing (k = 4.32 +/- 0.55%/min) and HFO at 12 cmH2O MAP (4.68 +/- 0.63%/min) groups. The clearance curves were biexponential in the former two groups. We conclude that pulmonary clearance of 99mTc-DTPA is accelerated in high surface tension pulmonary edema, and this effect is enhanced by both conventional ventilation and HFO at high mean airway pressure.
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PMID:Effect of increased surface tension and assisted ventilation on 99mTc-DTPA clearance. 245 99

Amiodarone (ADR), a new antiarrhythmic drug for life-threatening cardiac arrhythmias, causes pneumonitis or lung fibrosis in a sizeable minority of patients. The cause of lung damage is not known. We have shown that infusion of 10 mg amiodarone into the inflow circuit of ventilated and perfused rabbit lungs causes immediate increase in pulmonary artery pressure (mean +/- SEM) (from 13.6 +/- 1.2 to 40.6 +/- 9.5 mm Hg, p less than 0.01) and pulmonary edema with marked increase in the pulmonary generation of thromboxane and leukotrienes C4 and/or D4. Albumin (2 g%) in the perfusate prevents any increase in lung perfusion pressure or edema formation. When lung perfusion pressure increase is blocked with the combined cyclooxygenase and lipoxygenase inhibitor enolicam sodium (CG5391B, 35 microM in perfusate), significant lung edema still occurs after amiodarone, indicating that amiodarone causes increased alveolar-capillary membrane permeability. Addition of catalase (100 U/ml) or superoxide dismutase and catalase (100 U/ml each) to perfusate fails to protect from amiodarone lung injury. Immediate infusion of amiodarone (10 mg) into lungs ventilated with room air (ADR + RA) causes an increase in lung weight gain from baseline (delta W) of 5.7 +/- 1.5 g/min. Compared with ADR + RA, ventilation of lungs with 4% O2 (delta W = 0.7 +/- 0.3 g/min, p less than 0.05), pretreatment of rabbits for 3 days with butylated hydroxyanisole (BHA, 100 mg/kg/day i.p., delta W = 0.05 +/- 0.02 g/min, p less than 0.01), pretreatment of rabbits for 3 days with vitamin E (Vit E, 300 U/day orally, delta W = 0.6 +/- 0.2 g/min, p less than 0.05), or addition of N-acetylcysteine to the lung perfusate (NAC, 5 mM, delta W = 0.1 +/- 0.08 g/min, p less than 0.01) all protect from lung edema formation after amiodarone. Amiodarone (100 mg) also caused a marked increase in luminol-enhanced lung chemiluminescence, lung production of superoxide anion (O2-), and tissue levels of lung glutathione disulfide. These results suggest that amiodarone causes lung injury by an oxidant mechanism.
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PMID:Amiodarone causes acute oxidant lung injury in ventilated and perfused rabbit lungs. 245 31

The effect of blood exchange transfusion on experimental acute pancreatitis was investigated. Acute hemorrhagic pancreatitis was induced in rats by the injection of sodium taurocholate into the pancreatic duct. One hour after the induction of pancreatitis, blood exchange transfusion was carried out in these rats. The survival rates by 24 hr significantly increased in the exchange transfusion group as compared to those in the non-treated control group. Blood exchange transfusion, though had not significant effect on the macroscopic findings at autopsy, reduced pulmonary edema. These results suggested that blood purification by exchange transfusion may be beneficial for patients with acute pancreatitis, especially at an early stage.
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PMID:Effect of blood exchange transfusion as an initial treatment of acute hemorrhagic pancreatitis. 246 34


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