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

A smoke inhalation model was created in 22 adult male sheep with pine smoke inhalation through an endotracheal tube for 6 min. Arterial blood gases, HbCO, HbO2 and pulmonary compliance (Cdyn) were monitored, and the morphology of the tracheobronchial tree and pulmonary parenchyma were studied by light and electron microscopy. Severe carbon monoxide poisoning with fatal levels of HbCO (greater than 50 percent) was found at the end of smoke inhalation. Acute respiratory distress, progressive hypoxemia, decreased pulmonary compliance and increased P(A-a)O2 and Qs/QT occurred after injury. Tracheobronchial blockade by pseudomembrane cast, pulmonary edema, atelectasis and necrosis of pulmonary epithelia were demonstrated pathologically. The mechanisms of CO poisoning and ARF are discussed.
 ...
PMID:The pathophysiology of carbon monoxide poisoning and acute respiratory failure in a sheep model with smoke inhalation injury. 230 76

The contribution of maternal hormonal changes and pulmonary damage on the fetal toxicity of methyl isocyanate (MIC) was studied in mice and rats. Exposure to MIC decreased maternal plasma progesterone levels in mice that lost but not in mice that retained pregnancy. Fetal toxicity of MIC was not related to changes in maternal plasma corticosterone levels. Neither chronic administration of progesterone nor the suppression of pulmonary edema with dexamethasone decreased fetal toxicity of MIC. Embryos exposed in utero or in vitro to MIC vapor exhibited a concentration-dependent decrease in growth in culture. An acute dose (3 mmol/kg) of the MIC metabolites (methylamine, dimethylamine, trimethylamine, dimethyl urea) did not exert fetal toxicity. These data suggest that the fetal toxicity of MIC is partly independent of maternal toxicity and may result from its transfer across the placenta and interaction with fetal tissues.
 ...
PMID:Dissociation between maternal and fetal toxicity of methyl isocyanate in mice and rats. 234 77

The harmful effect of iron excess was studied in an experiment using fifteen adult sheep. The animals were divided into three groups of 5 each. The sheep of the group I were kept as controls, those of the group II and III were supplemented with iron in doses of 80 and 40 mg/kg body weight (BW)/24 h respectively. The animals of group II died after a period of 3-7 weeks showing anorexia, loss of weight, diarrhoea, depression and symptoms of circulatory and respiratory failure. From the animals of group III one died after 13 weeks, with symptoms of pulmonary oedema, while the other 4 survived for 22 weeks, together with the animals of the control group. The iron-supplemented animals presented increased values of Serum Iron (SI), Total Iron Binding Capacity (TIBC), percent Transferring Saturation (% SAT), Alanino aminotransferase (ALT), serum Alkalin Phosphatase (SAP), Serum Urea Nitrogen (SUN) Creatinine, Phosphorus and decreased values of serum Copper concentration. These parameters were greater in group II. The iron concentration in the liver, spleen, myocardium and kidneys was also much higher than in the controls. The histological examination revealed degeneration of the liver, spleen, myocardium and kidneys in both groups, while cells overloaded with hemosiderin were seen in the third group only. In conclusion, it was shown that chronic intoxication may occur in sheep overdosed with iron. The toxic dose of iron ranged between 40 and 80 (mg/Kg body weight) per day and was close to 40 mg, when iron was administered in the soluble from FeCl3.6H2O.
 ...
PMID:Iron toxicity in sheep. 253 32

27 cases of uremia with abnormal appearances on the chest films were analysed. The results showed that the clinical features were cough, expectoration dyspnea and hemoptysis. However, the degree of these symptoms was relatively mild as judged from the amount of pulmonary edema found on the chest films. The chest X-ray finding in these group of patients were characterized by pulmonary blood stasis, interstitial edema of the lung and edematous alveoli. The pathogenesis of uremic lung was said to be related to blood urea nitrogen and creatinine retention and the concurrent presence of left side heart failure may also play a role. Hemodialysis and other comprehensive treatments could help the patients with uremic lung for relief the symptoms. But the fundamental managements to improve the prognosis for this disease are early treatment of the primary renal diseases, in order to prevent the occurrence of renal failure. Kidney transplantation should be advised.
 ...
PMID:[The uremic lung]. 263 29

Hemodynamic changes after intravenous application of 10 mg celiprolol-HCl (3-[3-acetyl-4-(3-tert-butylamino-2-hydroxy-propoxy)-phenyl]-1,1-diethyl urea hydrochloride. Selectol; in the following briefly called celiprolol) were investigated over an interval of 30 min in 15 patients with angiographically determined coronary heart disease and depressed left ventricular function (ejection fraction less than 60%, left ventricular end-diastolic pressure (LVEDP) greater than 12 mmHg). One patient suffered from severe left ventricular failure with lung edema and could not be evaluated. The heart rate was not influenced, the arterial pressure was significantly reduced (p less than 0.01), similarly LVEDP (p less than 0.001), and pulmonary pressure (p less than 0.01). Cardiac output and total peripheral resistance were not changed significantly. The hemodynamic working profile of celiprolol in patients with depressed left ventricular function is that of a beta 1-receptor blocker with a strong intrinsic sympathomimetic activity (ISA = Intrinsic Sympathetic Activity) and vasodilating properties--even on preload. The intravenous application of celiprolol in patients with severely depressed left ventricular function can cause pump failure.
 ...
PMID:[Hemodynamic effects of intravenously administered celiprolol in patient with coronary heart disease and depressed left ventricular function]. 288 31

Severe falciparum malaria complicated by acute renal failure resulted in very high mortality. Ten patients with acute renal failure from falciparum malaria (infected rbc up to 80%) were continuously dialysed using Tenckhoff peritoneal catheter. Five were oliguric and BUN was maintained between 60 to 80 mg/dl (21.4 to 28.6 mmol/l) by hourly 1 to 1.5 liter dialysate exchange during the acute phase. The peritoneal urea clearance (mean +/- SD) was 12.1 +/- 1.2 ml/min with urea nitrogen removal of 13.4 +/- 2.3 g/day. In nonoliguric cases dialysis was also needed for additional removal of waste products since the remaining renal function could not cope with the hypercatabolic state. Peritoneal glucose absorption (135 to 565 g/day) gave considerable caloric supply without volume load and also contributed to the prevention of hypoglycemia. Varying degree of acute respiratory failure developed in all patients with 5 cases (2 oliguric and 3 nonoliguric) progressing to pulmonary edema. Swan-Ganz catheterization and hemodynamic study suggested the role of increased capillary permeability and volume overload from endogenous water formation in the development of pulmonary complication. Continuous removal of fluid and waste products minimized these problems and may prevent the progression of respiratory failure. One patient died of severe sepsis and the other nine survived. This study showed the beneficial contribution of continuous peritoneal dialysis in the management of acute renal failure from severe falciparum malaria.
 ...
PMID:Continuous peritoneal dialysis in acute renal failure from severe falciparum malaria. 312 24

After tripling of baseline lung water (EVLW), decreasing wedge pressure (PWP) alone for two hours did not decrease EVLW. In 11 of 16 dogs, triple baseline EVLW and a decrease in plasma colloid osmotic pressure (COP) from 21.1 +/- 0.8 to 17.8 +/- 0.8 mm Hg resulted from left atrial balloon inflation at PWP of 28 to 30 mm Hg. With subsequent lowering of PWP to 10 mm Hg, intravenously administered furosemide (1 mg/kg) was given to these 11 dogs. One half hour after furosemide, shunt decreased slightly without decreasing EVLW in all 11 dogs, but by two hours, seven dogs (group 1) decreased EVLW (from 23.2 +/- 1.8 to 11.1 +/- 1.4 ml/kg) and shunt (37.4 +/- 2.0 to 12.9 +/- 2.9 percent), while four dogs (group 2) did not (EVLW: 22.3 +/- 1.4 to 22.5 +/- 0.6 ml/kg: shunt, 36.8 +/- 1.7 to 36.5 +/- 1.9 percent). Group 1 had diuresis, maintained normal blood urea nitrogen and creatinine levels, and increased COP from 17.7 +/- 0.7 to 23.6 +/- 0.5 mm Hg while group 2 was oliguric with elevated BUN and creatinine values and showed no change in COP (17.9 +/- 0.9 to 18.3 +/- 0.6 mm Hg) after furosemide. After decreasing PWP in massive pulmonary edema (triple baseline EVLW), furosemide appeared to enhance edema clearance by changes in COP with diuresis.
 ...
PMID:Colloid osmotic pressure in pulmonary edema clearance with furosemide. 362 34

To determine whether circulating leukocytes contribute to gas exchange abnormalities in diffuse lung injury, we retrospectively examined oxygenation in 6 patients who met 3 criteria: leukopenia caused by marrow aplasia from remission-inducing chemotherapy for myelogenous leukemia, the eventual resolution of leukopenia, and concurrent acute respiratory failure diagnosed clinically as increased permeability pulmonary edema. Four of the 6 patients abruptly developed overt clinical evidence of pulmonary dysfunction within the 96 h preceding the resolution of the peripheral leukopenia. In all 6 patients, the alveolar to arterial oxygen tension difference increased between leukocyte counts. The mean value for the alveolar to arterial oxygen tension difference for the group doubled during this period (148 +/- 37 mmHg 3 days prior to resolution; 290 +/- 37 mmHg 1 day after resolution; p less than 0.05). As an index of lung capillary permeability, we measured the lung permeability-surface area product for urea (PSu) for an additional patient with oxygen toxicity and drug-induced leukopenia whose hypoxemia increased immediately before the resolution of leukopenia. The PSu in this patient was high, in the range previously reported as being highly specific for increased permeability pulmonary edema with a fatal outcome. We conclude that such diffuse lung injury resembling the adult respiratory distress syndrome can occur in leukopenic patients, but the resolution of leukopenia in such patients may be associated with worsening oxygenation and with abnormally high pulmonary microvascular permeability. These observations do not prove a causal relationship but provide a clinical parallel to several leukocyte-depletion studies reported in animal models of increased permeability pulmonary edema that implicate white blood cells in the pathogenesis of hypoxemia and lung edema.
 ...
PMID:Deterioration of oxygenation and abnormal lung microvascular permeability during resolution of leukopenia in patients with diffuse lung injury. 399 52

One case of severe varicella pneumonia with high microvascular permeability pulmonary edema and signs of multiple system organ disfunction was successfully treated by means of hemofiltration. The patient was discharged from the Intensive Care Unit 6 days after admission. Peptides showing molecular weight ranging between 600 (prostaglandins) and 4000 (B-endorphin) daltons were cleared from blood at the same rate as urea. Hemofiltration appears to be a valuable tool for treating septic ARDS.
 ...
PMID:Hemofiltration in severe septic adult respiratory distress syndrome associated with varicella. 408 8

During single pass indicator studies across the lungs [(14)C]urea remains in the vascular compartment, but its molecular size and solubility suggest it might escape abnormally permeable vessels. To test the hypothesis that [(14)C]urea might be used to distinguish pulmonary edema due to acutely increased intravascular pressure from that due to vascular damage by alloxan, we studied [(51)Cr]erythrocytes (r), [(125)I]albumin (a), [(14)C]urea (u), and tritiated water as dilution indicators in the pulmonary circulation of anesthetized dogs. In addition, the adequacy of albumin as an intravascular indicator was evaluated. Indicator curves, blood gases, hematocrit, and vascular pressures were determined during a base-line period and repeated 30 and 60 min after treatment in five groups of dogs: (a) saline control. (b) alloxan edema. (c) epinephrine infusion, (d) volume overload, and (e) left atrial (LA) balloon obstruction.Groups b, d, and e developed a similar degree of edema judging by wet/dry lung weights and histology. Groups a and c did not develop edema. In alloxan edema, differences between the mean transit time volume of u and r (V(v-r)) increased over base line at 30 (P < 0.001) and 60 min (P < 0.02); the differences between the mean transit time volume of a and r (V(e-r)) increased slightly at 30 (P < 0.03) and 60 min (P < 0.02); and V(u-r) significantly exceeded V(a-r) at 30 (mean difference = 9 ml, P < 0.02) and 60 min (mean difference = 11, P < 0.04). In none of the other groups did V(u-r) significantly exceed V(a-r). Thus, comparison of V(u-r) with V(a-r) may permit distinction between "high pressure" and "increased permeability" pulmonary edema. Albumin was not a consistently reliable indicator of intravascular volume as compared with composite red cell and albumin curve.
 ...
PMID:In vivo assessment of pulmonary vascular integrity in experimental pulmonary edema. 457 97


<< Previous 1 2 3 4 5 6 Next >>