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)

Reduced oxygen tension is regarded as the primary physiologic signal for the production of erythropoietin (EPO). There is little information available about early changes of EPO production in man due to severe hypoxia. The purpose of the present study was to examine the time course of EPO in serum of patients with acute cardiogenic pulmonary edema (ACPE). In 29 patients (seventy-five +/- six years, mean age +/- SEM) who were hospitalized within two hours after onset of symptoms of ACPE, serum EPO concentrations were monitored for up to seventy-two hours. At the moment of admission all patients showed significantly increased EPO concentrations of 121 +/- 64 mU/mL (mean +/- SEM) compared with a healthy population (15-35 mU/mL). Twenty-three patients who recovered within thirty minutes (group A) exhibited a quick return of their EPO serum levels to normal. The remaining 6 patients (group B) had a protracted clinical course and their EPO concentration showed a further increase up to the end of the observation period. The comparative monitoring of concentrations of alpha-1-proteinase inhibitor, antithrombin III, C-reactive protein, fibronectin, hapotoglobin, and transerrin in serum and plasma revealed no significant changes. Thus a major contribution of fluid shifts into or from the intravascular compartment to the observed changes in EPO concentration seems to be unlikely. The data suggest that the production and release of EPO in the kidneys due to altered oxygen delivery is a fast-responding mechanism.
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PMID:Serum-erythropoietin concentration during acute cardiogenic pulmonary edema. 201 19

Acute gestational pyelonephritis infrequently leads to nonhydrostatic permeability pulmonary edema known clinically as acute respiratory distress syndrome (ARDS). In this form of ARDS, sepsis is considered the primary cause of pulmonary dysfunction. Decreases in colloid osmotic pressure, plasma fibronectin, and arterial oxygen saturation are associated with a worsening prognosis in septic conditions. We sought to investigate the changes in these parameters with acute gestational pyelonephritis to gain insight into the factors that may place the patient at risk for sepsis-related morbidity. Colloid osmotic pressure, plasma fibronectin, and arterial oxygen saturation via pulse oximetry were prospectively measured during the inpatient treatment of 17 pregnant patients with acute gestational pyelonephritis. All three parameters achieved their nadir within 24 hours of hospitalization and the initiation of therapy. Although no patient developed significant pulmonary dysfunction, we believe that patient susceptibility for pulmonary edema and general morbidity could be maximal in the first 24 hours after therapy. Future studies using a larger number of patients may identify one or more of these laboratory parameters as helpful in identifying gravid patients who are at risk of developing gestational ARDS.
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PMID:Acute gestational pyelonephritis: the impact on colloid osmotic pressure, plasma fibronectin, and arterial oxygen saturation. 202 86

Basic therapeutic methods based on early diagnosis of septic ARDS were described. Concerning early diagnosis exertional hypoxemia and increased broncho-vascular markings on chest X-ray were observed in the pre-ARDS stage of septic patients. These findings were also observed in the initial stage of endotoxin-induced pulmonary edema in rabbits and the basic mechanisms were thought to be as follows, based or our experimental studies. The former is related on impairment of alveolar diffusion and the latter reflect increased peri-vascular cuffing due to increase in pulmonary edema. The diffuse infiltrative shadows on the both back area in CT scanning was also a helpful sign indicating the early stage of pulmonary edema. This finding was seen at the stage at which the edematous shadow had not yet appeared on conventional chest X-ray. Increase in serum laminin and decrease in plasma fibronectin were also important biochemical findings predicting ARDS in gram negative sepsis. Using these findings, it is considered that early prediction of septic ARDS is possible. Concerning therapeutic methods based on early prediction, the usefulness of cortico-steroids and the protease inhibitor "Urinastatin" were observed in experimental in vitro and in vivo studies. Some findings induced by endotoxin administration in rats or rabbits, such as the increase in endotoxin in peripheral blood, the distraction of PMN-elastase, the increase in pulmonary lymph flow and mortality within 48 hours were significantly suppressed by simultaneous treatment by corticosteroid. In an in vitro study, PMN superoxide production and elastase release following incubation of endotoxin and PMNs were significantly inhibited by adding a concomitant level of corticosteroid and/or urinastatin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Sepsis and ARDS]. 203 89

The effects of intravenous (IV) ritodrine therapy on capillary endothelial damage and colloid osmotic pressure were examined in 15 patients in premature labor. Plasma fibronectin, a marker for capillary endothelial damage, did not change significantly after IV ritodrine therapy. Plasma colloid osmotic pressure was lowered following ritodrine therapy (P less than 0.05). Pretreatment plasma fibronectin levels in the study and control groups were similar. Interestingly, pretreatment colloid osmotic pressure in the study group was significantly lower than that of the control group (P less than 0.05). Our data suggest that there is no evidence of capillary endothelial damage following ritodrine therapy. Lower levels of plasma colloid osmotic pressure in patients with preterm labor, which are further reduced with IV ritodrine therapy, may predispose these patients to pulmonary edema.
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PMID:Does intravenous ritodrine therapy cause capillary endothelial damage? 365 Nov 92

Plasma fibronectin (FNp) concentrations were measured in 63 patients with acute respiratory failure and 28 patients with circulatory failure, using Laurell's electroimmunoassay method. Measurements were made in the acute phase and repeated in the course of the disease. The mean FNp concentration in 20 controls was 262 +/- 59 mg/l. FNp values were normal in the acute phase of chronic obstructive pulmonary disease and in cardiogenic pulmonary oedema. In contrast, they were significantly decreased in adult respiratory distress syndrome and in acute pneumonia, as well as in acute circulatory failure, notably from septic shock. FNp values were also considerably reduced in patients with severe disseminated intravascular coagulation syndrome. Clinical improvement was accompanied by a return to normal of FNp concentrations. The mortality rate was greater in patients with low FNp values than in those with normal values.
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PMID:[Acute respiratory and circulatory failure. Prognostic value of plasma fibronectin levels]. 622 Mar 70

We produced an experimental adult respiratory distress syndrome model by intravenous administration of oleic acid (OA) in 30 dogs (Group I: 10 normal dogs; Group II: 10 dogs with 0.02 ml/kg of OA; Group III: 10 dogs with 0.04 ml/kg of OA; Group IV: 10 dogs with 0.08 ml/kg of OA). Changes in albumin (AL) and fibronectin (FN) in serum and BALF of these dogs were examined. The following results were obtained: 1) Serum values of AL and FN were significantly decreased after OA injection as compared with the baseline values. These changes were not correlated with the severity of pulmonary edema. 2) BALF values of AL and FN were significantly increased after OA injection as compared with the baseline values. Significant linear correlations were found between the BALF value of AL and ELWV, and between BALF value of AL and delta ELWV, [r = -0.682, 0.573 (p < 0.01)]. Significant linear correlations were also found between the BALF value of FN and ELWV, and the BALF value of FN and delta ELWV, [r = 0.722, 0.650 (p < 0.01)]. BALF value of AL increased significantly even with the low OA dose (0.02 ml/kg). Thus in comparison with BALF value of AL after OA injection, BALF value of FN was significantly higher than that in the normal group even when pulmonary edema were severe (Groups III and IV). We concluded that we could estimate the severity of pulmonary edema by measuring BALF value of AL and FN simultaneously.
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PMID:[Albumin and fibronectin dynamics in an experimental adult respiratory distress syndrome model]. 851 14

The monocrotaline pyrrole (MCTP)-treated rat is a useful model for the study of certain chronic pulmonary vascular diseases. A single, i.v. administration of a low dose of MCTP causes pneumotoxicity, pulmonary vascular remodeling, sustained increases in pulmonary arterial pressure, and right ventricular hypertrophy in rats. The pulmonary vascular lesions are characterized by endothelial cell alterations, platelet and fibrin microvascular thrombosis, pulmonary edema, and thickening of the intimal and medial layers of the vessel wall. These lesions suggest that some dysfunction of the hemostatic system occurs in the lungs of rats treated with MCTP. We evaluated the concentrations of two adhesion proteins, cellular fibronectin (cFn) and von Willebrand factor (vWF), in the plasma of rats treated with MCTP. We hypothesized that changes in these factors occur along with markers of pneumotoxicity and ventricular hypertrophy and that such changes might contribute to the genesis of the vascular lesions. Enzyme-linked immunosorbent assays were used to measure cFn and vWF concentrations in the plasma of rats after MCTP treatment. Rats treated with a single i.v. injection of 3.5 mg MCTP/kg body weight had delayed and progressive lung injury characterized at 5 days post-treatment by increases in the lung-to-body weight ratio and in lactate dehydrogenase activity and protein concentration in cell-free bronchoalveolar lavage fluid (BALF). Values for these markers were further increased at 8 days and reached a plateau thereafter. The number of nucleated cells within the BALF was increased at 8 and 14 days. Right ventricular hypertrophy, an indirect marker of pulmonary hypertension, was evident at 14 days. The cFn concentration was increased in plasma in rats at 8 and 14 days after treatment with MCTP. There was no difference between the vWF concentration in plasma of rats treated with MCTP and those treated with vehicle at any time. We conclude that an increase in plasma cFn concentration occurs prior to the onset of right ventricular hypertrophy and that this change is consistent with a role for cFn in the genesis of vascular remodeling and pulmonary hypertension in the MCTP-treated rat. The lung vascular injury and pulmonary hypertension in this model were not reflected in altered vWF concentration in the plasma.
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PMID:Cellular fibronectin and von Willebrand factor concentrations in plasma of rats treated with monocrotaline pyrrole. 861 88

Anti-CD7-dgA, DA7, consists of deglycosylated ricin A chain coupled to a mouse monoclonal anti-human CD7 antibody. This study determined the maximally tolerated dose (MTD) of this immunotoxin administered as a one hour infusion over five days to 11 patients with T-cell lymphoma (>30% CD7+ malignant cells). The MTD was 0.2 mg/kg/day or 1 mg/kg/120 hours (maximal toxicity grade 3) with vascular leak syndrome (VLS) as dose-limiting toxicity (DLT). Predictors of severe VLS included age and absence of circulating lymphoma cells. Two partial responses and one minimal response were seen. Patients with minimal lymphoma burden or T-cell large granular lymphocyte (LGL) leukemia showed the best responses. The mean maximal serum concentration of immunotoxin at the MTD was 2.5 ug/ml. The mean alpha-phase half-life was 1.5 hours and the mean beta-phase half-life was 8 hours. Repeated dosing had minimal effects on either peak serum immunotoxin concentrations or serum half-lives. While human antimouse antibodies were observed, they were low in concentration (<55 ng/ml). Human anti-ricin antibody was elevated in one patient (190 ng/ml). VLS presented with hypoalbuminemia, dyspnea, pulmonary edema, aphasia, and peripheral edema and cleared over a two week period. Serum fibronectin levels were measured in three patients and were very low in one patient who developed VLS. No specific binding of DA7 immunotoxin was seen with vascular endothelium in various human tissues.
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PMID:Therapy of patients with T-cell lymphomas and leukemias using an anti-CD7 monoclonal antibody-ricin A chain immunotoxin. 932 91

Fumonisin B(1) (FB(1)) is a mycotoxin produced by the phytopathogenic fungus Fusarium moniliforme, which structurally resembles sphingoid bases. FB(1) perturbs sphingolipid synthesis by inhibiting the activity of ceramide synthase. Depending on the host, ingestion of FB(1) causes equine leukoencephalomalacia or porcine pulmonary edema. It is also carcinogenic to rats and may play a role in certain human cancers. Previous studies showed that FB(1) repressed specific isoforms of protein kinase C and cyclin-dependent kinase 2 (CDK2) activity. Conversely, FB(1) induced expression of CDK inhibitors, p21(Waf1/Cip1), p27(Kip1), and p57(Kip2) in monkey kidney cells (CV-1). Consequently, FB(1) treatment of CV-1 cells leads to cell-cycle arrest and apoptosis. The baculovirus IAP gene (inhibitor of apoptosis), which blocks tumor necrosis factor (TNF)-induced apoptosis, protects several fibroblast cell types from apoptosis, suggesting the TNF pathway is important for FB(1)-induced apoptosis. To identify genes that are induced by FB(1), we used a PCR-based subtraction approach. Eight genes that showed high similarity (> 90%) to known mammalian genes were identified. These genes included: tumor necrosis factor type 1 receptor associated protein 2 (TRAP2), human leukemia virus receptor (GLVR1), human Scaffold attachment factor A (SAF-A) also called heterogeneous nuclear ribonucleoprotein U (hnRNP-U), human protein kinase C-binding protein (RACK7), human oligosaccharyl transferase STT3 subunit, mouse WW-domain binding protein 2 (WBP2), human fibronectin, and an unknown human clone. The ability of FB(1) to alter gene expression and signal transduction pathways may be necessary for its carcinogenic and toxic effects.
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PMID:Identification of differentially expressed genes following treatment of monkey kidney cells with the mycotoxin fumonisin B(1). 1125 50

Acute lung injury is usually a complication of sepsis, and endotoxin treatment of mice is a frequently used experimental model. To define this model and to clarify pathogenesis of the lung injury, we injected with 1 mg/kg endotoxin ip and measured pulmonary function, pulmonary edema, serum concentrations of cytokines and growth factors, and lung histology over 48 h. During the first 6 h, tidal volume and minute volume increased and respiratory frequency decreased. Serum concentrations of cytokines showed three patterns: 10 cytokines peaked at 2 h and declined rapidly, two peaked at 6 h and declined, and two had biphasic peaks at 2 and 24 h. Growth factors increased later and remained elevated longer. Both collagen and fibronectin were deposited in the lungs beginning within hours of endotoxin and resolving over 48 h. Histologically, lungs showed increased cellularity at 6 h with minimal persistent inflammation at 48 h. Lung water peaked at 6 h and gradually decreased over 48 h. We conclude that intraperitoneal administration of endotoxin to mice causes a transient systemic inflammatory response and transient lung injury and dysfunction. The response is characterized by successive waves of cytokine release into the circulation, early evidence of lung fibrogenesis, and prolonged increases in growth factors that may participate in lung repair.
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PMID:Endotoxin-induced lung injury in mice: structural, functional, and biochemical responses. 1547 80


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