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)

Rats were exposed under static conditions to phosgene at concentrations within the LCt50 range and above. Lungs were removed at various postexposure intervals. Degrees of pulmonary edema were estimated by increases in percentage of water in the lungs of exposed groups as opposed to control animals. Lungs were fractionated into four major subcellular organelle fractions: nuclear debris, mitochondrial-lysosomal, microsomal, and soluble (cytoplasmic). Activities of p-nitrophenyl phosphatase, cytochrome C oxidase, ATP'ase, and LDH within these fractions were decreased after phosgene exposure. There was a concomitant increase in serum LDH levels. One possible mechanism that may play a role in phosgene damage can be associated with either inhibition or loss of enzyme activities from the lung.
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PMID:Effect of phosgene on rat lungs after single high-level exposure. 20 Dec 20

A 63 year old female, who was admitted to a psychiatric hospital for schizophrenia, was referred to our emergency room because of sudden loss of consciousness and convulsions. On arrival, she was drowsy and hypoxemic. Her chest X-ray showed cardiomegaly with pulmonary edema. ECG showed marked ST depression in precordial leads and serum chemistry revealed marked elevation of CPK, GOT and LDH along with hyponatremia and hypochloremia. She was immediately admitted to CCU on suspicion of acute non-transmural myocardial infarction complicated with congestive heart failure. After fluid restriction and intravenous infusion of dopamine she passed large amount of urine, and her consciousness level, electrolyte imbalance and ECG change, improved gradually. Although serum CPK level increased as high as 32,307 IU/ml, there were no signs of left ventricular asynergy on UCG and CPK isozyme analysis performed later revealed more than 99% of serum cCPK was MM-type. We concluded that water intoxication was the cause of the ECG change and the elevated serum CPK, GOT and LDH levels. There are few reports on elevated CPK level in association with water intoxication, in which rhabdomyolysis is speculated as the cause of CPK elevation. But there is no report on ECG change complicated with water intoxication. In our case, electrolyte imbalance caused by water intoxication seemed to play a major role in ST depression and QT prolongation. Although water intoxication is a rare disorder in the general population, it is not infrequent among patients with psychiatric diseases. Care must be taken when such patients present ECG change and serum enzyme elevation mimicking ischemic heart disease.
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PMID:[A water intoxication patient who showed remarkable ST depression and suspected ischemic heart disease]. 152 80

Paraquat is a herbicide known to cause pulmonary edema in its acute toxic phase. Many investigators showed that paraquat induces morphological changes of alveolar epithelial cells even in its early phase. Controversy still exists, however, as to whether pulmonary vascular endothelial cells are also morphologically vulnerable to paraquat. To test the direct toxicity and metabolic changes of pulmonary vascular endothelial cells after paraquat addition, porcine pulmonary artery endothelial cells (PPAEC) were cultured. Thrombin- or bradykinin-stimulated PGI2 production was enhanced significantly, and the angiotensin converting enzyme (ACE) activity of cell lysate of PPAEC was significantly suppressed after a 24-hour incubation with 10(-4) M of paraquat. No further thrombin-induced enhancement of PGI2 production was noted after a 48-hour incubation. The alterations in arachidonic acid metabolism and ACE activity mentioned above did not result from cytotoxicity of paraquat because LDH release into culture medium was not increased during 72 hours of incubation with paraquat. Longer incubation more than 48 hours, in turn, induces obvious toxic effects on PPAEC.
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PMID:[Arachidonic acid metabolism and angiotensin converting enzyme activity by cultured porcine pulmonary artery endothelial cells are affected with paraquat]. 166 45

A 48-year-old man with small cell lung cancer developed ARDS, and massive pulmonary edema fluid was obtained with the fiberoptic bronchoscopy. The pulmonary edema fluid to serum ratios of total protein and albumin were 0.72 and 0.85 respectively. The ratio of LDH was higher (2.71), while that of cholesterol was lower (0.11) than that of total protein. Simultaneously, isopropyl N [I-123] p iodoamphetamine (I-123 IMP) and I-131 human serum albumin (I-131 HSA) were injected into this patient. Samples of blood and pulmonary edema fluid were collected to measure the clearance through the pulmonary microvasculature. The time activity curves of I-123 IMP and I-131 HSA in his blood samples revealed almost constant radioactivity from 5 minutes to 120 minutes after injection, while both radioactivity levels in pulmonary edema fluid samples increased with time. The clearance ratio of I-123 IMP to I-131 HSA was constant at each sampling time (mean +/- SD, 1.51 +/- 0.32). The linear correlation between I-123 IMP clearance and I-131 HSA clearance (r = 0.95, p less than 0.01) suggested that the clearance ratio of exudative plasma components may remain unchanged even if pulmonary microvasculature permeability has changed.
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PMID:[Assessment of the permeability of the pulmonary microvasculature using radiotracers in a case of adult respiratory distress syndrome]. 185 5

Methods of clinico-instrumental investigation and biochemical monitoring (CPK and its membranous fraction) were employed for examination of 432 patients with acute myocardial infarction (AMI). Among them there were patients with an uncomplicated course of disease (19.4%), recurrences (13.7%) and AMI spreading (9%). Lung edema, a cardiogenic shock, ventricular fibrillation and complicated cardiac rhythm disorders were not detected on the 1st day of disease. Clinico-anamnestic data provided no opportunity for defining factors promoting AMI recurrences whereas AMI spreading frequently developed in patients with repeated AMI, suffering from essential hypertension, obesity and heart failure. Higher diastolic pressure in the pulmonary artery, an increase in the cardiac volume, a decrease in the ejection fraction and left ventricular stroke work--changes which were most pronounced in AMI spreading, were noted in patients with AMI lingering forms. Signs of disseminated intravascular blood coagulation were noted in the venous and arterial blood of patients with lingering AMI forms. A high blood enzyme level was shown to be accompanied by a low level of antibodies to LDH and CPK.
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PMID:[Clinico-pathogenetic variants of protracted forms of acute myocardial infarct]. 361 39

In summary, we have described our method of treating phosgene inhalation injury. We have presented two serious cases in detail which demonstrate that survival was associated with aggressive therapy. Several points should be mentioned. The pulmonary edema and resulting fluid and foam production can be so copious as to overwhelm efforts to place an endotracheal tube. The solution is early intubation by the nearest experienced person at the first hint of edema or pulmonary failure. Adequate support of the patient's blood volume is imperative to avert hypovolemic shock and renal failure. A balloon flotation catheter is desirable to monitor pulmonary wedge pressure and avoid overload. Follow-up pulmonary function studies and chest x-rays are recommended 2-3 months after hospital discharge. We have not yet found a reliable test to determine which cases will progress to pulmonary edema. The LDH appears to be the only consistently elevated sign in more serious cases. Finally, we would like to make a plea for the sharing of information from instances of fatal phosgene injury so that the facts can be studied and applied to future cases.
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PMID:Review of clinical experience in handling phosgene exposure cases. 391 30

A case of subarachnoid hemorrhage complicated by neurogenic pulmonary edema and neurogenic myocardial damage is reported. A 50-year-old woman was admitted following the sudden onset of headache and disturbance of consciousness due to a ruptured internal carotid posterior communicating artery aneurysm on the right side. She showed respiratory failure due to pulmonary edema, which subsequently improved with the mechanical ventilation. After that, she manifested chest distress and hypotensive episode then occurred. An ECG showed QS wave and ST elevation which suggested the presence of inferolateral myocardial damage. Subsequent rises in serum GOT, GPT, LDH and CPK were noticed. CPK-MB and LDH I and V isozyme levels rose. An echo cardiogram showed hypokinesis of the apical half of the left ventricular septum. The patient died on 5th hospital day due to rerupture of the cerebral aneurysm. Autopsy revealed diffuse myocytolysis with coagulation necrosis of the heart muscle without occlusion of coronary arteries. A small hemorrhagic lesion was found in the hypothalamus. We suggested that a hypothalamic lesion due to subarachnoid hemorrhage stimulated the sympathetic nervous system which in turn discharged endogenic catecholamine. This was probably accompanied by vasospasm of the coronary arteries and systemic peripheral arterioles. Furthermore, myocardial oxygen consumption could have been increased by the increase in catecholamine. Finally, it gave rise to neurogenic pulmonary edema and extensive diffuse myocytolysis of the heart occurred.
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PMID:[Myocardial damage (myocytolysis) caused by subarachnoid hemorrhage]. 409 85

Toxicological effects of fenvalerate on rat lungs by bronchoalveolar lavage (BAL) and biochemical changes in 20 workers exposed to fenvalerate were studied. The results showed that the levels of CPK, albumin, TP, AKP, ACP, alpha 1-AT, MDH, LDH, glucose, and lactic acid in BAL fluid increased significantly, with a CPK level the most sensitive one. most of the above parameters in BAL fluid changed four hours after exposure and returned basically to normal on the fourth day after exposure. Only the levels of ACP, alpha 1-AT and albumin were found increased in their blood. It showed a good linear relationship between blood and BAL levels of alpha 1-AT and ACP. Changes in some biochemical parameters were also found in workers exposed to fenvalerate, which correlated to the length of their employment. The results suggested inhalation of fenvalerate may cause alveolitis, pulmonary edema, and damage to lung cells.
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PMID:[Biochemical and toxicological studies of fenvalerate on the lung]. 813 61

To evaluate the self-expandable metallic stent therapy for inferior vena caval obstruction (IVCO) secondary to malignant liver tumors, changes in caval pressure, the symptoms and hemobiochemical values were observed. Among 16 IVCO cases with higher caval pressure than 20 cmH2O at the peripheral caval lumen to the stenosis, nine cases consisting of five extracaval compression cases and four intravenous tumor thrombi cases subjected the stent therapy. Other three subjected radiotherapy and the other four cases inactive supportive care. Immediately after the Z-stent implantation, the averaged caval pressure distal to the stenosis decreased from 27.7 +/- 3.5 cmH2O to 14.7 +/- 2.6 cmH2O. One case developed 8 cmH2O increase of right atrial pressure but no lung edema. The urine excretion volume increased after stent. The decrease in caval pressure correlated with the urine volume of the day after the stenting (gamma = 0.83), symptomatic improvements of leg edema (gamma = 0.68), ascites (gamma v 0.51) and scrotal edema (gamma = 0.70). Five cases showed gradual increase in platelet number. All elevated LDH and elevated fibrinogen value decreased. These changes would suggest physiologic benefits of the IVC stent therapy. Compression cases showed better improvements and courses than the thrombi cases. Two thrombi cases endured severe conditions suspected of triggered by the procedure. Conclusively, the stent therapy to the IVC obstruction was thought to effect hemodynamically and hematobiochemically.
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PMID:[Self-expandable metallic stent therapy for inferior vena cava obstruction secondary to malignancy: clinical observations]. 819 Jun 8

We report three cases of drug-induced hemolytic uremic syndrome (HUS). Three patients with advanced gastrointestinal cancer underwent a curative operation and adjuvant chemotherapy with Mitomycin C (MMC), 5FU and Ara-C. Later, progressive anemia, thrombocytopenia, renal dysfunction and elevation of serum LDH were recognized. A diagnosis of HUS was made. As they had no symptoms of infectious diseases or relapse of cancer, the cause of HUS was thought to be MMC. Treatment with antiplatelet drugs and fresh frozen plasma was effective for two patients. However, one patient died of pulmonary edema.
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PMID:[Three cases of drug-induced hemolytic uremic syndrome]. 871 31


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