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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Purification of angiotensin I-converting enzyme from human lung and characteristics of the enzyme was studied. Experimental pneumonitis was produced in rabbits and the change of the activity of angiotensin I-converting enzyme was studied in purpose to clarify the role of this enzyme in the metabolism of vasoactive peptides in the lung. Purification was performed using trypsin treatment, acid treatment, DE52-cellulose column chromatography, hydroxyapatite chromatography and Sephadex G-200 gel filtration. The enzyme after final step showed a single band on disc gel electrophoresis. Experimental pneumonitis was produced by injection of Complete Freund's adjuvant (acute pneumonitis) and of N-nitroso-N-methylurethane (chronic pneumonitis). In acute experiment, angiotensin I-converting enzyme activity in pulmonary tissue and in plasma was significantly decreased. In perfusion experiment, conversion of angiotensin I to angiotensin II and inactivation of bradykinin were also significantly decreased. In case of decreased activity of angiotensin I-converting enzyme in the lung, less angiotensin II will be released into systemic circulation and bradykinin will pass through the pulmonary circulation into systemic circulation, thus this may result in the decrease of systemic blood pressure.
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PMID:Purification and properties of angiotensin I-converting enzyme in human lung and its role on the metabolism of vasoactive peptides in pulmonary circulation. 22 10

Substantial differences between mouse strains have been reported in the lesions present in the lung during the early phase of radiation injury. Some strains show only classical pneumonitis, while other strains develop substantial fibrosis and hyaline membranes which contribute appreciably to respiratory insufficiency, in addition to pneumonitis. Other strains are intermediate between these extremes. These differences correlate with intrinsic differences in activities of lung plasminogen activator and angiotensin converting enzyme. The genetic basis of these differences was assessed by examining histologically the early reaction in lungs of seven murine hybrids available commercially after whole-thorax irradiation. Crosses between fibrosing and nonfibrosing parents were uniformly nonfibrosing, and crosses between fibrosing and intermediate parents were uniformly intermediate. No evidence of sex linkage was seen. Thus the phenotype in which fibrosis is found is controlled by autosomal recessive determinants. Strains prone to radiation-induced pulmonary fibrosis and hyaline membranes exhibited intrinsically lower activities of lung plasminogen activator and angiotensin converting enzyme than either the nonfibrosing strains or the nonfibrosing hybrid crosses. The median time of death of the hybrids was genetically determined primarily by the longest-lived parent regardless of the types of lesions expressed.
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PMID:The genetic basis of strain-dependent differences in the early phase of radiation injury in mouse lung. 185 22

In spite of the development of various antibiotics, management of elderly patients with pneumonia remains an important problem. It is suggested that adult respiratory distress syndrome (ARDS) and disseminated intravascular coagulation (DIC) often occur in elderly patients with pneumonia. Although neutrophils are suggested to be involved in the genesis of these conditions, details remain unknown. We demonstrated that a highly cytotoxic substance, 9,10-epoxy-12-octadecenoate, is biosynthesized from linoleate by human neutrophils, thus it was named leukotoxin. Leukotoxin was detected in lung lavages from patients with ARDS. In these lung lavages, increases in albumin concentration and angiotensin converting enzyme (ACE) activity were also observed. Similar results were observed in lung lavages from rats after exposure to hyperoxia for 60 hours in an experimental model of ARDS. Intravenous administration of leukotoxin (100 mumol/kg) caused lung edema. Albumin concentration and ACE activity were increased in lung lavages of rats receiving leukotoxin. In contrast, these changes were not observed in rats administered with linoleate. Furthermore, administration of leukotoxin (100 mumol/kg) caused coagulation abnormality, i.e., increase in fibrin-fibrinogen degradation products, decrease in fibrinogen, and prolongation of activated partial thromboplastin time and prothrombin time. Administration of linoleate did not induce these changes. It is indicated that O2- was produced by respiratory burst enzyme located in neutrophil plasma membrane, and that hydroxyl radicals derived from O2- by Fenton reaction were responsible for leukotoxin synthesis. From our results, leukotoxin, a product of hydroxyl radicals and linoleate, might be responsible for the genesis of ARDS and DIC.
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PMID:[Leukotoxin and pulmonary injury]. 238 90

The ability of WR 2721 to protect endothelial cells and Type II cells in mouse lung after single doses of X rays was studied using specific assays of cell function to assess damage. The whole thorax of mice was exposed to a range of single doses of X rays either alone or 30 minutes after an i.p. injection of 400 mg/kg of WR 2721. Endothelial cell function was assayed by angiotensin converting enzyme (ACE) and Type II cell function by phosphatidylcholine and total protein present in lavage fluid 28 days after radiation. Similar protection factors (PFs) were found for the functional activity of both cell types, 1.2 and 1.24 for ACE and phosphatidylcholine respectively. These values were somewhat less than the PF of 1.37 for lethality from pneumonitis 7 to 9 months after irradiation for this mouse strain. The lack of a clear difference between the PFs for the functional activity of these two cell types suggests that neither the endothelial cell nor the Type II cell can be accepted or excluded as the target cell for radiation pneumonitis in lung.
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PMID:WR 2721 modification of type II cell and endothelial cell function in mouse lung after single doses of radiation. 304 Jun 47

At present we do not possess a specific marker of broncho-pulmonary cancers. We propose to test the specificity of six serum markers labelled by radio-immunological methods (CA-50, CA-19.9, CA-125, CA-15.3, enolase, ACE) in 60 patients suffering from non-tumoural broncho-pulmonary disorders: chronic airflow obstruction = 28, acute infective bronchopulmonary disorders = 23, allergy = 9. We have not found any correlation between the percentage of false positives and sex, age or smoking. On the other hand, the CA-125 was often found to be positive in cases of acute pneumonia. Overall the frequency of false positives with ACE (3.3%) enolase (6.7%) and CA-15.3 (5%) is weak. The threshold of positivity obtained is adequate. This is not the case with CA-50 (33.3%), CA-19.9 (13.3%) and above all CA-125 (53.3%), for these we suggest new thresholds of positivity.
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PMID:[Blood levels of CA-50, CA-19.9, CA-125, enolase, CA-15.3 and carcinoembryonic antigen in non-cancerous bronchopulmonary pathology]. 321 89

Abnormal serum angiotensin converting enzyme (ACE) activity has been reported in various human lung disorders and in laboratory animals with acute lung injuries. To test the value of serum ACE activity as an indicator of lung damage and its assistance in diagnosis or prognosis, 328 serum samples were obtained from 108 hospitalized patients with lung disease and 26 normal subjects. When patients were clinically grouped by disease entity, only the sarcoidosis group showed elevated mean serum ACE. Significantly increased serum ACE was found in 17 patients with various lung diseases (15% of hospitalized patients) 12 of whom also had concomitant liver disease. It is hypothesized that the liver may play a role in the normal metabolism of ACE being released by lung endothelial injury. Significantly low levels were seen in many acute and chronic lung injuries; specifically the groups with chronic obstructive lung disease, lung cancer, acute pneumonia, aspiration pneumonitis, gram-negative sepsis, acute myocardial infarction, and congestive heart failure. Serial measures of ACE in 71 patients with lung injuries showed that significantly decreasing levels over successive days were associated with a very high mortality. A single ACE measurement did not predict the presence or extent of lung injury, or aid in diagnosis or prognosis, but serial levels are of value prognostically.
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PMID:The value of serial serum angiotensin converting enzyme determinations in hospitalized patients with lung disease. 609 28

Thirty four beagle dogs, male and female were orally given 10, 30, 100 and 200 mg/kg/day of captopril, an angiotensin converting enzyme inhibitor, for 3 months followed by a recovery test for 4 weeks. One of 4 female dogs which were treated with the highest dose of 200 mg/kg/day throughout the experimental period died of bronchial pneumonia. Hypersalivation and occasionally vomiting was observed in dogs treated with 100 and 200 mg/kg/day. Skin eruption such as erythema and papules was observed mostly at the ventral surface of the neck, chest and upper abdomen in dogs in these two experimental groups. Histological examination of the lesion revealed cellular infiltration with edema and expansion in the dermis and slight hyperkeratosis with parakeratosis and acanthosis. Changes in erythrocyte counts, hematocrit values and hemoglobin contents during the course of administration were variable among dogs but these were obvious in animals treated with higher doses. An increase in erythropoiesis of the bone marrow, extramedullary hematopoiesis and slight hemosiderosis in liver and spleen were revealed by histological examination. Above histological observations suggest that captopril may cause hemolysis. Hypertrophy and hyperplasia of juxtaglomerular cells with increased number of JG granules were shown in the highest dosage group even 4 weeks after suspension of captopril administration. A distinct plasma renin activity supported the morphological changes. From the results of three months administration of captopril to beagle dogs, the maximum non-toxic dose may be around 10 mg/kg/day and toxic dose 100 mg/kg/day.
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PMID:[Three month subacute toxicity of captopril in beagle dogs]. 627 85

The effects of alacepril, an angiotensin converting enzyme inhibitor, on atherogenesis were examined in rabbits fed a hypercholesterol diet. The process of atherogenesis was evaluated in vitro by high-resolution transesophageal ultrasonography (TEE phi 4 mm, 7.5 MHz), by direct histological examination and by serum lipid examination. Of the 38 subjects, 18 were designated as the control hypercholesterol group (CH) and 20 received oral alacepril at 90 mg/day (ACE) for 13-22 weeks. Three rabbits in each group died due to pneumonia. TEE enabled a clear diagnosis as either normal, early stage or late stage of atherosclerosis. The intimal-medial thickness was significantly less in the ACE group than in the CH group, but only over the middle portion of the aorta. The ACE group had a smaller area of atheromatous plaque than the CH group (atheromatous index: 37 +/- 20* and 60 +/- 30% respectively, *p < 0.02). Serum cholesterol and triglycerides were similar in the CH group (1590 +/- 653, 258 +/- 224) and the ACE group (1574 +/- 824, 303 +/- 360 respectively). In conclusion, alacepril reduced both the area of atheromatous atheroma plaque and wall hypertrophy independent of serum lipids in cholesterol-fed rabbits. In vitro miniature TEE is a dependable method for evaluating atherosclerosis in rabbits with hypercholesterolemia.
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PMID:The ACE inhibitor alacepril suppresses atherogenesis independent of serum lipids in cholesterol-fed rabbits--critical analysis with new ultrasound technique. 780 84

Cough is known to be the major respiratory side effect of treatment with angiotensin converting enzyme inhibitors (ACEI). Recently, ACEI have been implicated in drug-induced lung disease. We report a new case of diffuse pneumonitis which occurred during treatment with ACEI. A 73-year-old man was admitted for cough, dyspnea at rest, fever and weight loss. The patient had been treated with the ACEI pirindopril during 6 months for systemic hypertension. Chest radiographs showed reticular infiltrates in the upper lung fields. A CT scan confirmed the infiltrates and showed pleural thickening and airspace opacities. White blood cell counts showed 15,700/mm3 leucocytes with 940 eosinophils/mm3. Transbronchial biopsy was consistent with infiltration of the lung with eosinophils. There was no evidence for another etiology. Once the drug was withdrawn, clinical and radiological abnormalities improved but steroids were required to control symptoms. This report suggests that pirindopril, as captopril, can induce the picture of drug-induced pulmonary disease.
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PMID:[Pneumopathy induced by pirindopril. A case report]. 804 99

In a 63-year-old woman with longstanding type I diabetes mellitus, CAD and chronic heart failure, a subacute myocardial infarction developed, together with decompensation of cardiac function and diabetes and concurrent pneumonia. Acute heart failure with acute renal failure on top of diabetic nephropathy, and interstitial pulmonary edema was initially treated with hemofiltration and catechol amines together with antibiotic and perfusor-regulated insulin therapy, and systemic heparinization. Subsequent chronic treatment with digitalis, acetyl salicylic acid, insulin and a combination of an ACE inhibitor and a loop diuretic resulted in an improvement of heart failure to NYHA functional class II where PTCA of coronary multi-vessel disease could be performed with low risk.
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PMID:[Heart failure after myocardial infarct in decompensated diabetes mellitus. Acute therapy with catecholamines--long-term therapy with ACE inhibitor-loop diuretic combination]. 937 33


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