ABSTRACT
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.
Subject(s)
Liver Diseases/enzymology , Lung Diseases/enzymology , Peptidyl-Dipeptidase A/metabolism , Adult , Female , Hospitalization , Humans , Liver Diseases/complications , Lung Diseases/complications , Male , Middle Aged , Peptidyl-Dipeptidase A/blood , PrognosisABSTRACT
Administration of endotoxin prior to an LD50 dose of thiourea protected rats against pulmonary edema and pleural effusion. These results are similar to those seen with endotoxin pretreatment and pulmonary O2 toxicity.
Subject(s)
Endotoxins/pharmacology , Pleural Effusion/prevention & control , Pulmonary Edema/prevention & control , Thiourea/antagonists & inhibitors , Animals , Escherichia coli , Male , Pleural Effusion/chemically induced , Pulmonary Edema/chemically induced , Rats , Time FactorsABSTRACT
Intraperitoneal administration of paraquat to mice produced a linear dose-response increase (20 to 50 mg/kg of body weight) in serum angiotensin converting enzyme (ACE). The peak increase (31%) in ACE occurred after 50 mg/kg of paraquat and began at approximately 4 h. ACE was still significantly elevated 8 h after the administration of paraquat, but it began to return to normal 24 h later. Although serum ACE increased during the first 5 h after the administration of paraquat, lung ACE decreased. The enzyme that we measured in mouse serum was inhibited 100% by 10(-7) M of SQ 20881, a known ACE inhibitor.
