Literature DB >> 8270718

Angiotensin-converting enzyme activity in serum and bronchoalveolar lavage fluid after damage to the alveolo-capillary barrier in the human lung.

R F De Jongh1, W A De Backer, R Mohan, P G Jorens, F J van Overveld.   

Abstract

OBJECTIVE: Angiotensin-converting enzyme (ACE) is considered as a possible marker for endothelial cell damage in serum or bronchoalveolar lavage fluid. This hypothesis was tested during cardiac surgery and during the adult respiratory distress syndrome.
DESIGN: We used patients with an expected different degree of endothelial cell damage. ACE levels in serum and bronchoalveolar lavage fluid were compared with indirect markers of alveolo-capillary barrier integrity.
SETTING: Interdisciplinary team in a university hospital.
METHODS: 13 Cardiac surgery patients received no glucocorticoids and 13 others received 2 g methylprednisolone before extracorporeal circulation. Thirteen patients were used as controls and 15 patients had nonseptic adult respiratory distress syndrome. All underwent bronchoalveolar lavage for ACE determination.
RESULTS: At different times during surgery serum angiotensin-converting enzyme levels were not significantly different between the two groups. In post-operative bronchoalveolar lavage fluid, angiotensin-converting enzyme levels were significantly higher in patients who received corticoids (27.8 +/- 1.7 U/l, mean +/- SEM), compared to patients without corticoids (19.8 +/- 1.4 U/l), control patients (18.2 +/- 1.3 U/l) or patients with full blown non-septic adult respiratory distress syndrome (18.8 +/- 1.1 U/l). There were no correlations between lavage angiotensin-converting enzyme and other parameters for alveolo-capillary membrane integrity in the lavage fluid such as the number of neutrophil cells, albumin or protein concentration, and between lavage angiotensin-converting enzyme and PaO2/FIO2 ratio during lavage.
CONCLUSION: Angiotensin-converting enzyme activity in serum or bronchoalveolar lavage fluid does not reflect damage of endothelial cells or damage of alveolocapillary integrity in acute pulmonary disease.

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Year:  1993        PMID: 8270718      PMCID: PMC7095338          DOI: 10.1007/bf01724878

Source DB:  PubMed          Journal:  Intensive Care Med        ISSN: 0342-4642            Impact factor:   17.440


  25 in total

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8.  Complement activation during cardiopulmonary bypass: quantitative study of effects of methylprednisolone and pulsatile flow.

Authors:  M J Boscoe; V M Yewdall; M A Thompson; J S Cameron
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9.  Angiotensin-converting enzyme substrates hydrolyzed by fibroblasts and vascular endothelial cells.

Authors:  D B Rubin; R J Mason; L J Dobbs
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10.  Corticosteroids inhibit complement-induced granulocyte aggregation. A possible mechanism for their efficacy in shock states.

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1.  Surfactant protein A (SP-A) and angiotensin converting enzyme (ACE) as early biomarkers for pulmonary edema formation in ventilated human lung lobes.

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