Τίτλος:
Pulmonary capillary endothelial metabolic function in chronic
thromboembolic pulmonary hypertension
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Background: Chronic thromboembolic pulmonary hypertension (CTEPH) causes
physical plugging of large pulmonary arteries as well as a distal
micro-vasculopathy. Pulmonary endothelium is an active metabolic tissue
in normal humans. The effects of CTEPH on pulmonary endothelial
metabolism are unknown. Objectives: We studied pulmonary capillary
endothelium-bound angiotensin converting enzyme (ACE) activity as an
index of endothelial metabolism in patients with CTEPH.
Patients/methods: We measured single-pass transpulmonary per cent
metabolism (%M) and hydrolysis of an ACE synthetic substrate and
calculated functional capillary surface area (FCSA), normalized to body
surface area (BSA), in 13 patients with CTEPH and 23 controls. Results:
Mean %M for CTEPH (71.6 +/- 4.0% SE) was similar to controls (74.7 +/-
2.7%). Substrate hydrolysis (v) was similar for CTEPH (1.47 +/- 0.22)
and controls (1.51 +/- 0.11). However, FCSA/BSA was reduced (P < 0.01)
for CTEPH (1530 +/- 218 mL min(-1)*m(-2)) as compared with controls
(2948 +/- 245). Conclusions: The metabolically functional pulmonary
capillary bed is reduced in CTEPH. However, because %M and hydrolysis
are preserved, this points to a reduction in functional capillary
surface area rather than reduced ACE activity on the pulmonary capillary
endothelial cell. The reduction in functional capillary surface area may
just be a result of decreased capillary recruitment because of upstream
vascular plugging by chronic organized thrombus.
Συγγραφείς:
Orfanos, S. E.
Hirsch, A. M.
Giovinazzo, M.
Armaganidis, A.
and Catravas, J. D.
Langleben, D.
Περιοδικό:
Journal of Thrombosis and Haemostasis
Λέξεις-κλειδιά:
angiotensin converting enzyme; endothelium; pulmonary hypertension;
pulmonary metabolism; thromboembolic disease
DOI:
10.1111/j.1538-7836.2008.03046.x
