Forskning
Udskriv Udskriv
Switch language
Rigshospitalet - en del af Københavns Universitetshospital
Udgivet

Downregulation of aquaporin-1 in alveolar microvessels in lungs adapted to chronic heart failure

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

DOI

  1. Clinical implications of electrocardiographic bundle branch block in primary care

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Associations between common ECG abnormalities and out-of-hospital cardiac arrest

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Lactate acidosis and cardiac output during initial therapeutic cooling in asphyxiated newborn infants

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  4. Rare truncating variants in the sarcomeric protein titin associate with familial and early-onset atrial fibrillation

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Vis graf over relationer
The threshold pressure for lung edema formation is increased in severe chronic heart failure (CHF) due to reduced microvascular permeability. The water channel aquaporin-1 (AQP1) is present in the pulmonary microvascular endothelium, and a number of studies suggest the importance of AQP1 as a molecular determinant of pulmonary microvascular water transport. The present study examined the abundance and localization of AQP1 in lungs from rats with CHF. We used two different models of CHF: ligation of the left anterior descending coronary artery (LAD ligation) and aorta-banding (AB). Sham-operated rats served as controls. Echocardiographic verification of left ventricular dysfunction, enhanced left ventricular end-diastolic pressure, and right ventricular hypertrophy confirmed the presence of CHF. Western blotting of whole-lung homogenates revealed significant downregulation of AQP1 in LAD-ligated rats (24 h: 58 ± 5% of sham; 3 weeks: 8 ± 3% of sham; 9 weeks: 16 ± 6% of sham) and after AB (30 weeks: 37 ± 5% of sham), whereas the protein levels of the specific endothelial cell marker PECAM-1 was increased 3 weeks after LAD ligation (229 ± 20% of sham), but unchanged after 9 weeks and in the AB rats compared to controls. Immunohistochemical examination 3 weeks after LAD ligation showed intact labeling of PECAM-1 but an almost complete absence of AQP1 in the pulmonary alveolar microvessels in the CHF rats. These results suggest that downregulation of AQP1 in the alveolar microvessels may act as a compensatory mechanism to protect against formation of excessive pulmonary edema in CHF.
OriginalsprogEngelsk
TidsskriftLung
Vol/bind189
Udgave nummer2
Sider (fra-til)157-66
Antal sider10
ISSN0341-2040
DOI
StatusUdgivet - 2011

ID: 33267722