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Circulating surfactant protein-B levels increase acutely in response to exercise-induced left ventricular dysfunction
Carmine G De Pasquale1, Leonard F Arnolda, Ian R Doyle
1Cardiac Services, Flinders Medical Centre, Adelaide, South Australia, Australia. carmine.depasquale@fmc.sa.gov.au
Clinical and Experimental Pharmacology & Physiology
|August 27, 2005
Summary
Exercise does not increase surfactant protein-B (SP-B) levels, but it does in individuals with exercise-induced myocardial dysfunction. This suggests increased pulmonary vascular pressure in dysfunction may compromise the alveolocapillary barrier, allowing SP-B to leak into circulation.
Area of Science:
- Cardiology
- Pulmonary Medicine
- Exercise Physiology
Background:
- The alveolocapillary barrier is susceptible to mechanical stress from increased pulmonary microvascular pressure (Pmv).
- Surfactant protein-B (SP-B) can leak into the bloodstream when this barrier is damaged.
Purpose of the Study:
- To investigate if exercise increases plasma SP-B levels.
- To determine if exercise-induced left ventricular dysfunction exacerbates SP-B elevation due to increased Pmv.
Main Methods:
- Twenty subjects underwent treadmill exercise stress echocardiography (ESE).
- Blood samples were collected pre- and post-exercise for atrial natriuretic peptide (ANP) and SP-B assays.
- Echocardiographic measures of pulmonary hemodynamics (pafAT, rVTI) were assessed.
Main Results:
- Circulating ANP increased post-exercise in all subjects, but SP-B did not change in the overall cohort.
- In subjects with exercise-induced ventricular dysfunction (positive ESE), SP-B levels significantly increased post-exercise.
- Hemodynamic parameters indicated increased pulmonary vascular pressure in the positive ESE group.
Conclusions:
- Standard exercise protocols do not elevate circulating SP-B despite increased pulmonary pressures.
- Exercise-induced myocardial dysfunction leads to a detectable increase in circulating SP-B.
- Elevated pulmonary vascular pressure in myocardial dysfunction may compromise the alveolocapillary barrier, increasing SP-B leakage.