Related Experiment Videos
Ventilatory dysfunction precedes pulmonary vascular changes in monocrotaline-treated rats
Y L Lai1, J W Olson, M N Gillespie
1Pharmacology and Experimental Therapeutics Division, College of Pharmacy, University of Kentucky, Lexington 40536.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|February 1, 1991
Summary
Monocrotaline-induced pulmonary hypertension in rats shows airway and lung dysfunction preceding pulmonary vascular changes. These early lung function alterations may contribute to the development of pulmonary hypertension.
Area of Science:
- Pulmonary Medicine
- Respiratory Physiology
- Cardiovascular Research
Background:
- Pulmonary hypertension is associated with increased lung resistance and decreased lung compliance.
- The temporal relationship between airway/lung dysfunction and pulmonary vascular disease in monocrotaline (MCT)-induced pulmonary hypertension is not fully understood.
Purpose of the Study:
- To establish the temporal sequence of events between the development of pulmonary hypertension and altered ventilatory function in MCT-treated rats.
Main Methods:
- 47 Sprague-Dawley rats were divided into control and three MCT-treated groups, receiving MCT injections 1, 2, or 3 weeks prior to functional studies.
- Lung resistance (RL), lung compliance, carbon monoxide diffusing capacity (DLCO), alveolar wall thickness, medial thickness of pulmonary arteries, right ventricular hypertrophy, and lung dry weight were assessed.
Main Results:
- One week post-MCT, significant increases in RL and alveolar wall thickness, and decreased DLCO were observed.
- Medial thickening of pulmonary arteries and right ventricular hypertrophy appeared at 2 and 3 weeks post-MCT, respectively.
- Pressure-volume curves showed rightward shifts in the first two weeks post-MCT, indicating altered lung mechanics.
Conclusions:
- MCT-induced alterations in airway and lung function precede the development of pulmonary vascular abnormalities.
- Early airway/lung dysfunction may play a role in the pathogenesis of MCT-induced pulmonary hypertension.