Microfocal CT was used to image the pulmonary arterial (PA) tree in rodent models of pulmonary hypertension (PH).
CT images were used to measure the arterial tree diameter along the main arterial trunk at several hydrostatic
intravascular pressures and calculate distensibility. High-resolution planar angiographic imaging was also used to
examine distal PA microstructure. Data on pulmonary artery tree morphology improves our understanding of vascular
remodeling and response to treatments. Angiotensin II (ATII) has been identified as a mediator of vasoconstriction and
proliferative mitotic function. ATII has been shown to promote vascular smooth muscle cell hypertrophy and
hyperplasia as well as stimulate synthesis of extracellular matrix proteins. Available ATII is targeted through angiotensin
converting enzyme inhibitors (ACEIs), a method that has been used in animal models of PH to attenuate vascular
remodeling and decrease pulmonary vascular resistance. In this study, we used rat models of chronic hypoxia to induce
PH combined with partial left pulmonary artery occlusion (arterial banding, PLPAO) to evaluate effects of the ACEI,
captopril, on pulmonary vascular hemodynamic and morphology. Male Sprague Dawley rats were placed in hypoxia
(FiO2 0.1), with one group having underwent PLPAO three days prior to the chronic hypoxia. After the twenty-first day
of hypoxia exposure, treatment was started with captopril (20 mg/kg/day) for an additional twenty-one days. At the
endpoint, lungs were excised and isolated to examine: pulmonary vascular resistance, ACE activity, pulmonary vessel
morphology and biomechanics. Hematocrit and RV/LV+septum ratio was also measured. CT planar images showed less
vessel dropout in rats treated with captopril versus the non-treatment lungs. Distensibility data shows no change in rats
treated with captopril in both chronic hypoxia (CH) and CH with PLPAO (CH+PLPAO) models. Hemodynamic
measurements also show no change in the pulmonary vascular resistance with captopril treatment in both CH and
CH+PLPAO.
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