Arterial morphology responds differently to Captopril then N-acetylcysteine in a monocrotaline rat model of pulmonary hypertension

Robert Molthen; Qingping Wu; Shelley Baumgardt; Laura Kohlhepp; Rahul Shingrani; Gary Krenz

doi:10.1117/12.844830

9 March 2010 Arterial morphology responds differently to Captopril then N-acetylcysteine in a monocrotaline rat model of pulmonary hypertension

Robert Molthen, Qingping Wu, Shelley Baumgardt, Laura Kohlhepp, Rahul Shingrani, Gary Krenz

Author Affiliations +

Proceedings Volume 7626, Medical Imaging 2010: Biomedical Applications in Molecular, Structural, and Functional Imaging; 762615 (2010) https://doi.org/10.1117/12.844830
Event: SPIE Medical Imaging, 2010, San Diego, California, United States

Abstract

Pulmonary hypertension (PH) is an incurable condition inevitably resulting in death because of increased right heart workload and eventual failure. PH causes pulmonary vascular remodeling, including muscularization of the arteries, and a reduction in the typically large vascular compliance of the pulmonary circulation. We used a rat model of monocrotaline (MCT) induced PH to evaluated and compared Captopril (an angiotensin converting enzyme inhibitor with antioxidant capacity) and N-acetylcysteine (NAC, a mucolytic with a large antioxidant capacity) as possible treatments. Twenty-eight days after MCT injection, the rats were sacrificed and heart, blood, and lungs were studied to measure indices such as right ventricular hypertrophy (RVH), hematocrit, pulmonary vascular resistance (PVR), vessel morphology and biomechanics. We implemented microfocal X-ray computed tomography to image the pulmonary arterial tree at intravascular pressures of 30, 21, 12, and 6 mmHg and then used automated vessel detection and measurement algorithms to perform morphological analysis and estimate the distensibility of the arterial tree. The vessel detection and measurement algorithms quickly and effectively mapped and measured the vascular trees at each intravascular pressure. Monocrotaline treatment, and the ensuing PH, resulted in a significantly decreased arterial distensibility, increased PVR, and tended to decrease the length of the main pulmonary trunk. In rats with PH induced by monocrotaline, Captopril treatment significantly increased arterial distensibility and decrease PVR. NAC treatment did not result in an improvement, it did not significantly increase distensibility and resulted in further increase in PVR. Interestingly, NAC tended to increase peripheral vascular density. The results suggest that arterial distensibility may be more important than distal collateral pathways in maintaining PVR at normally low values.

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Robert Molthen, Qingping Wu, Shelley Baumgardt, Laura Kohlhepp, Rahul Shingrani, and Gary Krenz "Arterial morphology responds differently to Captopril then N-acetylcysteine in a monocrotaline rat model of pulmonary hypertension", Proc. SPIE 7626, Medical Imaging 2010: Biomedical Applications in Molecular, Structural, and Functional Imaging, 762615 (9 March 2010); https://doi.org/10.1117/12.844830

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