지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 저널정보
- 대한약리학회 The Korean Journal of Physiology & Pharmacology The Korean Journal of Physiology & Pharmacology 제20권 제6호
- 발행연도
- 2016.11
- 수록면
- 641 - 647 (7page)
이용수
초록· 키워드
오류제보하기
Pulmonary arterial hypertension (PAH) is a progressive disease characterized by vascular remodeling of pulmonary arteries (PAs) and increased vascular resistance in the lung. Monocrotaline (MCT), a toxic alkaloid, is widely used for developing rat models of PAH caused by injury to pulmonary endothelial cells; however, characteristics of vascular functions in MCT-induced PAH vary and are not fully understood. Here, we investigated hypoxic pulmonary vasoconstriction (HPV) responses and effects of various vasoconstrictors with isolated/perfused lungs of MCT-induced PAH (PAH-MCT) rats. Using hematoxylin and eosin staining, we confirmed vascular remodeling (i.e., medial thickening of PA) and right ventricle hypertrophy in PAH-MCT rats. The basal pulmonary arterial pressure (PAP) and PAP increase by a raised flow rate (40 mL/min) were higher in the PAH-MCT than in the control rats. In addition, both high K+ (40 mM KCl)- and angiotensin II-induced PAP increases were higher in the PAH-MCT than in the control rats. Surprisingly, application of a nitric oxide synthase inhibitor, L-NG-Nitroarginine methyl ester (L-NAME), induced a marked PAP increase in the PAH-MCT rats, suggesting that endothelial functions were recovered in the three-week PAH-MCT rats. In addition, the medial thickening of the PA was similar to that in chronic hypoxia-induced PAH (PAH-CH) rats. However, the HPV response (i.e., PAP increased by acute hypoxia) was not affected in the MCT rats, whereas HPV disappeared in the PAH-CH rats. These results showed that vascular contractility and HPV remain robust in the MCT-induced PAH rat model with vascular remodeling.
목차
등록된 정보가 없습니다.
참고문헌 (33)
참고문헌 신청
Barst RJ / 2004 / Diagnosis and differential assessment of pulmonary arterial hypertension / J Am Coll Cardiol 43(12 Suppl S):40~47
Leopold JA / 2016 / Molecular mechanisms of pulmonary vascular remodeling in pulmonary arterial hypertension / Int J Mol Sci 17:761
Stenmark KR / 2009 / Animal models of pulmonary arterial hypertension : the hope for etiological discovery and pharmacological cure / Am J Physiol Lung Cell Mol Physiol 297:1013~1032
Sakao S / 2009 / Endothelial cells and pulmonary arterial hypertension : apoptosis, proliferation, interaction and transdifferentiation / Respir Res 10:95
Sumpio BE / 2002 / Cells in focus : endothelial cell / Int J Biochem Cell Biol 34:1508~1512
Leopold JA / 2016 / Molecular mechanisms of pulmonary vascular remodeling in pulmonary arterial hypertension / Int J Mol Sci 17:761
Stenmark KR / 2009 / Animal models of pulmonary arterial hypertension : the hope for etiological discovery and pharmacological cure / Am J Physiol Lung Cell Mol Physiol 297:1013~1032
Sakao S / 2009 / Endothelial cells and pulmonary arterial hypertension : apoptosis, proliferation, interaction and transdifferentiation / Respir Res 10:95
Sumpio BE / 2002 / Cells in focus : endothelial cell / Int J Biochem Cell Biol 34:1508~1512
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