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慢性去窦主动脉神经大鼠的动脉重塑

Arterial remodeling in chronic sinoaortic-denervated rats.

作者信息

Miao C Y, Tao X, Gong K, Zhang S H, Chu Z X, Su D F

机构信息

Department of Pharmacology, Basic Medical College, Second Military Medical University, Shanghai, China.

出版信息

J Cardiovasc Pharmacol. 2001 Jan;37(1):6-15. doi: 10.1097/00005344-200101000-00002.

Abstract

The spontaneous variation of blood pressure is defined as "blood pressure variability" (BPV). The chronic sinoaortic-denervated (SAD) rat is a model of high BPV without sustained hypertension. Little is known about vascular remodeling in this model. In the present study, we examined blood pressure, vascular remodeling, and aortic angiotensin II concentration in chronic SAD rats in separate experiments. In experiment 1, intra-arterial blood pressure was continuously recorded in conscious unrestrained rats. The 16-week SAD rats had a significant increase in BPV and no change in the mean level of blood pressure over a 24-h period. In experiment 2, we measured structural changes of seven kinds of arteries by histologic method and computer image analysis and functional changes of thoracic aortas by isolated artery preparation. Structural remodeling after 16-week sinoaortic denervation was characterized by increase in wall thickness, wall area, and ratio of wall thickness to internal diameter, with different changes in internal diameter and external diameter in different arteries, indicating that arterial structural remodeling expresses itself mainly as vascular growth. This vascular growth might be caused by medial smooth muscle cell growth and collagen accumulation. Aortic contraction induced by norepinephrine was potentiated, whereas aortic relaxation induced by acetylcholine was attenuated after sinoaortic denervation. In experiment 3, plasma and aortic angiotensin II concentrations were determined by radioimmunoassay. The former remained unchanged, whereas the latter was significantly increased in 10-week SAD rats. It is concluded that in rats chronic sinoaortic denervation can produce vascular remodeling that might be related to increased BPV and an activated tissue renin-angiotensin system.

摘要

血压的自发变化被定义为“血压变异性”(BPV)。慢性去窦弓神经(SAD)大鼠是一种具有高BPV但无持续性高血压的模型。关于该模型中的血管重塑知之甚少。在本研究中,我们在单独的实验中检查了慢性SAD大鼠的血压、血管重塑和主动脉血管紧张素II浓度。在实验1中,在清醒不受约束的大鼠中连续记录动脉内血压。16周龄的SAD大鼠在24小时内BPV显著增加,平均血压水平无变化。在实验2中,我们通过组织学方法和计算机图像分析测量了七种动脉的结构变化,并通过离体动脉制备测量了胸主动脉的功能变化。16周去窦弓神经后的结构重塑表现为管壁厚度、管壁面积以及管壁厚度与内径之比增加,不同动脉的内径和外径有不同变化,表明动脉结构重塑主要表现为血管生长。这种血管生长可能是由中膜平滑肌细胞生长和胶原蛋白积累引起的。去窦弓神经后,去甲肾上腺素诱导的主动脉收缩增强,而乙酰胆碱诱导的主动脉舒张减弱。在实验3中,通过放射免疫测定法测定血浆和主动脉血管紧张素II浓度。前者保持不变,而后者在10周龄的SAD大鼠中显著增加。结论是,在大鼠中,慢性去窦弓神经可导致血管重塑,这可能与BPV增加和组织肾素-血管紧张素系统激活有关。

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