Lin Le-Jian, Tang Fa-Kuan, Hua Ning, Lu Hong, Di Chun-Xia, Tang Xue-Zheng, Li Yu
Department of Cardiology, 309 Hospital of the Chinese People's Liberation Army, Beijing 100091, China.
Sheng Li Xue Bao. 2012 Feb 25;64(1):62-8.
To investigate the time-course changes of myogenic tone in mesenteric small artery (MSA) of spontaneously hypertensive rat (SHR), thirty-two 7-week aged SHR rats were randomly divided into four groups (8, 16, 24, 32 weeks of age), and 32 sex- and age-matched Wistar-Kyoto (WKY) rats were assigned to control groups (CON). On the day of the study, segments of MSA were isolated and then cannulated to the two pipettes. Vascular diameters in response to the increased intraluminal pressure (from 0 mmHg to 150 mmHg, by 25 mmHg steps) of isolated MSA under no-flow conditions were recorded by a Pressure Myograph System both in physiologic salt solution (PSS) (active diameter, Da) and calcium-free PSS (passive diameter, Dp). The myogenic tone was calculated by (Dp - Da)/Dp × 100%. The tail artery pressure and vascular myogenic tone in SHR rats were significantly higher than those of the CON rats. Before 24 weeks, the vascular myogenic tone of MSA in SHR group increased monotonically, but at the end of 32 weeks, the vascular myogenic tone decreased in comparison with that in 24-week group, but was significantly higher than that in CON group. The tail artery pressure in SHR group slowly increased monotonically with increasing weeks of age, and the tail arterial pressure in 32-week group remained significantly higher than that in 24-week group. Vascular myogenic tone may participate in the whole process of hypertension. Early in the development of hypertension, because of the compensatory role of vascular tone, the vascular function has been partially compensated, thus guaranteeing adequate blood supply to organs. Late in the development of hypertension, because of the decompensation of myogenic tone, the vascular function is damaged, leading to the occurrence of severe vascular disease.
为研究自发性高血压大鼠（SHR）肠系膜小动脉（MSA）肌源性张力的时程变化，将32只7周龄的SHR大鼠随机分为四组（8周龄、16周龄、24周龄、32周龄），并将32只性别和年龄匹配的Wistar-Kyoto（WKY）大鼠作为对照组（CON）。在研究当天，分离出MSA节段，然后插管连接到两个移液管。通过压力肌动描记系统记录在无血流条件下，分离的MSA对管腔内压力升高（从0 mmHg升至150 mmHg，以25 mmHg步长递增）的血管直径，记录介质为生理盐溶液（PSS）（主动直径，Da）和无钙PSS（被动直径，Dp）。肌源性张力通过（Dp - Da）/Dp×100%计算得出。SHR大鼠的尾动脉压力和血管肌源性张力显著高于CON组大鼠。在24周之前，SHR组MSA的血管肌源性张力单调增加，但在32周龄时，与24周龄组相比，血管肌源性张力下降，但仍显著高于CON组。SHR组的尾动脉压力随周龄增加而缓慢单调升高，32周龄组的尾动脉压力仍显著高于24周龄组。血管肌源性张力可能参与高血压的全过程。在高血压发展早期，由于血管张力的代偿作用，血管功能得到部分代偿，从而保证了器官的充足血液供应。在高血压发展后期，由于肌源性张力失代偿，血管功能受损，导致严重血管疾病的发生。
