Institute of Microcirculation, Chinese Academy of Medical Sciences & Peking Union Medical College, Key Laboratory of Microcirculation, Ministry of Health, Beijing, China.
Diabetes Research Center, Chinese Academy of Medical Sciences, Beijing, China.
Am J Hypertens. 2021 Feb 18;34(1):100-109. doi: 10.1093/ajh/hpaa164.
Emerging evidence indicates that the pancreas serves as a major source of degrading protease activities and that uncontrolled proteolytic receptor cleavage occurs under hypertensive conditions, which leading to systemic dysfunction and end-organic damage. However, changes in pancreatic microcirculation profiles during the progression of hypertension remain unknown.
Pancreatic microcirculatory blood distribution patterns and microvascular vasomotion of spontaneously hypertensive rats (SHRs) and normotensive control Wistar Kyoto rats at 5, 8, 13, and 18 weeks of age were determined. Wavelet transform analysis was performed to convert pancreatic microhemodynamic signals into time-frequency domains and construct 3-dimensional spectral scalograms. The amplitudes of characteristic oscillators including endothelial, neurogenic, myogenic, respiratory, and cardiac oscillators were compared among groups. Plasma nitrite/nitrate levels were measured using a Griess reaction. Additionally, endothelin-1, malondialdehyde, superoxide dismutase, and interleukin-6 levels were determined by enzyme-linked immunosorbent assay.
SHRs exhibited a reduced blood distribution pattern with progressively decreased average blood perfusion, amplitude, and frequency of microvascular vasomotion. Wavelet transform spectral analysis revealed significantly reduced amplitudes of endothelial oscillators from 8- to 18-week-old SHRs. Additionally, the blood microcirculatory chemistry complements explained the microhemodynamic profiles partially, as demonstrated by an increase in plasma nitrite/nitrate, endothelin-1, malondialdehyde, and interleukin-6 levels and a decreased superoxide dismutase level in SHRs.
Pancreatic microcirculation profiles are abnormal in the progression of hypertension in SHRs, including a disarranged blood distribution pattern, impaired microvascular vasomotion, and reduced amplitudes of endothelial oscillators.
新出现的证据表明，胰腺是降解蛋白酶活性的主要来源，并且在高血压条件下会发生不受控制的蛋白水解受体裂解，导致全身功能障碍和终末器官损伤。然而，高血压进展过程中胰腺微循环特征的变化尚不清楚。
在 5、8、13 和 18 周龄时，确定自发性高血压大鼠（SHR）和正常血压对照 Wistar Kyoto 大鼠的胰腺微循环血液分布模式和微血管舒缩运动。使用小波变换分析将胰腺微循环血液动力学信号转换为时频域，并构建三维频谱标度图。比较各组之间包括内皮、神经源、肌源、呼吸和心脏振荡器在内的特征振荡器的振幅。使用Griess 反应测量血浆硝酸盐/亚硝酸盐水平。此外，通过酶联免疫吸附测定测定内皮素-1、丙二醛、超氧化物歧化酶和白细胞介素-6 的水平。
SHR 表现出逐渐减少的平均血液灌注、微血管舒缩运动的振幅和频率的血液分布模式减少。小波变换频谱分析显示，从 8 到 18 周龄的 SHR 中内皮振荡器的振幅明显降低。此外，血液微循环化学补充物部分解释了微血流动力学特征，表现为 SHR 中血浆硝酸盐/亚硝酸盐、内皮素-1、丙二醛和白细胞介素-6 水平升高，超氧化物歧化酶水平降低。
SHR 高血压进展过程中胰腺微循环特征异常，包括血液分布模式紊乱、微血管舒缩运动受损和内皮振荡器振幅降低。
