From the Department of Internal Medicine, Beijing Obstetrics and Gynecology Hospital, Capital Medical University.
Department of Central Laboratory, Beijing Obstetrics and Gynecology Hospital, Capital Medical University, Beijing, China.
Pancreas. 2020 Aug;49(7):960-966. doi: 10.1097/MPA.0000000000001609.
The aim of this study was to investigate the changes of pancreatic microvascular vasomotion and blood distribution pattern in acute pancreatitis (AP), and whether Angiotensin (Ang)-(1-7) treatment could restore pancreatic microcirculation profiles.
Mice were randomly separated into control, AP, and Ang-(1-7)-treated AP (A-AP) group. Acute pancreatitis was induced in mice by intraperitoneal injection of cerulein and lipopolysaccharide. Pancreatitis was confirmed by histopathology, serum amylase, and high-sensitive C-reactive protein. Pancreatic microvascular vasomotion and blood distribution pattern in AP progression were assessed by laser Doppler. Meanwhile, ultrastructural changes of pancreatic microcirculation, including microvascular cavity and wall and endothelial mitochondria, were evaluated by transmission electron microscopy.
Acute pancreatitis mice exhibited pathological pancreatic injuries with lower blood distribution pattern and decreased average blood perfusion, relative velocity, effective frequency, and amplitude of microvascular vasomotion. The pancreatic pathological injuries in Ang-(1-7)-treated mice were significantly alleviated. Consistently, Ang-(1-7) treatment led to a restoration in pancreatic microcirculation profiles. Furthermore, non-Ang-(1-7)-treated mice showed an irregular microvascular wall, narrow cavity, and swelling mitochondria, and these ultrastructural impairments were reversed by Ang-(1-7) administration.
Pancreatic microcirculation profiles are abnormal in the progression of AP. Angiotensin-(1-7) administration could restore functional status of pancreatic microcirculation.
本研究旨在探讨急性胰腺炎(AP)时胰腺微血管舒缩运动和血流分布模式的变化,以及血管紧张素(Ang)-(1-7)治疗是否能恢复胰腺微循环特征。
将小鼠随机分为对照组、AP 组和 Ang-(1-7)治疗的 AP 组(A-AP 组)。通过腹腔内注射胆酸钠和脂多糖诱导小鼠急性胰腺炎。通过组织病理学、血清淀粉酶和高敏 C 反应蛋白来确认胰腺炎。通过激光多普勒评估 AP 进展过程中胰腺微血管舒缩运动和血流分布模式。同时,通过透射电子显微镜评估胰腺微循环的超微结构变化,包括微血管腔和壁以及内皮线粒体。
AP 小鼠表现出病理性胰腺损伤,血流分布模式降低,平均血流灌注、相对速度、有效频率和微血管舒缩运动幅度降低。Ang-(1-7)治疗的小鼠胰腺病理损伤明显减轻。同样,Ang-(1-7)治疗导致胰腺微循环特征得到恢复。此外,非 Ang-(1-7)治疗的小鼠显示出不规则的微血管壁、狭窄的腔和肿胀的线粒体,而这些超微结构损伤通过 Ang-(1-7)给药得到逆转。
AP 进展过程中胰腺微循环特征异常。血管紧张素(1-7)治疗可恢复胰腺微循环的功能状态。