Hargens A R, Zweifach B W
Am J Physiol. 1977 Jul;233(1):H57-65. doi: 10.1152/ajpheart.1977.233.1.H57.
Contractility was investigated in collecting lymph vessels of rat and guinea pig mesentery. Lymphatic diameter and micropressure were simultaneously recorded under normal conditions and during micromanipulation of intralymphatic pressure. Spontaneous activity involved characteristic changes in intralymphatic pressure coincident with opening and closure of upstream and downstream valves. Contractions were irregular but still predictable by noting the trend of intraluminal pressure as it approached a threshold level. Mechanical obstruction upstream of lymph vessels reduced lymph pressure and contraction frequency. Microinjection or withdrawal of fluid caused contraction frequency. Microinjection or withdrawal of fluid caused contraction frequency to rise and fall, respectively. Contraction rate was not affected by the level of general anesthesia. Lymphatic wall tension, as calculated from pressure-radius variables, correlated well with contraction frequency, suggesting a myogenic origin for the contractile mechanism. However, lymphatic smooth muscle may be inherently unstable since some contractility persists despite an absence of pressure stimuli.
在大鼠和豚鼠肠系膜的集合淋巴管中研究了收缩性。在正常条件下以及在对淋巴管内压力进行显微操作期间,同时记录淋巴管直径和微压力。自发活动涉及淋巴管内压力的特征性变化,这些变化与上游和下游瓣膜的开放和关闭同时发生。收缩不规则,但通过注意管腔内压力接近阈值水平时的趋势仍可预测。淋巴管上游的机械性阻塞降低了淋巴压力和收缩频率。微量注射或抽取液体导致收缩频率分别上升和下降。收缩率不受全身麻醉水平的影响。根据压力-半径变量计算得出的淋巴管壁张力与收缩频率密切相关,表明收缩机制起源于肌源性。然而,淋巴平滑肌可能本质上不稳定,因为即使没有压力刺激,仍存在一些收缩性。