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肝内神经支配在铯诱导的大鼠肝脏血流动力学振荡中的作用。

Involvement of intrahepatic innervation in caesium-induced haemodynamic oscillations in the rat liver.

作者信息

Hill C E, Myers J W, Pon D C

机构信息

Department of Biological Sciences, University of Calgary, Alberta, Canada.

出版信息

J Physiol. 1993 Jan;460:69-78. doi: 10.1113/jphysiol.1993.sp019459.

DOI:10.1113/jphysiol.1993.sp019459
PMID:8487213
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1175201/
Abstract
  1. Cs+ was used to study the mechanisms involved in the induction of haemodynamic and metabolic oscillations in the isolated rat liver perfused by the portal vein. 2. Cs+ (2.25 mM) in K(+)-free perfusate causes the appearance of periodic increases in portal pressure (3.87 +/- 0.6 mmHg, n = 24) and decreases in O2 uptake (111 +/- 26 microM) at a frequency of 0.013 +/- 0.002 Hz. A 19.8 +/- 1.2 min induction time occurs prior to the generation of periodicity. The oscillations are interspersed with low amplitude shoulders and peaks indicating multiple non-phasic components. 3. Cs+ concentrations higher or lower than 2.25 mM decrease oscillation amplitude and render them aperiodic. No oscillations are observed with 0.5 or 12.5 mM Cs+. 4. The oscillations are reversibly blocked by 1 mM K+, 1 mM EGTA, 5 microM verapamil or 0.17 microM tetrodotoxin. One micromolar chlorpheniramine, 10 microM propranolol, 12 microM phentolamine or 35 microM atropine also maximally inhibit the Cs(+)-induced vasoactivity. 5. The results show that the liver perfused by the portal vein has all of the components required to activate vascular synchrony including intrinsic neural input and responsive vasoactive cells.
摘要
  1. 采用铯离子(Cs+)研究门静脉灌注的离体大鼠肝脏中血流动力学和代谢振荡诱导所涉及的机制。2. 无钾灌注液中的Cs+(2.25 mM)导致门静脉压力出现周期性升高(3.87±0.6 mmHg,n = 24),同时氧气摄取量降低(111±26 μM),频率为0.013±0.002 Hz。在周期性产生之前有19.8±1.2分钟的诱导期。振荡夹杂着低幅度的波峰和波谷,表明存在多个非相位成分。3. 高于或低于2.25 mM的Cs+浓度会降低振荡幅度并使其变为非周期性。0.5 mM或12.5 mM的Cs+未观察到振荡。4. 振荡可被1 mM钾离子、1 mM乙二醇双乙醚二胺四乙酸(EGTA)、5 μM维拉帕米或0.17 μM河豚毒素可逆性阻断。1 μM氯苯那敏、10 μM普萘洛尔、12 μM酚妥拉明或35 μM阿托品也能最大程度抑制Cs+诱导的血管活性。5. 结果表明,门静脉灌注的肝脏具备激活血管同步性所需的所有成分,包括内在神经输入和反应性血管活性细胞。

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本文引用的文献

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