Takeuchi T, Horiuchi J, Terada N
Department of Physiology, Yamanashi Medical College, Japan.
Pflugers Arch. 1989 Feb;413(4):348-53. doi: 10.1007/BF00584482.
Contractile responses of the portal vein of the anesthetized rabbit were measured quantitatively by plethysmography during transmural electrical field stimulation (TES, 0.8 ms and 15 V) and during the cerebral ischemic pressor response at various volemic states. To evoke the cerebral ischemic response, the route of blood supply to the brain was surgically restricted to the right internal carotid artery, the artery was then compressed in a stepwise fashion by a micrometer device. The maximum contractile response of the portal vein segment that could be evoked by cerebral ischemia corresponded in magnitude to that produced by TES of 10-11 Hz. The contractile response began when the internal carotid blood flow was reduced to 4 ml/min from its normal value of 13.8 +/- 1.2 (mean +/- SE) ml/min and reached a maximum at 0 ml/min. The maximum contractile response was an increase of 26% from control value under normovolemic condition, 20% after hemorrhage and 31% after volume loading. It was estimated that the contractile response in normovolemia was 95% neurogenic, the rest was thought to be of humoral origin.
在麻醉兔的门静脉跨壁电场刺激(TES,0.8毫秒和15伏)期间以及在不同血容量状态下的脑缺血升压反应期间,通过体积描记法对门静脉的收缩反应进行了定量测量。为了诱发脑缺血反应,通过手术将脑供血途径限制在右颈内动脉,然后用微米装置逐步压迫该动脉。脑缺血可诱发的门静脉段最大收缩反应在幅度上与10 - 11赫兹的TES所产生的反应相当。当颈内动脉血流从其正常的13.8±1.2(平均值±标准误)毫升/分钟降至4毫升/分钟时,收缩反应开始,并在0毫升/分钟时达到最大值。最大收缩反应在正常血容量条件下比对照值增加26%,出血后增加20%,容量负荷后增加31%。据估计,正常血容量时的收缩反应95%是神经源性的,其余部分被认为是体液源性的。