Ping P, Johnson P C
Department of Physiology, University of Arizona, Tucson 85724.
Am J Physiol. 1992 Oct;263(4 Pt 2):H1177-84. doi: 10.1152/ajpheart.1992.263.4.H1177.
The effect of sustained sympathetic nerve stimulation on autoregulation of blood flow was examined in the exteriorized cat sartorius muscle using intravital microscopy. Without sympathetic nerve stimulation (SNS), second-order arterioles showed insignificant dilation (3%) during arterial pressure reduction from 110 to 60 mmHg; volume flow fell coincident with pressure reduction. During SNS, these arterioles constricted significantly (25%), and their dilation during pressure reduction (20%) was significant and was significantly greater than that without SNS. Volume flow increased significantly (20-60%) during pressure reduction, a phenomenon termed superregulation of flow. Elevation of ambient oxygen in the suffusate from 0 to 20% caused arteriolar constriction but did not abolish arteriolar dilation during pressure reduction under sustained SNS. Arteriolar response to venous pressure elevation was also affected significantly by sustained SNS. Without SNS, third-order arterioles showed slight dilation (4%) when femoral venous pressure was elevated by 10 mmHg. During SNS, these arterioles constricted significantly and constricted further (20%) when venous pressure was elevated. Using a local anesthetic (lidocaine), we determined that a local venous-arteriolar reflex was not involved in the arteriolar constriction. Our data suggest that superregulation of flow during sustained sympathetic nerve stimulation is not due to metabolic factors but rather to an enhanced myogenic response.
利用活体显微镜检查了去神经猫缝匠肌中持续交感神经刺激对血流自动调节的影响。在无交感神经刺激(SNS)的情况下,当动脉压从110 mmHg降至60 mmHg时,二级小动脉扩张不明显(3%);血流量随压力降低而下降。在SNS期间,这些小动脉显著收缩(25%),在压力降低期间它们的扩张(20%)显著,且显著大于无SNS时。在压力降低期间,血流量显著增加(20% - 60%),这一现象称为血流的超调节。灌流液中环境氧含量从0%升高至20%会导致小动脉收缩,但在持续SNS下压力降低期间并未消除小动脉的扩张。持续SNS也显著影响小动脉对静脉压升高的反应。在无SNS时,当股静脉压升高10 mmHg时,三级小动脉显示轻度扩张(4%)。在SNS期间,这些小动脉显著收缩,且在静脉压升高时进一步收缩(20%)。使用局部麻醉剂(利多卡因),我们确定局部静脉 - 动脉反射不参与小动脉收缩。我们的数据表明,持续交感神经刺激期间的血流超调节不是由于代谢因素,而是由于增强的肌源性反应。