Myocardial interstitial noradrenaline monitoring during occlusion of inferior vena cava in cats.
Myocardial interstitial noradrenaline monitoring during occlusion of inferior vena cava in cats.
复制标题
猫下腔静脉闭塞期间心肌间质去甲肾上腺素监测。
DOI：
10.1046/j.1365-201x.1998.00365.x
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
T. Yamazaki
中科院分区：
文献类型：
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作者：
H. Kitagawa;T. Akiyama;T. Yamazaki
为了研究全身交感神经激活过程中心肌间质去甲肾上腺素(NA)的动态变化，我们对麻醉猫左室应用透析技术，并在阻断下腔静脉(IVC)6分钟期间监测心肌间质NA的水平。将透析探头植入左室壁，用高效液相色谱-电化学检测法测定透析液NA水平，作为心肌间质NA水平的指标。在下腔静脉阻断期间，透析液NA水平从对照组的110+/-17pmoL L-1逐渐升高，在下腔静脉阻断4-6min时达到620+/-160pmoL L-1。局部应用欧米茄毒素GVIA 10微米可使对照透析液NA水平降至35+/-0.2pmoL L-1。下腔静脉阻断引起的透析液NA升高仅在下腔静脉阻断0~2min时被抑制。静脉注射欧米茄毒素GVIA(10微克·kg~(-1))不能增加下腔静脉阻断时透析液中NA的水平。局部应用100微米的地塞帕明使对照透析液NA水平增加到900+/-73pmoL L-1。下腔静脉阻断后2~6min，透析液NA进行性增加。这些结果表明，心肌间质NA水平的早期升高主要是由交感神经末梢的神经元释放NA引起的，而循环提取和神经元NA摄取是延迟几分钟后心肌间质NA水平变化的原因。
To investigate myocardial interstitial noradrenaline (NA) kinetics during activation of systemic sympathetic nerves, we applied a dialysis technique to the left ventricle of anaesthetised cats and monitored myocardial interstitial NA levels during 6-min occlusion of the inferior vena cava (IVC). Dialysis probes were implanted in the left ventricular wall, and dialysate NA levels as an index of myocardial interstitial NA levels, were measured with high-performance liquid chromatographic-electrochemical detection. During IVC occlusion, dialysate NA levels progressively increased from 110 +/- 17 pmol L-1 in the control and reached 620 +/- 160 pmol L-1 at 4-6 min of IVC occlusion. Local administration of omega-conotoxin GVIA at 10 microM decreased the control dialysate NA level to 35 +/- 0.2 pmol L-1. The IVC occlusion induced increase in dialysate NA was suppressed only at 0-2 min of IVC occlusion. Intravenous injection of omega-conotoxin GVIA (10 micrograms kg-1) did not increase the dialysate NA levels during IVC occlusion. Local administration of desipramine at 100 microM increased the control dialysate NA level to 900 +/- 73 pmol L-1. The IVC occlusion induced progressive increase in dialysate NA was augmented at 2-6 min of IVC occlusion. These results suggest that the early increase in myocardial interstitial NA levels is mainly caused by neuronal release of NA from cardiac sympathetic nerve terminals, and that extraction from the circulation and neuronal NA uptake contribute to changes in myocardial interstitial NA levels after a delay of several minutes.