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首页> 外文期刊>American Journal of Physiology >Preemptive, but not reactive, spinal cord stimulation mitigates transient ischemia-induced myocardial infarction via cardiac adrenergic neurons.
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Preemptive, but not reactive, spinal cord stimulation mitigates transient ischemia-induced myocardial infarction via cardiac adrenergic neurons.

机译：抢先但无反应性的脊髓刺激可通过心脏肾上腺素能神经元缓解短暂性缺血引起的心肌梗塞。

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Our objective was to determine whether electrical neuromodulation using spinal cord stimulation (SCS) mitigates transient ischemia-induced ventricular infarction and, if so, whether adrenergic neurons are involved in such cardioprotection. The hearts of anesthetized rabbits, subjected to 30 min of left anterior descending coronary arterial occlusion (CAO) followed by 3 h of reperfusion (control), were compared with those with preemptive SCS (starting 15 min before and continuing throughout the 30-min CAO) or reactive SCS (started at 1 or 28 min of CAO). For SCS, the dorsal C8-T2 segments of the spinal cord were stimulated electrically (50 Hz, 0.2 ms, 90% of motor threshold). For preemptive SCS, separate groups of animals were pretreated 15 min before SCS onset with 1) vehicle, 2) prazosin (alpha(1)-adrenoceptor blockade), or 3) timolol (beta-adrenoceptor blockade). Infarct size (IS), measured with tetrazolium, was expressed as a percentage of risk zone. In controls exposed to 30 min of CAO, IS was 36.4+/- 9.5% (SD). Preemptive SCS reduced IS to 21.8 +/- 6.8% (P < 0.001). Preemptive SCS-mediated infarct reduction was eliminated by prazosin (36.6 +/- 8.8%) and blunted by timolol (29.4 +/- 7.5%). Reactive SCS did not reduce IS. SCS increased phosphorylation of cardiac PKC. SCS did not alter blood pressure or heart rate. We conclude that preemptive SCS reduces the size of infarcts induced by transient CAO; such cardioprotection involves cardiac adrenergic neurons.
机译：我们的目标是确定使用脊髓刺激（SCS）进行的电神经调节是否能缓解短暂性缺血性心室梗塞，如果是，那么肾上腺能神经元是否参与这种心脏保护。将麻醉兔子的心脏进行左前降支30分钟冠状动脉闭塞（CAO），然后再灌注3小时（对照），与先发性SCS进行比较（从开始前15分钟开始并持续整个30分钟CAO） ）或反应式SCS（从CAO的1或28分钟开始）。对于SCS，对脊髓的背侧C8-T2节段进行电刺激（50 Hz，0.2 ms，运动阈值的90％）。对于先发性SCS，在SCS发作前15分钟用1）媒介物，2）哌唑嗪（α（1）-肾上腺素受体阻断剂）或3）噻吗洛尔（β-肾上腺素受体阻断剂）对单独的动物组进行预处理。用四唑鎓测量的梗塞面积（IS）以危险区的百分比表示。在暴露于30分钟的CAO的对照组中，IS为36.4 +/- 9.5％（SD）。抢先式SCS将IS降至21.8 +/- 6.8％（P <0.001）。先发性SCS介导的梗塞减轻被哌唑嗪（36.6 +/- 8.8％）消除，而噻吗洛尔（29.4 +/- 7.5％）减弱。反应性SCS并没有减少IS。 SCS增加了心脏PKC的磷酸化。 SCS并没有改变血压或心率。我们得出的结论是，先发制人的SCS可以减少短暂性CAO引起的梗塞面积。这种心脏保护涉及心脏肾上腺素能神经元。

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