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Ischaemia-induced sympathoexcitation in spinalyzed rats.

机译:缺血引起的大鼠缺血性交感神经兴奋。

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摘要

Systemic ischaemia increases sympathetic activity via both reflex and direct effects on the nervous system, which include the hypothalamus and brainstem structures that provide excitatory drive to sympathetic pre-ganglionic motoneurones. Using an arterially perfused working heart-brainstem preparation (WHBP), we evaluated the sympathoexcitatory response recorded from the thoracic sympathetic chain (tSC) in response to systemic ischaemia (produced by arresting perfusion for 30 s) before and after transecting consecutively at both the ponto-medullary and medullary-spinal cord junctions. Ischaemia produced a striking increase in tSC activity that persisted after transecting at both the ponto-medullary and medullary-spinal cord levels (intact: 70+/-3%; ponto-medullary: 77+/-7%; medullary-spinal cord: 61+/-6%; n=9). In sino-aortic denervated (SAD) rats (n=4), sympathoexcitatory responses were smaller in both intact and ponto-medullary, but not in medullary-spinal cord transected versus intact rats. Following administration of a ganglionic blocker [hexamethonium (hex), 25 mg/kg] after medullary-spinal cord transection the ischaemia-induced sympathoexcitatory response was reduced (12+/-6% increase relative to control, n=4). In medullary-spinal cord transected preparations, intrathecal injection of N2-saturated saline increased tSC discharge (22+/-3%, n=4), which was attenuated by hex (5+/-1%). We propose that neural mechanisms within the cervical-thoracic segments can make a substantial contribution to the sympathoexcitatory response during systemic ischaemia.
机译:全身性局部缺血通过对神经系统的反射和直接作用来增强交感神经活动,包括下丘脑和脑干结构,它们为交感神经节前运动神经元提供兴奋性驱动。使用动脉灌注的工作性心脑干制剂(WHBP),我们评估了从桥上交感神经链(tSC)记录到的对全身缺血(通过停止灌注30 s产生)的反应,该反应在桥体前后连续横切之前-髓质和髓质-脊髓连接。缺血导致tSC活性显着增加,在桥状和髓状脊髓水平横切后持续存在(完整:70 +/- 3%;桥状髓质:77 +/- 7%;髓状脊髓: 61 +/- 6%; n = 9)。在窦主动脉去神经支配的(SAD)大鼠中(n = 4),在完整和桥状髓中,交感神经兴奋反应均较小,但与完整大鼠相比,经脊髓-脊髓横断的交感兴奋反应却没有。脊髓脊髓横断后给予神经节阻滞剂[六甲铵(hex),25 mg / kg]后,局部缺血引起的交感兴奋反应减少(相对于对照增加12 +/- 6%,n = 4)。在截断脊髓的脊髓制剂中,鞘内注射N2饱和盐水可增加tSC排放量(22 +/- 3%,n = 4),十六进制衰减(5 +/- 1%)。我们建议颈椎-胸段内的神经机制可以对全身缺血期间的交感兴奋反应作出重大贡献。

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