Contribution of oxygen-sensitive neurons of the rostral ventrolateral medulla to hypoxic cerebral vasodilatation in the rat
Contribution of oxygen-sensitive neurons of the rostral ventrolateral medulla to hypoxic cerebral vasodilatation in the rat
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DOI：
10.1113/jphysiol.1996.sp021585
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发表时间：
1996-08-15
影响因子：
5.5
通讯作者：
Reis, DJ
中科院分区：
文献类型：
--
作者：
Golanov, EV;Reis, DJ
1.我们试图确定是否缺氧刺激的头端腹外侧网状核（RVL）的神经元将提高局部脑血流量（rCBP）在麻醉瘫痪2。微量注射氰化钠（NaCN; 150-450 pmol）快速进入RVL（1-2秒内），瞬时，剂量依赖性和部位特异性rCBF升高，通过激光多普勒血流仪测量，61.3 +/- 22.1%（P < 0.01），动脉压升高（AP; +30 +/- 8 mmHg; P < 0.01），触发同步的6 Hz节律的EEG活动.颈髓横断后，NaCN和二硝基苯酚（DNP）显著（P < 0.05）升高rCBF和同步EEG，但不升高AP;高氧和麻醉加深可减弱NaCN的反应。4.电刺激脊髓损伤大鼠RVL内NaCN敏感部位可增加放射自显影法测定的rCBF（凯蒂法）（182.3 +/- 17.2%; P < 0.05）和大脑皮层（172.6 +/- 15.6%; P < 0.05）区域，分别由RVL神经元直接或间接支配，以及在大脑的其余部分。相反，用C-14-2-脱氧葡萄糖（Sokoloff法）放射自显影测量的局部脑葡萄糖利用率（rCGU），中线丘脑mas与rCBP成比例增加（165.6 +/-17.8%，P < 0.05），但皮质无变化。RVL的NaCN敏感部位的双侧电解损伤，而不改变静息rCBF或高碳酸血症引起的升高（动脉CO2压，P-a，P-CO2类似于69 mmHg），减少了正常碳酸血症低氧血症引起的血管舒张（动脉氧分压，P-a，P-O2，与27 mmHg相似）降低67%（P < 0.01），并使P-a，P-O2-rCBP反应曲线的斜率变平. Pie得出结论，低氧血症在大脑皮层中产生的rCBF升高在很大程度上是神经源性的，通过内在神经元通路跨突触介导的，并由RVL中氧敏感神经元的兴奋引发。
1. We sought to determine whether hypoxic stimulation of neurons of the rostral ventrolateral reticular nucleus (RVL) would elevate regional cerebral blood flow (rCBP) in anaesthetized paralysed2. Microinjection of sodium cyanide (NaCN; 150-450 pmol) into the RVL rapidly (within 1-2 s), transiently, dose-dependently and site-specifically elevated rCBF, measured by laser Doppler flowmetry, by 61.3 +/- 22.1% (P < 0.01), increased arterial pressure (AP; +30 +/- 8 mmHg; P < 0.01), and triggered a synchronized 6 Hz rhythm of EEG activity.3. Following cervical spinal cord transection, NaCN and also dinitrophenol (DNP) significantly (P < 0.05) elevated rCBF and synchronized the EEG but did not elevate AP; the response to NaCN was attenuated by hyperoxia and deepening of anaesthesia. 4. Electrical stimulation of NaCN-sensitive sites in the RVL in spinalized rats increased rCBF measured autoradiographically with C-14-iodoantipyrine (Kety method) in the mid-line thalamus (by 182.3 +/- 17.2%; P < 0.05) and cerebral cortex (by 172.6 +/- 15.6%; P < 0.05) regions, respectively, directly or indirectly innervated by RVL neurons, and in the remainder of the brain. In contrast regional cerebral glucose utilization (rCGU), measured autoradiographically with C-14-2-deoxyglucose (Sokoloff method), mas increased in proportion to rCBP in the mid-line thalamus (165.6 +/- 17.8%, P < 0.05) but was unchanged in the cortex.5. Bilateral electrolytic lesions of NaCN-sensitive sites of RVL, while not altering resting rCBF or the elevation elicited by hypercarbia (arterial CO2 pressure, P-a,P-CO2 similar to 69 mmHg), reduced the vasodilatation elicited by normocapnic hypoxaemia (arterial O-2 pressure, P-a,P-O2, similar to 27 mmHg) by 67 % (P < 0.01) and flattened the slope of the P-a,P-O2-rCBP response curve.6. Pie conclude that the elevation of rCBF produced in the cerebral cortex by hypoxaemia is in large measure neurogenic, mediated trans-synaptically over intrinsic neuronal pathways,and initiated by excitation of oxygen-sensitive neurons in the RVL.