机构地区:[1]上海交通大学附属第一人民医院呼吸内科,200080
出 处:《中华医学杂志》2015年第12期933-937,共5页National Medical Journal of China
基 金:国家自然科学基金(81300020、81100033)
摘 要:目的探讨甲基丁香酚对气道迷走节前神经元(AVPNs)中枢性呼吸驱动的影响。方法应用逆行荧光示踪技术,标记3—5d新生SD大鼠疑核腹外侧区的吸气激活性一气道迷走节前神经元(IA-AVPNs);制备具有呼吸节律的离体延髓脑片,记录舌下神经根放电活动;应用膜片钳技术,记录IA—AVPNs的兴奋性突触活动。将脑片分为应用甲基丁香酚前的对照组及应用甲基丁香酚的甲基丁香酚组。选择对照组最后10个、甲基丁香酚组呼吸节律消失前5个呼吸周期连续的舌下神经根放电及对应的兴奋性突触活动进行统计学分析。结果甲基丁香酚组舌下神经根放电的频率、幅度、时程及面积显著低于对照组[(2.14±0.87)次/min、(1.27±0.53)mV、(178±37)ms、(330±173)mV·ms比(5.394±1.93)次/min、(2.94±0.92)mV、(249±54)ms、(983±534)mV·ms,均P〈0.001],IA—AVPNs吸气期相位性内向电流的幅度、时程及面积分别为对照组的(66.3±4.4)%、(58.5±4.3)%、(44.9±7.5)%(均P〈0.05),IA—AVPNs吸气期相位性兴奋性突触后电流(EPSCs)的频率显著低于对照组[(29.87±3.70)比(42.27±11.95)Hz]、但幅度显著高于对照组[(83.13±15.97)比(49.26±7.40)pA](均P〈0.05);两组IA—AVPNs吸气间期紧张性的EPSCS频率及幅度差异均无统计学意义(均P〉0.05)。结论甲基丁香酚通过抑制IA—AVPNs吸气期兴奋性突触传入抑制IA—AVPNs的中枢性呼吸驱动。Objective To explore the effects of methyleugenol (MEG) on central respiratory drive to inspiratory-activated airway vagal preganglionic neurons ( IA-AVPNs ). Methods The 3 to 5-day-old Sprague-Dawley rats were anesthetized and rhodamine was injected into trachea wall for labelling IA-AVPNs in ventrolateral vicinity of nucleus ambiguous (vNA). And then a brainstem slice preparation with hypoglossal rootlets was made. IA-AVPNs were identified and excitatory synaptic inputs were recorded with patch-clamp techniques. Brainstem slice preparations were divided into the groups of control prior to application of MEG and MEG during MEG application. The data from the last 10 consecutive inspiratory phases prior to application of MEG were chosen as control. And the data from the last 5 respiratory cycles prior to rhythm blockade were used to represent the maximal effects of MEG group. Paired Student's t-test was used for comparing inter-group differences. Results Compared with control, MEG group had lower frequency, amplitude, duration and area of hypoglossal bursts ( 2. 14 ± 0. 87 vs 5.39 ± 1.93 burst/rain, 1.27±0.53 vs 2.94 ±0.92 mV, 178 ±37 vs 249 ±54 ms, 330 ±173 vs 983 ±534 mV · ms, all P〈 0. 001 ). The duration, amplitude and area of phasic inspiratory inward current were lower in MEG group, accounting for ( 66. 3 ± 4. 4 ) %, ( 58. 5 ± 4. 3 ) %, ( 44. 9 ± 7.5 ) % ( all P 〈 0. 05 ) of control respectively. Compared with control, the frequency of phasic excitatory postsynaptic currents (EPSCs) was lower (29. 87 ±3.70 vs 42. 27 ± 11.95 Hz) during inspiratory bursts but the amplitude was higher (83.13 ± 15.97 vs 49.26 ± 7.40 pA) ( all P 〈 0. 05 ). However, compared with control, no significant differencesexisted in the frequency and amplitude of tonic EPSCs during inspiratory intervals ( all P 〉 0.05 ) . Conclusion MEG inhibits central respiratory drive to IA-AVPNs through inhibiting excitatory synaptic transmission.
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