南方医科大学学报
南方醫科大學學報
남방의과대학학보
JOURNAL OF SOUTHERN MEDICAL UNIVERSITY
2010年
2期
245-248
,共4页
李国才%焦勇钢%吴中海%方芳%程静
李國纔%焦勇鋼%吳中海%方芳%程靜
리국재%초용강%오중해%방방%정정
多沙普仑%面神经后核内侧区%呼吸节律性放电%延髓
多沙普崙%麵神經後覈內側區%呼吸節律性放電%延髓
다사보륜%면신경후핵내측구%호흡절률성방전%연수
doxapram%medial region of the nucleus retrofacialis%respiratory rhythmical discharge activity%medulla oblongata
目的 观察多沙普仑对新生大鼠延髓脑片呼吸节律性放电(RRDA)的调节作用.方法 制作主要包含延髓面神经后核内侧区(mNRF)的大鼠离体脑片标本,并保留舌下神经根的完整.将36只新生SD大鼠随机分为Ⅰ~Ⅵ组(n=6).Ⅰ组为对照组;Ⅱ~Ⅳ组为多沙普仑组(浓度分别为2、5、10μmol/L),V组给予丙泊酚(20 μmol/L),Ⅵ组给予丙泊酚(20μmol/L)+多沙普仑(5μmol/L),观察给药后1、3、5、10、15、30 min时舌下神经根呼吸节律性放电的变化,并分析吸气时程(TI)、呼气时程(TE)、呼吸周期(RC)、放电积分幅度(IA)的改变.结果 Ⅱ组在给药前后脑片RRDA并无明显改变;Ⅲ、Ⅳ组在给药后1 min开始,吸气时程明显延长,放电积分幅度增加;呼气时程于第5 min时开始缩短(P<0.05),但呼吸周期仅于第10 min时缩短,其余时间点无明显改变;V组在第3 min时开始出现吸气时程缩短、放电积分幅度下降,并伴有呼气时程及呼吸周期延长(P<0.05),第10 min时达最大变化值;Ⅵ组RRDA各时间点均无明显改变(P>0.05).结论5 μmol/L多沙普仑可直接兴奋延髓脑片的RRDA,且可完全拮抗丙泊酚对脑片RRDA的抑制作用,此作用主要通过兴奋吸气中枢实现.
目的 觀察多沙普崙對新生大鼠延髓腦片呼吸節律性放電(RRDA)的調節作用.方法 製作主要包含延髓麵神經後覈內側區(mNRF)的大鼠離體腦片標本,併保留舌下神經根的完整.將36隻新生SD大鼠隨機分為Ⅰ~Ⅵ組(n=6).Ⅰ組為對照組;Ⅱ~Ⅳ組為多沙普崙組(濃度分彆為2、5、10μmol/L),V組給予丙泊酚(20 μmol/L),Ⅵ組給予丙泊酚(20μmol/L)+多沙普崙(5μmol/L),觀察給藥後1、3、5、10、15、30 min時舌下神經根呼吸節律性放電的變化,併分析吸氣時程(TI)、呼氣時程(TE)、呼吸週期(RC)、放電積分幅度(IA)的改變.結果 Ⅱ組在給藥前後腦片RRDA併無明顯改變;Ⅲ、Ⅳ組在給藥後1 min開始,吸氣時程明顯延長,放電積分幅度增加;呼氣時程于第5 min時開始縮短(P<0.05),但呼吸週期僅于第10 min時縮短,其餘時間點無明顯改變;V組在第3 min時開始齣現吸氣時程縮短、放電積分幅度下降,併伴有呼氣時程及呼吸週期延長(P<0.05),第10 min時達最大變化值;Ⅵ組RRDA各時間點均無明顯改變(P>0.05).結論5 μmol/L多沙普崙可直接興奮延髓腦片的RRDA,且可完全拮抗丙泊酚對腦片RRDA的抑製作用,此作用主要通過興奮吸氣中樞實現.
목적 관찰다사보륜대신생대서연수뇌편호흡절률성방전(RRDA)적조절작용.방법 제작주요포함연수면신경후핵내측구(mNRF)적대서리체뇌편표본,병보류설하신경근적완정.장36지신생SD대서수궤분위Ⅰ~Ⅵ조(n=6).Ⅰ조위대조조;Ⅱ~Ⅳ조위다사보륜조(농도분별위2、5、10μmol/L),V조급여병박분(20 μmol/L),Ⅵ조급여병박분(20μmol/L)+다사보륜(5μmol/L),관찰급약후1、3、5、10、15、30 min시설하신경근호흡절률성방전적변화,병분석흡기시정(TI)、호기시정(TE)、호흡주기(RC)、방전적분폭도(IA)적개변.결과 Ⅱ조재급약전후뇌편RRDA병무명현개변;Ⅲ、Ⅳ조재급약후1 min개시,흡기시정명현연장,방전적분폭도증가;호기시정우제5 min시개시축단(P<0.05),단호흡주기부우제10 min시축단,기여시간점무명현개변;V조재제3 min시개시출현흡기시정축단、방전적분폭도하강,병반유호기시정급호흡주기연장(P<0.05),제10 min시체최대변화치;Ⅵ조RRDA각시간점균무명현개변(P>0.05).결론5 μmol/L다사보륜가직접흥강연수뇌편적RRDA,차가완전길항병박분대뇌편RRDA적억제작용,차작용주요통과흥강흡기중추실현.
Objective To investigate the effects of doxapram on the respiratory rhythmical discharge activity (RRDA) in the brainstem slices of neonatal rats. Methods Thirty neonatal SD rats (of either sex, 0-3 days old) were randomly divided into 6 equal groups (groups Ⅰ-Ⅵ), and the brainstem slices which contained the medial region of the nucleus retrofacialis (mNRF)were prepared. All the slices were perfused with modified Kreb's solution (MKS), and in group Ⅰ (control group), the slices were perfused with MKS only; in groups Ⅱ to Ⅳ, the slices were perfnsed with doxapram in MKS continuously at the concentrations of 2, 5, and 10 μmol/L, respectively; in groups Ⅴ and Ⅵ, the slices were peffused with 20 μmol/L propofol and 20 μmol/L propofol plus 5 μmol/L doxapram, respectively. The RRDA in the hypoglossal nerve was recorded by suction electrode. The discharge time course of the inspiratory (TI), expiratory (TE), respiratory cycle (RC) and integral amplitude of the inspiratory discharge (IA) were recorded at 1, 3, 5, 10, 15, and 30 rain after the application of the drugs. Results The hypoglossal nerve in groups Ⅰ , Ⅱ and Ⅵ showed no significant changes of RRDA in the entire course of the experiment (P>0.05). In groups Ⅲ and Ⅳ, the TI, IA increased and TE decreased significantly 5 min after doxapram application (P<0.05),and the RC was shortened only at 10 min. In group V, the TI and IA decreased and the RC and TE increased significantly after the drug application (P<0.05). Conclusion Doxapram (>5 μmol/L) can directly stimulate the RRDA and prevent propofol-induced inhibitory effects in the brainstem slice of neonatal rats, and the effects are mediated by its actions upon the inspiratory neurons in the mNRF.