CAJ | 학술논문

背景:迄今为止呼吸节律的准确起源位置和其形成机制仍不清楚.作者以前的实验发现轻触压延髓腹侧表面舌下神经根部,家兔呼吸会立即停止.目的:观察在整体情况下,机械损毁家兔面神经后核内侧区对呼吸节律的影响.设计:随机对照实验.单位:昆明医学院生理教研室.材料:实验于2002-02/12在昆明医学院生理教研室进行.动物为实验用健康家兔54只,其中22只从延髓背侧面定位并机械损毁双侧面神经后核内侧区,18只从延髓腹侧面定位损毁,14只用于观察机械损毁面神经后核内侧区后血压和心率的变化.方法:分别暴露家兔延髓腹面侧和背面侧,切断双侧迷走神经,记录一侧膈神经放电作为呼吸指标,应用直径为0.8 mm或0.4 mm的不锈钢管损毁面神经后核内侧区,观察机械损毁对呼吸的影响.另取家兔14只,机械损毁双侧面神经后核内侧区,在机械损毁后1～3 min家兔血压和心率的变化.主要观察指标:①机械损毁双侧面神经后核内侧区致呼吸节律改变.②膈神经放电数及呼吸频率.③②损毁后1～3 min内血压和心率的变化.结果:54只家兔均进入结果分析.①从延髓腹侧面机械损毁双侧面神经后核内侧区致呼吸节律不可逆消失的总阳性率为67%(12/18),而从延髓背侧面机械损毁的总阳性率仅为14%(3/14).②出现呼吸节律不可逆消失的所有家兔的膈神经节律性放电明显稀少,不规则.膈神经放电的吸气时程和呼气时程显著延长,当呼气时程极度延长时,呼吸节律消失,动物呼吸停止于呼气相.②部分机械损毁双侧面神经后核内侧区时,家兔(n=27)的呼吸仍存在,但立即表现出明显的呼吸抑制,呼吸频率显著变慢[(43.5±6.4)%,P＜0.001],膈神经放电数显著减少[(42.0±3.7)%,P＜0.001],膈神经放电的吸气时程和呼气时程均显著延长,但以呼气时程的延长极为显著.④对上述各损毁点做组织学检查,引起呼吸停止或呼吸明显减弱的位点均在面神经后核内侧区内.⑤在损毁后1～3 min内,兔的心率和血压略有波动,变化幅度5%～7%,和正常值相比差异无显著性(P＞0.05).结论:面神经后核内侧区可能是呼吸节律产生的主要部位,而面神经后核内侧区中的呼吸相关神经元则可能是形成呼吸节律的重要组成部分. 揹景:迄今為止呼吸節律的準確起源位置和其形成機製仍不清楚.作者以前的實驗髮現輕觸壓延髓腹側錶麵舌下神經根部,傢兔呼吸會立即停止.目的:觀察在整體情況下,機械損燬傢兔麵神經後覈內側區對呼吸節律的影響.設計:隨機對照實驗.單位:昆明醫學院生理教研室.材料:實驗于2002-02/12在昆明醫學院生理教研室進行.動物為實驗用健康傢兔54隻,其中22隻從延髓揹側麵定位併機械損燬雙側麵神經後覈內側區,18隻從延髓腹側麵定位損燬,14隻用于觀察機械損燬麵神經後覈內側區後血壓和心率的變化.方法:分彆暴露傢兔延髓腹麵側和揹麵側,切斷雙側迷走神經,記錄一側膈神經放電作為呼吸指標,應用直徑為0.8 mm或0.4 mm的不鏽鋼管損燬麵神經後覈內側區,觀察機械損燬對呼吸的影響.另取傢兔14隻,機械損燬雙側麵神經後覈內側區,在機械損燬後1～3 min傢兔血壓和心率的變化.主要觀察指標:①機械損燬雙側麵神經後覈內側區緻呼吸節律改變.②膈神經放電數及呼吸頻率.③②損燬後1～3 min內血壓和心率的變化.結果:54隻傢兔均進入結果分析.①從延髓腹側麵機械損燬雙側麵神經後覈內側區緻呼吸節律不可逆消失的總暘性率為67%(12/18),而從延髓揹側麵機械損燬的總暘性率僅為14%(3/14).②齣現呼吸節律不可逆消失的所有傢兔的膈神經節律性放電明顯稀少,不規則.膈神經放電的吸氣時程和呼氣時程顯著延長,噹呼氣時程極度延長時,呼吸節律消失,動物呼吸停止于呼氣相.②部分機械損燬雙側麵神經後覈內側區時,傢兔(n=27)的呼吸仍存在,但立即錶現齣明顯的呼吸抑製,呼吸頻率顯著變慢[(43.5±6.4)%,P＜0.001],膈神經放電數顯著減少[(42.0±3.7)%,P＜0.001],膈神經放電的吸氣時程和呼氣時程均顯著延長,但以呼氣時程的延長極為顯著.④對上述各損燬點做組織學檢查,引起呼吸停止或呼吸明顯減弱的位點均在麵神經後覈內側區內.⑤在損燬後1～3 min內,兔的心率和血壓略有波動,變化幅度5%～7%,和正常值相比差異無顯著性(P＞0.05).結論:麵神經後覈內側區可能是呼吸節律產生的主要部位,而麵神經後覈內側區中的呼吸相關神經元則可能是形成呼吸節律的重要組成部分.
배경:흘금위지호흡절률적준학기원위치화기형성궤제잉불청초.작자이전적실험발현경촉압연수복측표면설하신경근부,가토호흡회립즉정지.목적:관찰재정체정황하,궤계손훼가토면신경후핵내측구대호흡절률적영향.설계:수궤대조실험.단위:곤명의학원생리교연실.재료:실험우2002-02/12재곤명의학원생리교연실진행.동물위실험용건강가토54지,기중22지종연수배측면정위병궤계손훼쌍측면신경후핵내측구,18지종연수복측면정위손훼,14지용우관찰궤계손훼면신경후핵내측구후혈압화심솔적변화.방법:분별폭로가토연수복면측화배면측,절단쌍측미주신경,기록일측격신경방전작위호흡지표,응용직경위0.8 mm혹0.4 mm적불수강관손훼면신경후핵내측구,관찰궤계손훼대호흡적영향.령취가토14지,궤계손훼쌍측면신경후핵내측구,재궤계손훼후1～3 min가토혈압화심솔적변화.주요관찰지표:①궤계손훼쌍측면신경후핵내측구치호흡절률개변.②격신경방전수급호흡빈솔.③②손훼후1～3 min내혈압화심솔적변화.결과:54지가토균진입결과분석.①종연수복측면궤계손훼쌍측면신경후핵내측구치호흡절률불가역소실적총양성솔위67%(12/18),이종연수배측면궤계손훼적총양성솔부위14%(3/14).②출현호흡절률불가역소실적소유가토적격신경절률성방전명현희소,불규칙.격신경방전적흡기시정화호기시정현저연장,당호기시정겁도연장시,호흡절률소실,동물호흡정지우호기상.②부분궤계손훼쌍측면신경후핵내측구시,가토(n=27)적호흡잉존재,단립즉표현출명현적호흡억제,호흡빈솔현저변만[(43.5±6.4)%,P＜0.001],격신경방전수현저감소[(42.0±3.7)%,P＜0.001],격신경방전적흡기시정화호기시정균현저연장,단이호기시정적연장겁위현저.④대상술각손훼점주조직학검사,인기호흡정지혹호흡명현감약적위점균재면신경후핵내측구내.⑤재손훼후1～3 min내,토적심솔화혈압략유파동,변화폭도5%～7%,화정상치상비차이무현저성(P＞0.05).결론:면신경후핵내측구가능시호흡절률산생적주요부위,이면신경후핵내측구중적호흡상관신경원칙가능시형성호흡절률적중요조성부분.
BACKGROUND: Until now, the definite source of respiratory rhythm generation and the ontogenic mechanism are still in controversy. Previous our investigating indicated that respiration would stop due to the gentle press on the hypoglossal root under the surface of ventral medulla of rabbit. OBJECTIVE: To observe the influence of mechanical lesion in medial re gion of nucleus retrofacialis on respiratory rhythm of a living rabbit model.DESIGN: Randomized controlled study.SETTING: At the Physiology Teaching Room of Kunming Medical College.MATERIALS: This study was carried out at the Physiology Teaching Room of Kunming Medical College from February 2002 to December 2002. Totally 54 healthy rabbits were randomly selected, amongst which 22 rabbits were submitted to the mechanical damage of the medial region of bilateral nucleus retrofacialis by the dorsal processes, and 18 received the same damage by the ventral process, 14 rabbits used for observing the changes of blood pressure andheart rate due to the mechanical damage.METHODS: The ventral and dorsal medullar of rabbits were exposed and the bilateral vagotomy at the cervical level were cut. Discharge of the phrenic nerve was used as the respiratory index. Stainless pipe of 0. 8 mm or 0.4 mm diameter was used to make mechanical damage at the medial region in order to investigate the changes of respiration. Fourteen rabbits were selected and submitted to the bilateral mechanical damage, the changes of blood pressure and heart rate were observed at post-traumatic 1 -3 minutes.MAIN OUTCOME MEASURES: ① The changes of respiratory rhythm induced by the mechanical damage of the medial region of bilateral nucleus retrofacialis. ② The number of phrenic nerve discharge and respiratory frequency. ③ The changes of blood pressure and heart rate at post-lesion 1-3minutes.RESULTS: Data of 54 rabbits were analyzed. ① Irreversible disappearance of respiratory rhythm was found in 12 out of 18 rabbits (the positive rate was 67% ) due to the mechanical damage by the ventral processes, comparing to 3 / 14 (14%) by the dorsal process. ② Rhythmic discharge of phrenic nerve became scarce and irregular in all rabbits who has irreversible disappearance of respiratory rhythm, the inspiratory and expiratory discharging phase were significantly prolonged, moreover respiratory rhythm would disappear if expiratory phase was extremely extended, respiration stopped at expiratory phase. ③ When the medial region of bilateral nucleus retrofacialis was partially destroyed, the still existed respiration of 27 rabbits was found immediately inhibited, phrenic nerve discharge frequency obviously decreased [ (43.5 ± 6.4)%, P ＜ 0. 001 ], and its discharge number was significantly decreased [ (42.0 ± 3.7 )%, P ＜ 0. 001 ], moreover the inspiratory and expiratory discharging phase were found obviously extended, with expiratory phase was in particular. ④ From the results of histological examination on the above mechanical lesion. Respiration stop or obvious attenuation was found mostly due to the damage at the medial region of nucleus retrofacialis.⑤ The blood pressure and heart rate changed slightly by 5% -7% at post-traumatic 1 -3 minutes, there was not significantly different from the normal value ( P ＞ 0. 05).CONCLUSION: The medial region of nucleus retrofacialis might be the main source of respiratory rhythm generation, and the related neuron within it would be the important component involving in the generation of respiratory rhythm.