生理学报
生理學報
생이학보
ACTA PHYSIOLOGICA SINICA
2005年
6期
689-695
,共7页
Edward WINNER%张静文%Mary PROCTOR%於峻
Edward WINNER%張靜文%Mary PROCTOR%於峻
Edward WINNER%장정문%Mary PROCTOR%어준
迷走神经%肺%反射%机械感受器%传入神经
迷走神經%肺%反射%機械感受器%傳入神經
미주신경%폐%반사%궤계감수기%전입신경
vagus nerve%lung%reflex%mechanoreceptor%afferent nerve
钠钾泵抑制剂--哇巴因能引起气道内慢适应感受器异相发放,表现为冲动在正常时的吸气相发放,呼气相终止转变为在呼气相发放,吸气相终止.我们推测异相发放由过度兴奋所致,如果假设正确,那么降低气道压力从而减少对感受器刺激,将能防止异相发放.本工作在麻醉、开胸、机械通气(在呼气末附加3 cm水柱的正压)的家兔中记录颈迷走神经中慢适应感受器的单位放电,向感受野注射微量哇巴因(1 μmol/L,20μl),可观察到感受器活动发生变化.感受器放电经历紧张性发放、异相发放、以及不规则发放三个时期,随后放电终止,进入静息状态.在紧张期,感受器呈持续发放,冲动频率随肺部通气变化的波动幅度明显减小.在异相发放期,感受器活动出现突然发放(呼气相)与终止(吸气相),其冲动快速转换于高频发放和静止之间.此时,若撤除呼气末正压而减少气道内压力,感受器活动恢复正常,即冲动频率于气管压峰值时为最高,在呼气相减少或终止.在不规则期,感受器通常处于静止状态,时而出现突发高频冲动,且与呼吸周期无关.可以设想:在吸气相,感受器受到牵拉,引起钠、钙等阳离子内流,产生感受器电位.正常时,由于激活钠泵,将钠离子泵出细胞,使感受器电位回复.当钠泵受到抑制后,钠外流受阻,感受器电位加大.在异相发放期,肺充气时牵拉感受器,进一步增加感受器电位,当它超越了产生动作电位的活动范围后,则感受器因过度去极化而失去兴奋性.
鈉鉀泵抑製劑--哇巴因能引起氣道內慢適應感受器異相髮放,錶現為遲動在正常時的吸氣相髮放,呼氣相終止轉變為在呼氣相髮放,吸氣相終止.我們推測異相髮放由過度興奮所緻,如果假設正確,那麽降低氣道壓力從而減少對感受器刺激,將能防止異相髮放.本工作在痳醉、開胸、機械通氣(在呼氣末附加3 cm水柱的正壓)的傢兔中記錄頸迷走神經中慢適應感受器的單位放電,嚮感受野註射微量哇巴因(1 μmol/L,20μl),可觀察到感受器活動髮生變化.感受器放電經歷緊張性髮放、異相髮放、以及不規則髮放三箇時期,隨後放電終止,進入靜息狀態.在緊張期,感受器呈持續髮放,遲動頻率隨肺部通氣變化的波動幅度明顯減小.在異相髮放期,感受器活動齣現突然髮放(呼氣相)與終止(吸氣相),其遲動快速轉換于高頻髮放和靜止之間.此時,若撤除呼氣末正壓而減少氣道內壓力,感受器活動恢複正常,即遲動頻率于氣管壓峰值時為最高,在呼氣相減少或終止.在不規則期,感受器通常處于靜止狀態,時而齣現突髮高頻遲動,且與呼吸週期無關.可以設想:在吸氣相,感受器受到牽拉,引起鈉、鈣等暘離子內流,產生感受器電位.正常時,由于激活鈉泵,將鈉離子泵齣細胞,使感受器電位迴複.噹鈉泵受到抑製後,鈉外流受阻,感受器電位加大.在異相髮放期,肺充氣時牽拉感受器,進一步增加感受器電位,噹它超越瞭產生動作電位的活動範圍後,則感受器因過度去極化而失去興奮性.
납갑빙억제제--왜파인능인기기도내만괄응감수기이상발방,표현위충동재정상시적흡기상발방,호기상종지전변위재호기상발방,흡기상종지.아문추측이상발방유과도흥강소치,여과가설정학,나요강저기도압력종이감소대감수기자격,장능방지이상발방.본공작재마취、개흉、궤계통기(재호기말부가3 cm수주적정압)적가토중기록경미주신경중만괄응감수기적단위방전,향감수야주사미량왜파인(1 μmol/L,20μl),가관찰도감수기활동발생변화.감수기방전경력긴장성발방、이상발방、이급불규칙발방삼개시기,수후방전종지,진입정식상태.재긴장기,감수기정지속발방,충동빈솔수폐부통기변화적파동폭도명현감소.재이상발방기,감수기활동출현돌연발방(호기상)여종지(흡기상),기충동쾌속전환우고빈발방화정지지간.차시,약철제호기말정압이감소기도내압력,감수기활동회복정상,즉충동빈솔우기관압봉치시위최고,재호기상감소혹종지.재불규칙기,감수기통상처우정지상태,시이출현돌발고빈충동,차여호흡주기무관.가이설상:재흡기상,감수기수도견랍,인기납、개등양리자내류,산생감수기전위.정상시,유우격활납빙,장납리자빙출세포,사감수기전위회복.당납빙수도억제후,납외류수조,감수기전위가대.재이상발방기,폐충기시견랍감수기,진일보증가감수기전위,당타초월료산생동작전위적활동범위후,칙감수기인과도거겁화이실거흥강성.
Ouabain, a Na+/K+-ATPase inhibitor, induces slowly adapting pulmonary stretch receptors (SARs) to discharge paradoxically.Paradoxical discharge is characterized by increased SAR activity during lung deflation coupled with silence during lung inflation. We hypothesized that over-excitation silences the SARs. Accordingly, if cyclic inflation pressure was reduced so as to lower SAR stimulation,paradoxical discharge would be prevented. In the present study, single-unit activity of SARs was recorded in anesthetized, open-chest and mechanically ventilated rabbits with positive-end-expiratory pressure (PEEP). After microinjection of ouabain into the receptive field,SAR activity initially increased and then gradually became paradoxical. During paradoxical cycling, SAR activity started and stopped abruptly, oscillating between high frequency discharge during lung deflation and silence during peak inflation. Removing PEEP reduced basal cyclic stimulation and returned the discharge pattern to normal, that is, SAR activity was highest at peak inflation pressure but silent during deflation. It is speculated that stretching SARs causes Na+ influx, producing generator potential (GP). Normally, GP recovers by Na+ extrusion via Na+/K+-ATPase. Ouabain inhibits the ATPase, which limits Na+ extrusion, and thus sustains the GP. Therefore, after ouabain microinjection, lung inflation will further increase GP, causing over-excitation to silence the SARs.