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机构地区:[1]西安医学院解剖学教研室,西安710021 [2]解放军第一医院检验科,兰州730030 [3]陕西省博爱医院,西安710065
出 处:《中国药学杂志》2012年第18期1473-1477,共5页Chinese Pharmaceutical Journal
基 金:国家自然科学基金资助项目(30700266);陕西省卫生厅资助课题(06E05)
摘 要:目的 Salusin-α在大鼠尾端延髓腹外侧区(caudal ventrolateral medulla,CVLM)对心血管活动的调节作用及其机制研究尚不清楚。本实验主要探讨salusin-α在麻醉大鼠尾端延髓腹外侧区的心血管效应机制。方法雄性SD大鼠61只,其中25只大鼠单侧尾端延髓腹外侧区注射不同剂量salusin-α(0.04~4 pmol)或人工脑脊液(artificial cerebrospinalfluid,aCSF),观察salusin-α对大鼠血压和心率产生的影响。36只大鼠分别预先在尾端延髓腹外侧区给予人工脑脊液、非选择性谷氨酸受体拮抗剂犬尿希酸(kynurenic acid,Kyn)、毒蕈碱受体(M受体)阻断剂阿托品(atropine)、烟碱能受体(N受体)阻断剂六烃季铵(hexamethonium,Hex)或在头端延髓腹外侧区(rostral ventrolateral medulla,RVLM)用人工脑脊液/γ-氨基丁酸受体激动剂蝇蕈醇(5 pmol)预处理,观察对尾端延髓腹外侧区内salusin-α心血管效应受体机制。结果在尾端延髓腹外侧区单侧微量注射salusin-α产生剂量依赖性降低血压、减缓心率的作用。尾端延髓腹外侧区预先注射犬尿希酸(1 nmol)或六烃季铵均不影响尾端延髓腹外侧区微量注射salusin-α产生的降低血压、减缓心率的效应(P>0.05)。预先在尾端延髓腹外侧区微量注射阿托品或在头端延髓腹外侧区预先注射蝇蕈醇均能有效阻断salusin-α(4pmol)在尾端延髓腹外侧区产生的降低血压、减缓心率的效应(P<0.05)。结论 Salusin-α在大鼠尾端延髓腹外侧区产生的降低血压、减缓心率的作用可能由尾端延髓腹外侧区内M胆碱能受体介导,通过抑制头端延髓腹外侧区内前交感神经元活动产生的抑制效应。OBJECTIVE To determine the cardiovascular actions of salusin-ct in the caudal ventrolateral medulla (CVLM) in anesthetized rats. METHODS Sixty-one anesthetic male SD rats were employed in the present study. The dose-dependant effects of salusin-α (0. 04 -4 pmol ) on blood pressure and heart rate in the CVLM were determined by unilateral microinjection of salusin-α or artificial cerebrospinal fluid (aCSF) into the CVLM in 25 rats. In the other 36 rats, a CSF, kynurenic acid ( Kyn), atropine, hexametho- nium (Hex) in the CVLM or aCSF/ muscimol in the RVLM were given in advance to determine the mechanism of the cardiovascular actions of intra-CVLM salusin-α. RESULTS Unilateral microinjection of salusin-α into the CVLM produced a dose-dependent hypo- tension and bradycardia. Prior administration of Kyn( 1 nmol) or Hex ( 120 pmol) into the CVLM did not alter the hypotension and bradycardia induced by intra-CVLM salusin-ct ( P 〉 0. 05 ). But prior administration of atropine into the CVLM or pretreatment with muscimol within RVLM almost completely abolished the hypotension and bradycardia evoked by intra-CVLM salusin-u ( P 〈 0. 05 ). CONCLUSION Microinjection of salusin-α into the CVLM produces significantly hypotension and bradycardia,which probably origi- nates from suppressing the activities of presympathetic neurons in the RVLM.
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