Yuan B X, Ardell J L, Hopkins D A, Armour J A
Department of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada.
Cardiovasc Res. 1993 May;27(5):760-9. doi: 10.1093/cvr/27.5.760.
The aim was to study the locations and functions of atrial and ventricular nicotine sensitive neurones.
In anaesthetised open chest dogs, cardiovascular effects elicited by nicotine (100 micrograms in 0.1 ml 0.9% saline), administered at specific loci of in situ atrial and ventricular ganglionated plexi, were studied before and after decentralisation.
Cardiovascular responses were elicited when 41% of atrial and 36% of ventricular ganglionated plexus loci were studied. Subsequently, ganglia were identified adjacent to active sites. When cardiovascular responses were elicited, either tachycardia or bradycardia was induced, depending on the locus investigated. When tachycardia occurred, atrial and/or ventricular forces were augmented. When bradycardia occurred, atrial forces were suppressed. Ventricular fibrillation was induced in two animals when ventricular ganglionated plexus loci were investigated. Cardiovascular responses were not elicited when up to 2000 micrograms of nicotine were administered adjacent to intrinsic cardiac axons, indicating that responses were not primarily due to axonal effects. Control injections of saline (0.1 ml) into active loci did not elicit cardiovascular responses. Following acute decentralisation, responses initiated by nicotine were attenuated or eliminated. Depressor responses were no longer elicited following atropine administration, nor augmentor ones following propranolol administration.
(1) The canine heart contains nicotine sensitive neurones which can induce either augmentor or depressor cardiac effects. (2) Nicotine sensitive atrial neurones modify primarily, but not exclusively, atrial tissues, whereas ventricular ones modify primarily, but not exclusively, ventricular tissues. (3) Nicotine sensitive intrinsic cardiac neurones can interact with central neurones to modulate the heart.
研究心房和心室尼古丁敏感神经元的位置及功能。
在麻醉开胸犬身上，研究在原位心房和心室神经节丛的特定部位给予尼古丁（100微克溶于0.1毫升0.9%盐水中）所引发的心血管效应，观察在去神经支配前后的变化。
在研究41%的心房和36%的心室神经节丛部位时引发了心血管反应。随后，在活跃部位附近识别出神经节。引发心血管反应时，根据所研究的部位，会诱发心动过速或心动过缓。出现心动过速时，心房和/或心室力量增强。出现心动过缓时，心房力量受到抑制。在研究心室神经节丛部位时，两只动物诱发了心室颤动。当在心脏固有轴突附近给予高达2000微克尼古丁时，未引发心血管反应，表明反应并非主要由轴突效应所致。向活跃部位注射对照盐水（0.1毫升）未引发心血管反应。急性去神经支配后，尼古丁引发的反应减弱或消除。阿托品给药后不再引发降压反应，普萘洛尔给药后不再引发升压反应。
（1）犬心脏含有尼古丁敏感神经元，可诱发心脏的升压或降压效应。（2）尼古丁敏感的心房神经元主要但非唯一地影响心房组织，而心室神经元主要但非唯一地影响心室组织。（3）尼古丁敏感的心脏固有神经元可与中枢神经元相互作用以调节心脏。
