Blockage of the habenular nucleus can eliminate dyspnea induced by electrostimulation of the insular cortex  期刊论文  

BACKGROUND: The insular cortex and habenular nucleus may be a regulatory center for obstructive sleep apnea syndrome, and dyspnea may be caused by insular cortex activity. The insular cortex is a cortical representation of obstructive sleep apnea syndrome. The habenular nucleus is a station for descending insular cortex activity.
OBJECTIVE: Through actively stimulating the rat insular cortex, to observe rat respiratory movement, myoelectric activities of genioglossus, arterial partial pressure of oxygen, partial pressure of carbon dioxide and acidity-alkalinity, and to verify a hypothesis that the insular cortex is a superior-position regulation center, and the habenular nucleus is an inferior-position nervous nuclei of the insular cortex in patients with obstructive sleep apnea syndrome.
DESIGN, TIME AND SETTING: The randomized, controlled animal study was performed at the Laboratory of Electrophysiology, Department of Physiology, Norman Bathune College of Medicine, Jilin University, China from September 2004 to June 2008.
MATERIALS: We used L-glutamic acid (Dingguo Biological Product Research Center, Beijing, China), lidocaine hydrochloride (Seventh Pharmacy Co., Ltd., Wuxi, China), electric stimulator (Nihon Kohden, Japan), and an AVL-OPTI blood gas analyzer (AVL Scientific Co., Roswell, GA, USA).
METHODS: The insular cortex of healthy adult Wistar rats underwent electrostimulation and L-glutamic acid stimulation to record changes in the myoelectric activity of genioglossus and respiratory movement. Some rats were injected with lidocaine to block the habenular nucleus before electrostimulation or L-glutamic acid stimulation. L-glutamic acid and lidocaine were injected by microelectrodes embedded in nuclear groups.
MAIN OUTCOME MEASURES: Myoelectric activities of genioglossus, arterial partial pressure of oxygen, partial pressure of carbon dioxide and acidity-alkalinity Were measured following apnea in rats undergoing electrostimulation in the insular cortex and following blockade of the habenular nucleus.
RESULTS: Following electrostimulation and L-glutamic acid stimulation, rats developed apnea or respiratory rhythm disorders. Simultaneously, the amplitude of myoelectric activity of the genioglossus was reduced (P < 0.01), and the electromyogram integral was decreased (P < 0.01). Arterial blood gas analysis showed arterial blood acidosis, a decrease in pH (P < 0.05), and an increase in the negative value of alkaline reserve (P < 0.01). Lidocaine in the habenular nuclear blocked respiratory and other index changes after insular cortex stimulation.
CONCLUSION: Dyspnea induced by stimulating the insular cortex may require the habenular nucleus. Paralysis of the habenular nucleus can completely eliminate insular cortex stimulation-induced dyspnea.