摘要
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.
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.
基金
the National Natural Science Foundation of China,No.V30270502,C010703
