摘要
Background： Obstructive sleep apnea is strongly associated with obesity, particularly abdominal obesity common in centrally obese males. Previous studies have demonstrated that intra-abdominal pressure （IAP） is increased in morbid obesity, and tracheal traction forces may influence pharyngeal airway collapsibility. This study aimed to investigate that whether IAP plays a role in the mechanism of upper airway （UA） collapsibility via IAP-related caudal tracheal traction. Methods： An abdominal wall lifting （AWL） system and graded CO2 pneumoperitoneum pressure was applied to four supine, anesthetized Guizhou miniature pigs and its effects on tracheal displacement （TD） and airflow dynamics of UA were studied. Individual run data in 3 min obtained before and after AWL and obtained before and after graded pneumoperitoneum pressure were analyzed. Differences between baseline and AWL/graded pneumoperitoneum pressure data of each pig were examined using a Student＇s t-test or analysis of variance. Results： Application of AWL resulted in decreased IAP and significant caudal TD. The average displacement amplitude was 0.44 mm （P 〈 0.001 ）. There were three subjects showed increased tidal volume （TV） （P 〈 0.01 ） and peak inspiratory airflow （P 〈 0.01 ）; however, the change of flow limitation inspiratory UA resistance （Rua） was not significant. Experimental increased lAP by pneumoperitoneum resulted in significant cranial TD. The average displacement amplitude was 1.07 mm （P 〈 0.001） when lAP was 25 cmH2O compared to baseline. There were three subjects showed reduced Rua while the TV increased （P 〈 0.01 ）. There was one subject had decreased TV and elevated Rua （P 〈 0.001）. Conclusions： Decreased IAP significantly increased caudal TD, and elevated lAP significantly increased cranial TD. However, the mechanism of UA collapsibility appears primarily mediated by changes in lung volume rather than tracheal traction effect. TV plays an independent role in the mechanism of UA collapsibility.
Background： Obstructive sleep apnea is strongly associated with obesity, particularly abdominal obesity common in centrally obese males. Previous studies have demonstrated that intra-abdominal pressure （IAP） is increased in morbid obesity, and tracheal traction forces may influence pharyngeal airway collapsibility. This study aimed to investigate that whether IAP plays a role in the mechanism of upper airway （UA） collapsibility via IAP-related caudal tracheal traction. Methods： An abdominal wall lifting （AWL） system and graded CO2 pneumoperitoneum pressure was applied to four supine, anesthetized Guizhou miniature pigs and its effects on tracheal displacement （TD） and airflow dynamics of UA were studied. Individual run data in 3 min obtained before and after AWL and obtained before and after graded pneumoperitoneum pressure were analyzed. Differences between baseline and AWL/graded pneumoperitoneum pressure data of each pig were examined using a Student＇s t-test or analysis of variance. Results： Application of AWL resulted in decreased IAP and significant caudal TD. The average displacement amplitude was 0.44 mm （P 〈 0.001 ）. There were three subjects showed increased tidal volume （TV） （P 〈 0.01 ） and peak inspiratory airflow （P 〈 0.01 ）; however, the change of flow limitation inspiratory UA resistance （Rua） was not significant. Experimental increased lAP by pneumoperitoneum resulted in significant cranial TD. The average displacement amplitude was 1.07 mm （P 〈 0.001） when lAP was 25 cmH2O compared to baseline. There were three subjects showed reduced Rua while the TV increased （P 〈 0.01 ）. There was one subject had decreased TV and elevated Rua （P 〈 0.001）. Conclusions： Decreased IAP significantly increased caudal TD, and elevated lAP significantly increased cranial TD. However, the mechanism of UA collapsibility appears primarily mediated by changes in lung volume rather than tracheal traction effect. TV plays an independent role in the mechanism of UA collapsibility.
基金
Financial support and sponsorship This study was supported by a grant from National Natural Science Foundation of China （No. 81200735）.
