Obstructive Sleep Apnea Syndrome And Ventilatory Control

IntroductionVentilatory control is one of the key center of human body. Studies indicated that abnormal Ventilatory made active roles for the occurrence of respiratory disease such as chronical obstructive pulmonary disease (COPD) , hypothyroid-ism and sleep apnea syndrome. The obvious manifestations for obstructive sleep apnea syndrome ( OSAS) are loud snore, daytime sleepiness and recurrent obstructive apnea during sleep. It is known that the abnormal upper airway structure could cause OSAS. However, it is uncertain what kind of roles the vertilato-ry control could take for the occurrence of OSAS. The OSAS family aggregation has been reported by some researches, does the genetic abnormalities of ventila-tory control could induce such trend? OSAS is related to the obesity and sex, which also could influence other diseases such as diabetes etc. So, obesity -related hormones - leptin, estrogen, testrone, resistin may also change in patients with OSAS. What are their functions? Are they concerned with Ventilatory control?Since all these problems are still obscure, some are even not studied yet, we entered into OSAS studies mainly in terms of the occurrence, genetic role, body fluid mechanisms and treatment of ventilatory control.1. Ventilatory Control in Obstructive Sleep ApneaObjective: To evaluate the role of ventilatory control in the occurrence of OSAS. Methods: Comparing 35 OSAS patients with 15 obese controls in arterial blood gas analysis, pulmonary function, hypoxic ventilatory response ( HVR ) , hypercapnic ventilatory response ( HCVR ) and results of polysomonograph ( PSG). Results: (1) P0.1 of OSAS was higher than that of control. There were no differences in HVR and HCVR between OSAS and control. HVR of OSASwas related to FEV1%PEF% ( r = 0. 54) and nocturnal nadir oxygen saturation ( r = -0.46). HCVR of OSAS was correlated to FEV1%/PEF% ( r = 0. 53). (2) Patients with mild and moderate OSAS had higher HVR than those with severe OSAS, when 5 ≤AHI <40, HVR was negatively related to AHI ( r = -0.50) , while P0.1was positively correlated with AHI ( r = 0.80 ). For those whose AHI≥ 40, the HVR was obviously correlated with nocturnal nadir oxygen saturation ( r = -0.57 ) and HCVR ( r = 0. 82 ) , their P0.1 was related to apnea time ( r = 0.57 ) and PLMI ( r = 0. 83 ). Conclusion: (1) The P0.1, of patients with OSAS constantly increased and closely related with apnea time and AHI; (2) HVR of OSAS showed two phase change - increase first and then decrease - following the elevation of AHI.