Objective To develope a novel rabbit carotid body and carotid common artery model in vivo for the simulation of various intermittent hypoxia ( IH) intensities, IH durations, IH reoxygenation ( ROX) durations and continuous hypoxia ( CH) modes. Methods Forty-five adult New Zealand rabbits ( 2. 5-3. 0 kg) were anesthetized while spontaneous breathing kept intact. The tissue surrounding the right carotid common artery and carotid sinus nerve ( CSN) were cleared and " single" chemoreceptor bundle of the CSN was revealed. Then suction electrodes were placed and CSN afferent activity was monitored and recorded carefully. The right common carotid artery was exposed, cannulated to distal part and its proximal part was ligated. Preparations were challenged by changing the PO2 of the gas mixture equilibrating the perfusate. Alternatively perfusion ( 2 mL/min) of equilibrated perfusate bubbled with normoxia or hypoxia gas mixtures formed IH/ROX cycles in carotid common artery, simulating the pattern of hypoxic episodes seen in obstructive sleep apnea syndrome ( OSAS) , or with continuously perfusing hypoxia perfusate to form CH modes. All the perfusing procedures were regulated by a customized computer-controlled set and monitored using O2 gas analyzer. After the systematic exposures, carotid body, carotid common artery part distal to cannula, and carotid bifurcation were harvested as samples. Results The frequencies and average amplitudes of CSN chemoreceptor bundles afferent activities with normoxia perfusion were ( 0. 17 ±0. 03) impulse/ s and ( 46. 2 ±4. 4) μV, and with hypoxia perfusion were ( 0. 64 ±0. 09) impulse/ s and ( 87. 4 ±6. 6) μV, respectively. PO2 was ( 139 ±1. 5) mm Hg in normoxia perfusate and ( 35. 2 ±1. 3) mm Hg in hypoxia perfusate. Conclusion This new carotid body and carotid common arterymodel is a valuable tool to study neurological and biochemical changes in various IH and CH modes.
Objective To investigate whether the sleep-induced hypoxemia ( SIH) at different time and different level have different effects on pulmonary emphysema and coagulation systemfunction in the rats with pulmonary emphysema. Methods Thirty Wistar rats were randomly divided into three groups( n = 10 in each group) . All rats were exposed to cigarette smoke twice a day ( 30 min each time) . From29th day on, the rats in Group A ( pulmonary emphysema with short SIH) were also exposed to mixed gas of 12. 5% oxygen for 1. 5 hours during sleeping time every day ( the expose time was divided into 4 periods, 22. 5 min each) . The rats in Group B ( pulmonary emphysema with mild SIH) were also exposed to mixed gas of 15% oxygen for three hours during sleeping time every day( the expose time was divided into 4 periods, 45 min each) . The rats in Group C( pulmonary emphysema with standard SIH) were also exposed to mixed gas of 12. 5% oxygen for three hours during sleeping time every day( the expose time was divided into 4 periods,45 min each) . After continuous exposure for 56 days, the rats were sacrificed. Semi-quantitative image analytic method was employed for histopathological analysis including pathological score of lungs, mean linear intercept ( MLI) and mean alveolus number( MAN) . ATⅢ, FIB, vWF, FⅧ were measured. Results All animals in three groups manifested the histopathological features of emphysema. Pathological scores of lungs and MLI of every group were significantly different from each other( F = 21. 907, F = 18. 415, all P lt; 0. 05) , Group A [ ( 61. 90 ±4. 25) % , ( 92. 45 ±1. 78) μm] and Group B[ ( 64. 60 ±3. 95) % , ( 92. 80 ±3. 65) μm] were significantly lower than Group C[ ( 73. 30 ±3. 86) % , ( 99. 32 ±2. 81) μm, q= 8. 96, q =6. 84, q = 12. 64, q =9. 65, all P lt; 0. 05] . Levels of FIB were significantly different among three groups ( F = 20. 592, P lt; 0. 05) while FIB in Group A[ ( 189. 98 ±5. 29) mg/ dL] and Group B[ ( 182. 70 ±2. 78) mg /dL] were significantly lower than that in Group C[ ( 198. 40 ±7. 37) mg/ dL, q = 4. 86, q= 9. 07, all P lt; 0. 05] , and FIB in Group A was significantly higher than that in Group B( q = 4. 20, P lt; 0. 05) . Levels of FⅧ were significantly different from each other( F = 33. 652, P lt;0. 05) while FⅧ in Group A[ ( 232. 26 ±4. 17) % ]and Group B[ ( 242. 53 ±14. 50) % ] were significantly lower than that in Group C[ ( 303. 25 ±32. 93) % ,q= 10. 73, q = 9. 18, all P lt; 0. 05] . Conclusions Pulmonary emphysema and hypercoagulable states increases with time and severity of SIH in rats with pulmonary emphysema. The elevated activity of blood coagulation factor may be a critical role in the hypercoagulable states.