Pathologic and hemodynamic changes of common carotid artery in obstructive sleep apnea hypopnea syndrome in a porcine model

Abstract

Background/aim: To prepare a porcine model of obstructive sleep apnea-hypopnea syndrome (OSAHS) and observe the pathological and hemodynamic changes in the common carotid artery. Materials and methods: Twelve male miniature pigs were randomly divided into the model and control group (n = 6). Pigs in the model group were kept in an air-flow negative pressure chamber at 0.96 ± 0.01 kPa, and the air oxygen content, temperature, and humidity were kept at normal culture conditions in both groups. After pigs in the model group presented symptoms of OSAHS, changes in the hemodynamics and morphology of the carotid artery were analyzed using color Doppler, and light and electron microscopy. Results: An animal model of OSAHS was successfully created. The internal diameter of the carotid artery of pigs in the model group was decreased, while the intima thickness, peak-systolic mean velocity, and resistance index were increased when compared to the control group (P < 0.05). The results of the light and electron microscopy revealed an incomplete elastic plate, increased media thickness, irregular morphology of the smooth muscle cells, increased collagen fiber bundles, partially disordered elastic fibers, and smooth muscle layers. The quantitative analysis showed significantly increased elastic fibers in the media of the carotid artery in the model group (P < 0.01). Conclusion: Pathological changes in the tissue structure and hemodynamics in the negative pressure-induced pig OSAHS model were observed. We suggest that alterations in the upper airway pressure during OSAHS may lead to cardiovascular conditions through its pathological effects on the carotid artery.

Advances in animal models of obstructive sleep apnea

“…But meanwhile the experimental group showed activity decreased, sleep time increased, snoring intensity increased (43–51 dB), respiratory rate increased, peak value of negative respiratory pressure increased (3.5–4 kPa), and respiratory pressure waveform became irregular. The above characteristics are partly consistent with the parameter characteristics of human OSA patients ( 30 ).…”

“…In healthy people, the transmural pharyngeal pressure is maintained from 0 to +10 mmHg during sleep. Upper airway obstruction in OSA patients is associated with transmural negative pressure during sleep ( 30 ). King et al found that when healthy controls were exposed to an environment of -10 cm H 2 O to sleep, polysomnography (PSG) results showed that upper respiratory tract obstruction did occur during sleep and induce OSA ( 31 ).…”