Role of Chronic Intermittent Hypoxia and Hypercapnia Induced Hypertension in Regulation of Blood Pressure




Cunningham, J. Thomas
Little, Joel


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Role of Chronic Intermittent Hypoxia and Hypercapnia Induced Hypertension in Regulation of Blood Pressure Purpose Sleep apnea is a prevalent disease characterized by momentary cessations in respiration leading to sustained hypertension. The hypertension experienced can be mimicked by periodic decreases in oxygen or chronic intermittent hypoxia (CIH) in humans and animal models. More recently, CIH has been combined with hypercapnia (CIH-H) to determine if an increase in circulating carbon dioxide, which is also experienced by patients that suffer from sleep apnea, contributes to neural adaptations related to sustained hypertension. CIH has been shown to have a significant effect on increased blood pressure due to increased sympathetic outflow from initiation and maintenance of hypertension. However, it is not known if the additional hypercapnic component significantly affects blood pressure or central autonomic control. Methods Male Sprague-Dawley rats are instrumented with radio telemetry one week after arrival. The radio telemetry provides information regarding cardiovascular variables continuously over a specified period of time. Animals were monitored for recovery for one week and then acclimated to the CIH or CIH-H rooms for 6 days, and monitored during this period for baseline data before experiencing 7 days of CIH, CIH-H or normoxic conditions. The CIH exposure is applied for 8 hours during the light (nocturnal) period from 8:00 AM to 4:00 PM, during which time hypoxia is produced using 3 min on-3 min off cycles that reduces oxygen from 21% to 10% to then being flushed with room air, so the inspired oxygen rises back to 21% before the cycle repeats. During CIH-H, rats are exposed to the same conditions with the addition of carbon dioxide that is raised from 0% to 8% during hypoxia to also produce hypercapnia. Results Rodents exposed to hypoxic and hypercapnic conditions did exhibit a greater increase in blood pressure than rodents exposed to only hypoxic conditions in the light period. The difference was not sustained during the return to normoxic conditions. Conclusions The results are consistent with previous studies which showed periods where there were greater increases in blood pressure in CIH-H animals than those exposed to hypoxia alone. Both CIH and CIH-H produced a greater increase in blood pressure during the light period. The difference did not appear to be sustained when rats were breathing room air.