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Physiological Adaptations During the Acclimatization To‐ and Deacclimatization From‐Chronic Hypercapnia
Author(s) -
Buchholz Kirstyn,
Burgraff Nicholas,
Neumueller Suzanne,
Pan Lawrence,
Hodges Matthew,
Forster Hubert
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.04267
Subject(s) - hypercapnia , acclimatization , medicine , respiratory system , copd , hypoxia (environmental) , anesthesia , ventilation (architecture) , biology , chemistry , oxygen , ecology , mechanical engineering , organic chemistry , engineering
Respiratory disturbances, such as chronic obstructive pulmonary disease (COPD), are often associated with chronically elevated arterial CO 2 (P a CO 2 >45mmHg), which has been linked to an increase risk of all‐cause mortality. Additionally, acute exacerbations of respiratory symptoms may lead to greater levels of P a CO 2 that require mechanical intervention to restore P a CO 2 to control levels. Many physiological effects of chronic hypercapnia have been previously reported, and include robust adaptations in acid/base, and respiratory control mechanisms. However, the effects of restoring P a CO 2 to control levels following chronically elevated P a CO 2 are largely unknown. Thus, the goal of my project is to gain insight into the physiological and ventilatory control adaptations during the acclimatization to‐ and deacclimatization from‐chronic hypercapnia. Based on studies focusing on the deacclimatization from chronic hypoxia, I hypothesize that deacclimatization from chronic hypercapnia would not be completed within 24 hours of return to normoxia. To assess the effects of deacclimatization from chronic hypercapnia, I measured the temporal pattern of ventilation, ventilatory CO 2 /[H + ] chemoreflex, and acid‐base status during acclimatization to‐ and deacclimatization from‐chronic exposure to elevated inspired CO 2 (InCO 2 ) in goats. Goats were chronically housed in environmental chambers that allowed for modification of ambient CO 2 levels. Following a room air control period, goats were exposed to an InCO 2 of 6% for 30 days, followed by returned to room air for 24 hours (hrs). Within 1 hour of 6% InCO 2 , V I increased to 322% above control, but decreased slightly to 293% above control after 24 hours. By Day 2 of exposure, P a CO 2 increased 15 Torr and changed minimally thereafter. pH decreased by 0.06 units upon initial exposure but was partially compensated by Day 5 due to an 8mEq/L increase in arterial [HCO3 − ]. Within 4hrs of deacclimatization, V I decreased to 123% above control, and continued to decrease to near control levels by 24hrs. P a CO 2 decreased 13mmHg by 24hrs, while pH increased 0.04 units. The CO 2 /[H + ] chemoreflex was assessed by increasing InCO 2 to 3, 5, and 7% at 4 and 24 hours of deacclimatization. The chemoreflex was above control at 4 and 24 hours of deacclimatization. The steady‐state ventilation/[H + ] relationship was also slightly elevated at 4 and 24hrs. Taken together, these data suggest that deacclimatization from chronic hypercapnia is nearly complete by 24 hours. Further studies will extend the recovery time to 5 days to see if the deacclimatization is complete. Additional studies will aim to use western blotting to investigate neurological adaptations underlying the deacclimatization process Support or Funding Information Department of Veteran Affairs