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Departments of 1 Medicine and 2 Pediatrics, Case Western Reserve University, Cleveland, Ohio 44106
Given the environmental forcing by extremes in
hypoxia-reoxygenation, there might be no genetic effect on posthypoxic
short-term potentiation of ventilation. Minute ventilation
(
E), respiratory frequency (f), tidal volume
(VT), and the airway resistance during chemical loading
were assessed in unanesthetized unrestrained C57BL/6J (B6) and A/J mice
using whole body plethysmography. Static pressure-volume curves
were also performed. In 12 males for each strain, after 5 min of 8%
O2 exposure, B6 mice had a prominent decrease in
E on reoxygenation with either air (
11%) or 100% O2 (
20%), due to the decline of f. In contrast, A/J
animals had no ventilatory undershoot or f decline. After 5 min of 3%
CO2-10% O2 exposure, B6 exhibited significant
decrease in
E (
28.4 vs.
38.7%, air vs. 100%
O2) and f (
13.8 vs.
22.3%, air vs. 100% O2) during reoxygenation with both air and 100%
O2; however, A/J mice showed significant increase in
E (+116%) and f (+62.2%) during air reoxygenation
and significant increase in
E (+68.2%) during 100%
O2 reoxygenation. There were no strain differences in
dynamic airway resistance during gas challenges or in steady-state total respiratory compliance measured postmortem. Strain differences in
ventilatory responses to reoxygenation indicate that genetic mechanisms
strongly influence posthypoxic ventilatory behavior.
ventilatory control; genetics; mouse strains; short-term potentiation
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