Given the environmental forcing by extremes in hypoxia-reoxygenation, there
might be no genetic effect on posthypoxic short-term potentiation of venti
lation. Minute ventilation ((V) over dot E), respiratory frequency (f), tid
al volume ((V) over dot T), and the airway resistance during chemical loadi
ng were assessed in unanesthetized unrestrained C57BL/6J (B6) and A/J mice
using whole body plethysmography. Static pressure-volume curves were also p
erformed. In 12 males for each strain, after 5 min of 8% O-2 exposure, B6 m
ice had a prominent decrease in V E on reoxygenation with either air (-11%)
or 100% O-2 (-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% O-2 expo
sure, B6 exhibited significant decrease in (V) over dot E (-28.4 vs. -38.7%
, air vs. 100% O-2) and f (-13.8 vs. -22.3%, air vs. 100% O-2) during reoxy
genation with both air and 100% O-2; however, A/J mice showed significant i
ncrease in (V) over dot E (+116%) and f (+62.2%) during air reoxygenation a
nd significant increase in V E (+68.2%) during 100% O-2 reoxygenation. Ther
e were no strain differences in dynamic airway resistance during gas challe
nges or in steady-state total respiratory compliance measured postmortem. S
train differences in ventilatory responses to reoxygenation indicate that g
enetic mechanisms strongly influence posthypoxic ventilatory behavior.