Hyperventilation in normoxia following myocardial infarction in rats: a shift in the set point of the hypoxic ventilatory response.

AIM

The peripheral chemoreflex is augmented in heart failure, and it may contribute to sympathoexcitation. This study aimed to investigate both the chemoreflex and the cardiac sympathetic nerve activity in the acute-stage post-myocardial infarction.

METHODS

Myocardial infarction was induced in male adult Sprague-Dawley rats by permanent ligation of the left anterior descending coronary artery. Within-animal repeated measure assessment of normoxic and hypoxic ventilation patterns was determined with whole-body plethysmography and compared to sham-operated controls. Cardiac function, morphology and cardiac sympathetic nerve activity were determined 14 days later.

RESULTS

Infarction induced increases in normoxic ventilation through increases in tidal volume within 3 days. At the same time points, the hypoxic ventilatory response to short durations (10 min) of hypoxia (8, 10 and 12% inspired O2 ) was blunted. At the end of the experiment (D14), increases in nerve activity, specifically through increased firing rate, and significant cardiac dysfunction (ejection fraction 43%) were observed in myocardial infarction (MI) group.

CONCLUSIONS

An augmentation of normoxic ventilation caused by myocardial infarction occurs before the amplification of the hypoxic ventilatory response. It occurs much earlier following myocardial injury than previously demonstrated and may have a role in initiating cardiac sympathoexcitation. The difference in the augmentation of hypoxic response between early and late stages post-myocardial infarction suggest that the initial change in the chemoreflex is an alteration to the operating point of chemoreflex.