Influence of acute hypoxia combined with nitrous oxide on cardiovascular variability in conscious hypertensive rats

Anesthetics have been reported to depress autonomic nervous system (ANS) responses to hypoxia. The mechanisms by which cardiovascular variability responds to acute progressive hypoxia (APH) under nitrous oxide (N(2)O) inhalation, however, remain unclear. Additionally, the effect of hypertension on ANS responses in such cases has not been fully clarified. The present study examined the influence of APH (10% O(2)) under 60% N(2)O inhalation on cardiovascular variability in conscious, spontaneously hypertensive rats (SHR). Twenty-seven male SHR were randomly assigned to 3 treatment groups receiving N(2)O inhalation alone, APH stress alone or APH stress under N(2)O inhalation, using Wistar Kyoto rats (WKY) or non-N(2)O inhalation rats as controls. Systolic blood pressure (SBP) and heart rate (HR) variability were evaluated time-dependently using the wavelet method. While inhalation of N(2)O alone induced more powerful sympathomimetic actions in SHR than in WKY, circulatory and parasympathetic reactions were weaker. APH stress alone evoked significant inhibition of cardiac parasympathetic activity from immediately after exposure to hypoxic stress in SHR in contrast to WKY, facilitating tachycardia. This inhibition of parasympathetic activity in SHR continued without coupled changes in sympathetic activity. In SHR, APH under N(2)O inhalation decreased SBP and sympathetic activity more prominently and earlier than APH alone, and earlier than APH under N(2)O inhalation in WKY. Additionally, APH under N(2)O inhalation inhibited cardiac parasympathetic activity in SHR as compared to APH stress alone. In conclusion, APH under N(2)O inhalation in SHR potentially results in exacerbation of circulatory suppression from the earlier hypoxic phase, compared with non-N(2)O inhalation.