The purpose of the present study was to assess changes in heart period, heart‐period variance (HPV), and respiratory sinus arrhythmia (RSA) during manipulations of the baroreceptor reflex in anesthetized cats. Hypertension, induced via phenylephrine infusion, reflexly increases parasym‐pathetic activity and decreases sympathetic activity. Hypotension, produced by infusion of nitroprusside, leads to increased sympathetic activity and an inhibition of vagal influences on the heart. Specific autonomic contributions were assessed following administration of practolol, a β‐adrenergic blocker, or atropine methyl nitrate.
Spectral analysis was used to quantify the component of HPV associated with respiration, i.e., RSA, which is proposed to be sensitive to vagal influences on the heart. The respiratory component of HPV is described by a statistic, V̂, which is the sum of the spectral densities of the heart period spectrum across the band of frequencies associated with normal respiration.
Hypertension produced an increase in V̂ which was blocked by atropine infusion, but unaltered by beta‐adrenergic blockade. Hypotension decreased V̂ to near‐zero values which persisted after atropine and practolol infusion. These data suggest that V̂ is determined primarily by vagal factors. Correlations between V̂ and a previously used criterion measure of vagal tone further support this hypothesis. In contrast, heart period was sensitive to vagal and sympathetic factors. Heart period increases during hypertension were abolished with atropine and heart period decreases due to hypotension were eliminated by beta‐adrenergic blockade. These responses are consistent with the notion that heart period is under the control of both sympathetic and vagal factors. Since in an anesthetized preparation RSA is the major source of heart‐period variability, HPV responded similarly to V̂.
The results suggest that the spectral estimate of RSA, V̂, is particularly sensitive to blood pressure induced reflexive changes in vagal efferent influences on the heart. It also appears that V̂ is less influenced by sympathetic factors than heart period, a commonly used estimate of vagal activity.
Changes in heart period (HP), heart-period variance (HPV), and the respiratory component of HPV in freely moving rats were examined following pharmacological manipulations known to influence vagal control of the heart. Spectral analysis was used to quantify the component of HPV associated with respiration which is proposed to be sensitive to vagal influences on the heart. The respiratory component of HPV is described by a statistic, V', which is the sum ofthe spectral densities ofthe heart period spectrum across the band of frequencies associated with normal respiration, Vagai tone was reflexively enhanced hy phenylephrine or peripherally blocked by atropine.Phenylephrine produced biphasic changes in HP and V, with the increases lasting from 0.5 to 2 hrs. Atropine resulted in significant decreases in HP, HPV and V. These decreases were immediate and sustained throughout the experiment, although there were signiflcant linear increases in HP and HPV from their initial post-injection values. In the saline condition, HP increased linearly across time.Results were discussed in terms of vagal and non-vagal control of the heart. It was suggested that, while all three variables are altered by manipulations of vagal influences on the heart, V seems to be influenced less by non-vagal control than HP and HPV.
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