Detection and sources of nonlinearity in the variability of cardiac R-R intervals and blood pressure in rats

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Abstract
Beat-to-beat R-R interval (RRV) and systolic blood pressure (SPV) variability signals were obtained from unrestrained rats in baseline and under different pharmacological treatments. The origin and extent of the nonlinearity in both signals, as well as their degree of mutual coupling, was estimated using measurements from the correlation integral (CI) and recurrence quantification analysis (RQA). After the respiratory component of baseline signals was removed, the nonlinearity was lower in the RRV and disappeared in the SPV. This also decreased the RRV-SPV coupling. The nonlinearity of RRV was also reduced after atropine, and the nonlinearity of SPV was strengthened after prazosin and N ω-monomethyl-l-arginine (l-NMMA). Atropine and prazosin decreased CI measures of both signals, whereas propranolol, phenylephrine, andl-NMMA decreased only those of SPV. RQA indexes of RRV increased after atropine and decreased after propranolol, whereas the reverse occurred for the RRV-SPV coupling. These results suggest that: 1) the nonlinearity of RRV appears to be very dependent on the parasympathetic activity, whereas that of SPV seems to come from its respiratory component through a nonneural pathway; 2) respiratory component appears to be involved, through the parasympathetic system, in the RRV-SPV coupling; and 3) CI and RQA measures seems to be useful in assessing autonomic mediation of RRV and RRV-SPV coupling.