Recruitment of cardiac parasympathetic activity: effects of clonidine on cardiac vagal motoneurones, pressure lability, and cardiac baroreflex slope in rats

Abstract

Association of low cardiac vagal activity and poor outcome is demonstrated in the cardiology setting. This has not been addressed in the postoperative setting. Cardiac vagal motoneurones (CVMs) in the brain stem generate sinus arrhythmia. They may reduce blood pressure (BP) variability ('pressure lability'). An alpha-2 agonist, clonidine, was administered to assess whether cardiac vagal activity could be recruited from a very low baseline activity, increase the sensitivity of the cardiac baroreflex and sinus arrhythmia, and reduce the pressure lability. In ventilated anaesthetized rats, single-unit activity from antidromically identified CVMs was recorded. Given complex interactions within the cardiac ganglion, a peripherally acting beta-blocker, atenolol, was administered before clonidine. Atenolol 2 mg kg(-1) i.v. did not change systolic BP (SBP), CVM firing rate and slope of the cardiac baroreflex analysed at CVM (SBP-CVM unit activity relationship) level, or at the heart level (SBP-RR interval relationship) but evoked a significant bradycardia. In the presence of atenolol 2 mg kg(-1) h(-1), clonidine 10-100 microg kg(-1) i.v. evoked a significant reduction in SBP, a large increase of CVM firing rate from a very low base line [0.16 (sd 0.28) to 1.37 (1.21) spikes s(-1), n=7 cells], and increased the slope of the cardiac baroreflex analysed at the CVM level or at the heart level. sds of SBP were reduced, and that of RR interval was increased. Following peripheral beta-blockade, clonidine activated CVMs from a very low baseline, increased the slope of the cardiac baroreflex and sinus arrhythmia, and reduced pressure lability.