Algogen-induced vasosensory reflexes modulate short-term heart rate variability parameters in experimental rat models.

Abstract

The present work was designed to study the modulatory effects of algogen-induced vasosensory reflex responses on short-term heart rate variability (HRV) parameters in naïve and vagotomized rat models. In this study, vasosensory reflex responses were elicited by instilling algogens (bradykinin/histamine), a component of inflammatory mediators into a local segment of medium-sized peripheral blood vessel (femoral artery) while a continuous electrocardiogram (ECG) was recorded. Short-term (5min) ECG segments obtained from original recordings were examined in detail and relevant data of HRV parameters were pooled. Time domain and frequency domain analyses were performed using dedicated software (LabChart 8, AD Instruments®, Australia) and results were analyzed. Bradykinin-induced vasosensory reflexes caused significant alterations in both time domain and frequency domain HRV parameters as compared to the time-matched saline control group. Instillation of bradykinin caused a transient increase in NN interval, RMSSD, TSP, HF power (HFP) along with a decrease in the standard deviation of all normal NN intervals (SDNN), SDNN/RMSSD, LF power (LFP), LFP/HFP. Histamine produced a similar pattern of responses, but HRV alterations were less pronounced compared to those with bradykinin. Further analysis revealed that algogen-induced vasosensory reflex responses caused an increase in the parasympathetic influence on the heart accompanied by a decrease in sympathetic influence. In addition, HRV modulation by algogen-induced vasosensory reflexes was significantly attenuated in vagotomized rats, illustrating the principal role of vagus in the reflex HRV modulation. The present study proposes a novel hypothesis regarding the cardio-protective role of inflammatory mediators during acute stress, by potentiating the vagal impact and attenuating the sympathetic impact on the heart.