Photoplethysmography as a Potential Alternative to Electrocardiography for Recording Heart Rate Intervals Used in Variability Analysis.

Rationale. This study investigates the use of photoplethysmography (PPG) as a comfortable alternative to electrocardiography (ECG) for heart rate variability (HRV) analysis. Although HRV is typically analyzed from an ECG trace, PPG poses a likely alternative, as arterial pulsations and peripheral tissue perfusion (as measured by PPG) are coupled with cardiac electrical activity (as measured by ECG). PPG may be more desirable in some clinical circumstances, as a fingertip optical sensor is more comfortable for patients than ECG electrodes, and can reduce waste by not needing to be disposed after each use. Objective. The aim of this study is to assess the efficacy of using PPG as an alternative to ECG for recording cardiac activity for HRV analysis by comparing HRV data obtained using both methods. Methods and results. The study was conducted on 10 healthy human subjects, aged 20 to 25 years (4 males, 6 females). Three lead ECG and fingertip PPG traces were simultaneously recorded with a two-channel analog-to-digital converter and HRV parameters were calculated from each data set. The two sets of HRV data simultaneously obtained from the same subjects were compared. The results showed a high correlation between ECG-derived and PPG-derived HRV data (R2>0.95). Time-domain parameters, frequency-domain parameters and Poincaré geometry and analysis showed no significant difference between HRV analyses using PPG as compared to ECG for heart beat detection. Discussion. The comparison between the two methods indicates that PPG is a reliable instrument to precisely assess HRV parameters, showing no statistically significant differences when compared to HRV assessments calculated using ECG.

Vagal afferent innervation and remodeling in the aortic arch of young-adult fischer 344 rats following chronic intermittent hypoxia.

Previously, we have shown that chronic intermittent hypoxia (CIH) impairs baroreflex control of heart rate and augments aortic baroreceptor afferent function. In the present study, we examined whether CIH induces structural changes of aortic afferent axons and terminals. Young-adult Fischer 344 (F344, 4 months old) rats were exposed to room air (RA) or CIH for 35-45 days. After 14-24 days of exposure, they received tracer DiI injection into the left nodose ganglion to anterogradely label vagal afferent nerves. After surgery, animals were returned to their cages to continue RA or CIH exposure. Twenty-one days after DiI injection, the animals were sacrificed and the aortic arch was examined using confocal microscopy. In both RA and CIH rats, we found that DiI-labeled vagal afferent axons entered the wall of the aortic arch, then fanned out and branched into large receptive fields with numerous terminals (flower-sprays, end-nets and free endings). Vagal afferent axons projected much more to the anterior wall than to the posterior wall. In general, the flower-sprays, end-nets and free endings were widely and similarly distributed in the aortic arch of both groups. However, several salient differences between RA and CIH rats were found. Compared to RA control, CIH rats appeared to have larger vagal afferent receptive fields. The CIH rats had many abnormal flower-sprays, end-nets, and free endings which were intermingled and diffused into "bush-like" structures. However, the total number of flower-sprays was comparable (P>0.05). Since there was a large variance of the size of flower-sprays, we only sampled the 10 largest flower-sprays from each animal. CIH substantially increased the size of large flower-sprays (P<0.01). Numerous free endings with enlarged varicosities were identified, resembling axonal sprouting structures. Taken together, our data indicate that CIH induces significant remodeling of afferent terminal structures in the aortic arch of F344 rats. We suggest that such an enlargement of vagal afferent terminals may contribute to altered aortic baroreceptor function following CIH.

Impaired baroreflex control of renal sympathetic nerve activity in type 1 diabetic mice (OVE26).

To investigate the effects of chronic diabetes on baroreflex control of renal sympathetic nerve activity (RSNA), OVE26 diabetic (transgenic mouse line which develops hyperglycemia within the first 3 weeks after birth) and FVB control mice 5-6 months old were studied. Under anesthesia, RSNA in response to sodium nitroprusside (SNP)- and phenylephrine (PE)-induced mean arterial pressure changes (DeltaMAP) were measured. Baroreflex-induced inhibition of RSNA during PE infusion was characterized using the sigmoid logistic function curve. Baroreflex-induced excitation of RSNA during SNP infusion was characterized by the RSNA vs. DeltaMAP relationship. Mean arterial pressure (MAP) responses to the left aortic depressor nerve (ADN) stimulation were evaluated. Compared to FVB control, we found in OVE26 mice that (1) RSNA in response to MAP increase during PE infusion was dramatically reduced, as characterized by the maximal gain of the RSNA sigmoid logistic function curve (FVB: -20.0+/-5.1; OVE26: -7.6+/-0.8%/mm Hg, P<0.05); (2) RSNA in response to MAP decrease during SNP infusion was also attenuated (P<0.05); (3) MAP responses to ADN stimulation were reduced (P<0.05). We concluded that chronic diabetes impairs baroreflex control of RSNA in OVE26 diabetic mice. The use of the transgenic OVE26 diabetic mouse model may underlie a foundation for the further understanding of diabetes-induced autonomic neuropathy.