Effects of Transcutaneous Electrical Nerve Stimulation in Autonomic Nervous System of Hypertensive Patients: A Randomized Controlled Trial.

BACKGROUND: Patients with hypertension have altered autonomic nervous system function, which are increased sympathetic activity. Transcutaneous Electrical Nerve Stimulation (TENS) is a useful modality for pain control and has also been shown to be effective in the reduction of sympathetic activity in healthy subjects and individuals with cardiovascular diseases. OBJECTIVE: The aim of this study was to verify the effects of transcutaneous electrical nerve stimulation by the evaluation of heart rate variability (HRV) in patients with essential hypertension. METHOD: Twenty-eight patients received an application of low-frequency TENS(4 Hz) n=8, highfrequency TENS (100 Hz) n=10 or placebo TENS n=10 in paravertebral ganglionar region during thirty minutes. RESULTS: After 4 Hz TENS, there was a decrease in the low-frequency (LFn.u.) component (57.71±9.46 vs 45.58±13.51, p<0.026) and an increase in the high-frequency (HFn.u.) component (33.03±13.83 vs 45.83±20.19, p <0.05) of HRV. After 100 Hz TENS and placebo, there were no changes in the LF and HF components. No significant differences were found in systolic blood pressure with low-frequency TENS (129.37± 15.48 vs 126.69 ± 15.21, p<0.490). There was an increase, although not significant, with high-frequency TENS (131.00 ± 15.97 vs 138.75 ± 25.79, p<0.121) and placebo (133.80 ± 29.85 vs 134.80 ± 29.72, p< 0.800). No differences were found in the diastolic blood pressure with low-frequency TENS and placebo, but there was a significant increase in high-frequency TENS (81.00 ± 11.78 vs 85.65 ± 13.68, p< 0.018). CONCLUSION: Low-frequency TENS decreases sympathetic nervous system activity and increases parasympathetic nervous system activity and high-frequency TENS increases diastolic blood pressure, when applied on the paravertebral ganglionar region in the hypertensive patients.

Cardiac autonomic dysfunction and neuroganglionitis in a rat model of chronic Chagas' disease.

OBJECTIVE: The aim was to evaluate whether the cardiac parasympathetic function in a rat model of chronic Chagas' disease is impaired as in the human disease, and to correlate the functional state to histopathology of the intrinsic autonomic innervation of heart. METHODS: 70 male Wistar rats 8 months infected with strains Y (n = 22), São Felipe (n = 18), and Colombia (n = 30) of Trypanosoma cruzi, were compared with 20 age and sex matched non-infected controls. Baroreflex bradycardia was quantified after multiple bolus injections of phenylephrine (3 to 12 micrograms). For each rat studied a mean was obtained of the absolute and relative (delta %) ratio (index) between the maximum heart rate decrease and the maximum systolic blood pressure increase. RESULTS: For the relative index the means were smaller (p less than 0.05) in the Y [-0.52(SD 0.19)%], São Felipe [-0.45(0.28)%], and Colombia [-0.53(0.21%)] subgroups, as well as in the pooled chagasic group [-0.51(0.22)%], than in the control group [-0.64(0.13)%]. In 32% (7/22), 33% (6/18), and 20% (6/30) of rats infected with Y, São Felipe, and Colombia strains, respectively, and in 27% (19/70) of the pooled group rats, the index exceeded the control group mean by -2 SD. After atropinisation, a similar pronounced reduction (p less than 0.01) in the index was observed in all groups [-84(28)% to -95(17)%]; however, rats with depressed bradycardia showed a smaller (p less than 0.05) reduction in the relative index than control rats, at -70(34) v -92(16%). Inflammatory and degenerative lesions of the intrinsic cardiac innervation were observed in 87% of the rats with autonomic dysfunction. Rats with the lesions showed a mean relative index that was smaller than those without lesions, at -0.44(0.23) v -0.64(0.20)% (p less than 0.01), and also smaller than in the controls. CONCLUSIONS: Cardiac autonomic dysfunction expressed by reduced baroreflex bradycardia was detected in rats chronically infected with T cruzi, as in human Chagas' disease. The disturbance, shown for the first time in an animal model of chagasic infection, resulted primarily from impaired efferent parasympathetic activity caused by intrinsic neuroganglionar lesions.