Power spectra of arterial pressure and heart rate in streptozotocin-induced diabetes in rats

Background Chronic diabetes is associated with alterations in autonomic modulation of the cardiovascular system. Although the rat has been used extensively in studies of experimental diabetes, there have been no reports on the changes in autonomic modulation of the cardiovascular function in chronic diabetic rats. Objective To examine chronic diabetic rats to determine the autonomic modulation of arterial pressure and heart rate variabilities in the time and frequency domain. Materials and methods Diabetes was induced in rats by a single injection of streptozotocin, and 30 min of pulsatile arterial pressure was recorded in conscious rats, 5, 10-20 days and 12-18 weeks after the streptozotocin injection. Control rats were injected with vehicle. Beat-by-beat systolic arterial pressure and heart rate were obtained from pulsatile pressure. The spectral density powers of systolic arterial pressure and heart rate were calculated using fast Fourier transformation, and integrated in low- (0.015-0.25 Hz), mid- (0.25-0.75 Hz) and high- (0.75-3.0 Hz) frequency bands. The standard deviations of systolic arterial pressure and heart rate were also calculated. Results Basal systolic arterial pressure and heart rate were reduced in diabetic animals studied 10-20 days and 12-18 weeks after the streptozotocin injection. The standard deviations of systolic arterial pressure and heart rate were also reduced in the chronically diabetic animals. Diabetes reduced low- and mid-frequency variability but not the high-frequency variability of systolic arterial pressure. The low-frequency variability, but not the midfrequency variability, of the heart rate was also reduced, while the high-frequency variability of the heart rate was reduced in the more chronically diabetic rats. Conclusion Our findings that the mid-frequency band variability of arterial pressure was reduced in diabetic patients suggest that sympathetic modulation of the cardiovascular system is impaired, corroborating other studies in such patients using this and other approaches. J Hypertens 1999, 17:489-495 (C) Lippincott Williams & Wilkins.