Spectral Analysis of Blood Pressure and Heart Rate Variability during Hemorrhage after Losartan Administration into the Lateral Ventricle

Lee, Dong Wook; Kim, Kyoung Soon; Kim, Hyeong Jin; Lee, Won Jung

Abstract

This study was aimed to elucidate the effect of intracerebroventricular losartan administration on arterial pressure regulation during hemorrhage in rats by power spectral analysis of blood pressure and heart rate variability. Nineteen male Sprague-Dawley rats weighing 240-300g were divided into losartan-administered(n=10) and control(n=9) groups. Hemorrhage was induced with a withdrawal pump from the femoral artery at 3ml/kg/min for 5min. Arterial presure was measured with a pressure transducer connected to the contralateral femoral artery for 5min before, during and after hemorrhage. The blood pressure signal digitized at 500 Hz through a data acquisition system was analyzed with fast Fourier transform algorithm to yield power spectra of systolic(SP) and diastolic(DP) blood pressure and instantaneous heart rate(HR). Powers of very low frequency (VLF, 0.02-0.26 Hz), low frequency(LF, 0.26-0.75 Hz) and high frequency(HF, 0.75-5.00 Hz) band were obtained. Basal systolic and diastolic blood pressure was 149+/-9 and 99+/-2mmHg, respectively, and was not changed by hemorrhage in control rats. Basal blood pressure in losartan group was 143+/-9 and 97+/-6mmHg and was significantly lowered to 116+/-13 and 77+/-9mmHg, respectively. HR was significantly increased during and after hemorrhage in both groups. Total power of SP variability in losartan group was 13.9+/-3.2mmHg2 before hemorrhage and was significantly increased to 66.6+/-25.3mmHg2 during hemorrhage. VLF, LF and HF powers of SP variability were 7.3+/-2.0, 3.8+/-1.1 and 2.8+/-0.7mmHg2, respectively, in losartan group and 5.5+/-1.4, 3.7+/-1.5 and 2.8+/-0.8mmHg2 in control rats. VLF and HF powers of SP were increased to 33.0+/-15.2 and 20.3+/-6.4mmHg2 in losartan group, and VLF power was increased to 7.9+/-1.5mmHg2 in control group. VLF power of DP variability increased from 3.3+/-0.9 before hemorrhage to 5.9+/-1.0mmHg2 during hemorrhage in control group. Powers of DP variability in losartan group and those of HR variability in both groups were not changed by hemorrhage. The above results suggested that losartan aggravated the arterial pressure fall during hemorrhage by impairing the sympathetic nerve activation by central angiotensin II.