scholarly journals Effect of Losartan, an Angiotensin II Type 1 Receptor Antagonist on Cardiac Autonomic Functions of Rats During Acute and Chronic Inhibition of Nitric Oxide Synthesis

2012 ◽  
pp. 135-144
Author(s):  
M. CHASWAL ◽  
S. DAS ◽  
J. PRASAD ◽  
A. KATYAL ◽  
A. K. MISHRA ◽  
...  

We studied the effect of losartan on baroreflex sensitivity (BRS) and heart rate variability (HRV) of adult Wistar rats during acute and chronic inhibition of nitric oxide synthesis by NG-nitro-L-arginine methyl ester (L-NAME). Chronic L-NAME administration (50 mg/kg per day for 7 days, orally through gavage) increased mean arterial pressure (MAP), heart rate but significantly decreased BRS. In addition, a significant fall of standard deviation of normal RR intervals, total spectral power, high frequency spectral power and a rise of low frequency to high frequency (LF: HF) ratio was seen. Acute L-NAME administration (30 mg/kg, i.v. bolus dose) also raised MAP and impaired HRV but it was associated with augmented BRS for bradycardia reflex. Losartan treatment (10 mg/kg, i.v.) in both acute and chronic L-NAME treated rats, decreased MAP but the difference was not significant. On the other hand, losartan administration normalized depressed BRS for bradycardia reflex and significantly reduced LF to HF ratio in chronic L-NAME treated rats. But this improvement was not observed in acute L-NAME group. These results indicate importance of mechanisms other than renin-angiotensin system in the pressor response of both acute as well as chronic L-NAME. However, autonomic dysregulation especially following chronic L-NAME appears to be partly angiotensin dependent.

2017 ◽  
Vol 27 (9) ◽  
pp. 1662-1669 ◽  
Author(s):  
Cagdas Vural ◽  
Ener Cagri Dinleyici ◽  
Pelin Kosger ◽  
Ozge Bolluk ◽  
Zubeyir Kilic ◽  
...  

AbstractIntroductionCarbon monoxide poisoning may cause myocardial toxicity and cardiac autonomic dysfunction, which may contribute to the development of life-threatening arrhythmias. We investigated the potential association between acute carbon monoxide exposure and cardiac autonomic function measured by heart rate variability.MethodThe present study included 40 children aged 1–17 years who were admitted to the Pediatric Intensive Care Unit with acute carbon monoxide poisoning and 40 healthy age- and sex-matched controls. Carboxyhaemoglobin and cardiac enzymes were measured at admission. Electrocardiography was performed on admission and discharge, and 24-hour Holter electrocardiography was digitally recorded. Heart rate variability was analysed at both time points – 24-hour recordings – and frequency domains – from the first 5 minutes of intensive care unit admission.ResultsTime domain and frequency indices such as high-frequency spectral power and low-frequency spectral power were similar between patient and control groups (p>0.05). The ratio of low-frequency spectral power to high-frequency spectral power was significantly lower in the carbon monoxide poisoning group (p<0.001) and was negatively correlated with carboxyhaemoglobin levels (r=−0.351, p<0.05). The mean heart rate, QT dispersion, corrected QT dispersion, and P dispersion values were higher in the carbon monoxide poisoning group (p<0.05) on admission. The QT dispersion and corrected QT dispersion remained longer in the carbon monoxide poisoning group compared with controls on discharge (p<0.05).ConclusionThe frequency domain indices, especially the ratio of low-frequency spectral power to high-frequency spectral power, are useful for the evaluation of the cardiac autonomic function. The decreased low-frequency spectral power-to-high-frequency spectral power ratio reflects a balance of the autonomic nervous system, which shifted to parasympathetic components.


1999 ◽  
Vol 91 (6) ◽  
pp. 1604-1604 ◽  
Author(s):  
Isabelle Constant ◽  
Marie-Claude Dubois ◽  
Véronique Piat ◽  
Marie-Laure Moutard ◽  
Maggie McCue ◽  
...  

Background This study was design to assess clinical agitation, electroencephalogram (EEG) and autonomic cardiovascular activity changes in children during induction of anesthesia with sevoflurane compared with halothane using noninvasive recording of EEG, heart rate, and finger blood pressure. Methods Children aged 2-12 yr premedicated with midazolam were randomly assigned to one of three induction techniques: 7% sevoflurane in 100% O2 (group SevoRAPID); 2%, 4%, 6%, and 7% sevoflurane in 100% O2 (group SevoINCR); or 1%, 2%, 3%, and 3.5% halothane in 50% N2O-50% O2 (group HaloN2O). An additional group of children who received 7% sevoflurane in 50% N2O-50% O2 (group SevoN2O) was enrolled after completion of the study. Induction was videotaped. EEG, heart rate, and finger blood pressure were continuously recorded during induction until 5 min after tracheal intubation and analyzed in frequency domain using spectral analysis. Results Agitation was more frequent when anesthesia was induced with 100% O2 compared to the mixture of oxygen and nitrous oxide. No seizures were recorded in any group. In the four groups, induction of anesthesia was associated with an increase in EEG total spectral power and a shift toward the low-frequency bands. Sharp slow waves were present on EEG tracings of the three sevoflurane groups, whereas slow waves and fast rhythms (spindles) were observed in the halothane group. Sevoflurane induced a greater withdrawal of parasympathetic activity than halothane and a transient relative increase in sympathetic vascular tone at loss of eyelash reflex. Conclusions Agitation observed during sevoflurane induction was not associated with seizures. Sevoflurane induction induced a marked inhibition of parasympathetic control of heart rate.


1994 ◽  
Vol 77 (6) ◽  
pp. 2537-2542 ◽  
Author(s):  
R. L. Hughson ◽  
Y. Yamamoto ◽  
R. E. McCullough ◽  
J. R. Sutton ◽  
J. T. Reeves

The adaptive responses of the cardiovascular system to altitude appear to be dominated by increased sympathetic neural activity. We investigated the combined roles of the sympathetic and parasympathetic nervous systems (SNS and PNS, respectively) in the early (days 4–5) and subsequent (days 11–12) phases of acclimatization on Pike's Peak, CO (4,300 m), by spectral analysis of heart rate variability. Male subjects were randomly assigned to groups receiving oral propranolol (240 mg/day; n = 6) or a matched placebo (n = 3). On ascent to altitude, the high-frequency, fractal, and total spectral powers were reduced in the placebo group during days 4–5 and 11–12. At altitude during days 4–5, all three placebo group subjects increased SNS and decreased PNS activities compared with at sea level, and during days 11–12 SNS decreased and PNS increased compared with days 4–5. Relative to the placebo group, propranolol caused lengthening of the R-R interval; increases in high-frequency power, total spectral power, and the PNS indicator; and a decrease in the SNS indicator. Total spectral power tended to decrease at altitude, but there were no effects of altitude on PNS and SNS indicators in the propranolol group. The data from the placebo and propranolol groups suggest that both the PNS and SNS are involved in the elevated heart rate during the early phase of altitude acclimatization. Changes in heart rate variability during days 11–12 at altitude must be considered in light of the possible reductions in sympathetic receptor number noted in previous studies.


2011 ◽  
Vol 89 (12) ◽  
pp. 865-874 ◽  
Author(s):  
Meenakshi Chaswal ◽  
Shobha Das ◽  
Jagdish Prasad ◽  
Anju Katyal ◽  
Mohammad Fahim

We evaluated the role of the sympathetic nervous system and oxidative stress in hemodynamic and autonomic control after acute inhibition of the synthesis of nitric oxide, using intravenous (i.v.) injection of 30 mg·kg–1 NG-nitro-l-arginine methyl ester (L-NAME) in adult Wistar rats. Baroreflex sensitivity (BRS) and heart rate variability (HRV) were measured as indices of cardiac autonomic control, before and after L-NAME treatment in rats with intact autonomic innervation, and in rats with chemical sympathectomy by 6-hydroxydopamine. Serum malondialdehyde (MDA) was measured as a marker of oxidative stress. In control rats, L-NAME treatment resulted in a significant rise in blood pressure, augmentation of BRS, and enhanced serum MDA. HRV showed an attenuation of total spectral power and high frequency spectral power, along with a rise of the low to high frequency ratio (LF:HF). Administration of L-NAME produced a pressor response even in sympathectomised rats, but augmented BRS was not observed, and the high frequency spectral power showed an increase, in addition to a significant decline of LF:HF and serum MDA. We therefore conclude that even though pressor response was unaffected, reversal of cardiac autonomic responses and decline in oxidative stress following sympathectomy in L-NAME-treated rats reflects a significant role for sympathetic innervation in acute L-NAME-induced hypertension.


Heart rate variability (HRV) is a useful measure to evaluate activity of the autonomic nervous system (ANS) and monitor both pathological and psychological conditions. However, HRV analysis still has difficulties with changes in HRV parameters due to an increase or decrease in the average heart rate. At present, the interpretation of the average changes in HRV datasets and their HRV parameters is not fully understood. Therefore, this study aimed to analyze how much deviation in HRV parameters occurs from rescaling tachograms and normalizing HRV datasets. Four rescaled tachograms and their corresponding normalized HRV datasets were created by increasing the average heartbeat from 50 to 110 bpm in 20 bpm steps. The difference in low frequency powers (Ln LFs) calculated between two successive rescaled groups was 0.89, 1.03, and 1.04, as the average heartbeat increased from slow to fast, while the difference in high frequency powers (Ln HFs) was 1.06, 1.53, and 1.37. However, in the four normalized HRV datasets, the difference in Ln LFs and Ln HFs between two successive normalized groups was -0.28 and -0.12, 0.31 and 0.27, and 0.31 and 0.37, respectively. The results suggest that the normalized HRV datasets are more valuable than the individual rescaled-tachogram HRV dataset for obtaining measurements using frequency-domain HRV parameters for HRV analysis in clinical applications.


1997 ◽  
Vol 272 (6) ◽  
pp. H2630-H2638 ◽  
Author(s):  
F. E. Seier ◽  
M. Kellner ◽  
A. Yassouridis ◽  
R. Heese ◽  
F. Strian ◽  
...  

To compare autonomic and neuroendocrine responses during lactate-induced panic attacks, heart rate variability and cortisol and atrial natriuretic hormone (ANH) levels were measured in patients with panic attacks and in healthy control subjects. In a randomized double-blind design, all subjects received either 10 ml/kg body weight of 0.5 M racemic sodium lactate or normal saline from 1100 to 1120. Spectral analysis of the R-R interval of analog electrocardiograms was performed, and total (0.001-0.45 Hz), low-frequency (0.01-0.05 Hz), midfrequency (0.05-0.15 Hz), and high-frequency power (0.15-0.45 Hz) were computed. Cortisol was measured 12 times in the period from 0900 to 1300, and ANH was measured at 1100, 1120, and 1200 by radioimmunoassay. In both panickers (n = 6) and nonpanickers (n = 8), an infusion of lactate resulted in an acceleration of heart rate, a reduction in total spectral power, and a decrease in the high- and low-frequency components of spectral power. Panickers showed a significant enhancement of the high-frequency power, whereas in nonpanickers, a shift from the mid- and high-frequency toward the low-frequency power emerged. ANH plasma concentrations during lactate infusion in panickers showed a significant increase (115 and 131% at 1120 and 1200, respectively, over concentrations at 1100) in contrast to nonpanickers (20 and 74%, respectively). No group or treatment effects on cortisol secretion emerged, which is in line with former reports. Our study supports preliminary observations that lactate-induced panic attacks enhance the release of ANH, a vasodilatator and inhibitor of sympathetic activity. Hence this hormone not only could inhibit the secretion of the stress hormone cortisol but, in parallel, could also attenuate the sympathetic stimulation to the heart. These inhibitory effects of ANH could explain the so-far-unresolved dissociation between psychopathological alterations and autonomic and endocrine responses of panic attacks.


2016 ◽  
Vol 12 (1) ◽  
pp. 117-125
Author(s):  
Soroor Behbahani ◽  
Nader Jafarnia Dabanloo ◽  
Ali Motie Nasrabadi ◽  
Antonio Dourado

Recently, heart rate variability (HRV) analysis has been used as an indicator of epileptic seizures. As women have a lower sudden, unexpected death in epilepsy risk and greater longevity than men, the authors postulated that there are significant gender-related differences in heart rate dynamics of epileptic patients. The authors analyzed HRV during 5-minute segments of continuous electrocardiogram recording of age-matched populations. The middle-aged epileptic patients included males ( n = 12) and females ( n = 12), ranging from 41 to 65 years of age. Relatively high- (0.15 Hz-0.40 Hz) and low-frequency (0.01 Hz-0.15 Hz) components of HRV were computed using spectral analysis. Poincaré parameters of each heart rate time series were considered as nonlinear features. The mean heart rate markedly differed between gender groups including both right- and left-sided seizures. High-frequency heart rate power and the low-frequency/high-frequency ratio increased in the pre-ictal phase of both male and female groups ( p < .01), but men showed more increase especially in right-sided seizures. The standard deviation ratio, SD2/ SD1, of pre-ictal phase was greater in males than females ( p < .01). High-frequency spectral power and parasympathetic activity were higher in the female group with both right- and left-sided seizures. Men showed a sudden increase in sympathetic activity in the pre-ictal phase, which might increase the risk of cardiovascular disease in comparison to women. These complementary findings indicate the need to account for gender, as well as localization in HRV analysis.


2010 ◽  
Vol 298 (6) ◽  
pp. H2226-H2231 ◽  
Author(s):  
Jonas Spaak ◽  
George Tomlinson ◽  
Cheri L. McGowan ◽  
George J. Soleas ◽  
Beverley L. Morris ◽  
...  

In healthy subjects a standard drink of either red wine (RW) or ethanol (EtOH) has no effect on muscle sympathetic nerve activity or on heart rate (HR), whereas two drinks increase both. Using time- and frequency-domain indexes of HR variability (HRV), we now tested in 12 subjects (24–47 yr, 6 men) the hypotheses that 1) this HR increase reflects concurrent dose-related augmented sympathetic HR modulation and 2) RW with high-polyphenol content differs from EtOH in its acute HRV effects. RW, EtOH, and water were provided on 3 days, 2 wk apart according to a randomized, single-blind design. Eight-minute segments were analyzed. One alcoholic drink increased blood concentrations to 36 ± 2 mg/dl (mean ± SE), and 2 drinks to 72 ± 4 (RW) and 80 ± 2 mg/dl (EtOH). RW quadrupled plasma resveratrol ( P < 0.001). HR fell after both water drinks. When compared with respective baselines, one alcoholic drink had no effect on HR or HRV, whereas two glasses of both increased HR (RW, +5.4 ± 1.2; and EtOH, +5.7 ± 1.2 min−1; P < 0.001), decreased total HRV by 28–33% ( P < 0.05) and high-frequency spectral power by 32–42% (vagal HR modulation), and increased low-frequency power by 28–34% and the ratio of low frequency to high frequency by 98–119% (sympathetic HR modulation) (all, P ≤ 0.01). In summary, when compared with water, one standard drink lowered time- and frequency-domain markers of vagal HR modulation. When compared with respective baselines, two alcoholic drinks increased HR by diminished vagal and augmented sympathetic HR modulation. Thus alcohol exerts dose-dependent HRV responses, with RW and EtOH having a similar effect.


2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Reuben Howden ◽  
Eva Gougian ◽  
Marcus Lawrence ◽  
Samantha Cividanes ◽  
Wesley Gladwell ◽  
...  

Nrf2protects the lung from adverse responses to oxidants, including 100% oxygen (hyperoxia) and airborne pollutants like particulate matter (PM) exposure, but the role ofNrf2on heart rate (HR) and heart rate variability (HRV) responses is not known. We hypothesized that genetic disruption ofNrf2would exacerbate murine HR and HRV responses to severe hyperoxia or moderate PM exposures.Nrf2-/-andNrf2+/+mice were instrumented for continuous ECG recording to calculate HR and HRV (low frequency (LF), high frequency (HF), and total power (TP)). Mice were then either exposed to hyperoxia for up to 72 hrs or aspirated with ultrafine PM (UF-PM). Compared to respective controls, UF-PM induced significantly greater effects on HR (P<0.001) and HF HRV (P<0.001) inNrf2-/-mice compared toNrf2+/+mice.Nrf2-/-mice tolerated hyperoxia significantly less thanNrf2+/+mice (~22 hrs;P<0.001). Reductions in HR, LF, HF, and TP HRV were also significantly greater inNrf2-/-compared toNrf2+/+mice (P<0.01). Results demonstrate thatNrf2deletion increases susceptibility to change in HR and HRV responses to environmental stressors and suggest potential therapeutic strategies to prevent cardiovascular alterations.


2014 ◽  
Vol 2014 ◽  
pp. 1-19 ◽  
Author(s):  
Joanne W. Y. Chung ◽  
Vincent C. M. Yan ◽  
Hongwei Zhang

Aim.To summarize all relevant trials and critically evaluate the effect of acupuncture on heart rate variability (HRV).Method.This was a systematic review with meta-analysis. Keyword search was conducted in 7 databases for randomized controlled trials (RCTs). Data extraction and risk of bias were done.Results.Fourteen included studies showed a decreasing effect of acupuncture on low frequency (LF) and low frequency to high frequency ratio (LF/HF ratio) of HRV for nonhealthy subjects and on normalized low frequency (LF norm) for healthy subjects. The overall effect was in favour of the sham/control group for high frequency (HF) in nonhealthy subjects and for normalized high frequency (HF norm) in healthy subjects. Significant decreasing effect on HF and LF/HF ratio of HRV when acupuncture was performed on ST36 among healthy subjects and PC6 among both healthy and nonhealthy subjects, respectively.Discussion.This study partially supports the possible effect of acupuncture in modulating the LF of HRV in both healthy and nonhealthy subjects, while previous review reported that acupuncture did not have any convincing effect on HRV in healthy subjects. More published work is needed in this area to determine if HRV can be an indicator of the therapeutic effect of acupuncture.


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