Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2012 May 10:3:131.
doi: 10.3389/fphys.2012.00131. eCollection 2012.

Heart rate variability predicts cell death and inflammatory responses to global cerebral ischemia

Greg J Norman  1 , Kate Karelina, Gary G Berntson, John S Morris, Ning Zhang, A Courtney Devries
Affiliations

Heart rate variability predicts cell death and inflammatory responses to global cerebral ischemia

Greg J Norman et al. Front Physiol. .

Abstract

This study examines the relationship between autonomic functioning and neuropathology following cardiac arrest (CA) in mice. Within 24 h of CA, parasympathetic cardiac control, as indexed by high frequency (HF) heart rate variability, rapidly decreases. By day 7 after CA, HF heart rate variability was inversely correlated with neuronal damage and microglial activation in the hippocampus. Thus, by virtue of its sensitivity to central insult, HF heart rate variability may offer an inexpensive, non-invasive method of monitoring neuropathological processes following CA. The inverse linear relationships between heart rate variability and brain damage after CA also may partially explain why low heart rate variability is associated with increased morbidity and mortality in myocardial infarction patients.

Keywords: autonomic; cardiac; cardiac arrest; ischemia; parasympathetic.

PubMed Disclaimer

Figures

Figure 1
Figure 1
The CA/CPR procedure increased levels of hippocampal cell death (A) and microglial expression (B) at 7 days following CA, as measured by Fluoro-Jade C and MAC-1 staining, respectively. The data are presented as mean ± SD and an asterisk indicates a significant difference vs. control at p < 0.05.
Figure 2
Figure 2
(A) When cardiac arrest is accompanied by neurological damage (CA/CPR), there is a significant reduction in HF heart rate variability, a well validated measure of parasympathetic cardiac control. The mice in the ischemic control group (control) displayed similar levels of HF heart rate variability throughout the study. (B) Cardiac arrest also significantly increases heart rate. In contrast, the mice in the ischemic control group displayed similar heart rates throughout the study. (C) At 7 days following normothermic CA/CPR, high frequency heart rate variability values were significantly and inversely correlated with measures of neuronal cell damage(c) and microglial activation (D) within the CA1 region of the hippocampus of mice. Data are presented as mean ± SD and an asterisk indicates a significant difference (p < 0.05) at the given time point relative to the ischemic controls.
Figure 3
Figure 3
(A) When cardiac arrest is accompanied by neurological damage (CA/CPR), there is a significant reduction in body temperature and dysregulation of the diurnal rhythm. In contrast, body temperature and its diurnal rhythm did not differ from baseline among the ischemic control group that did not sustain neurological damage. (B) Likewise, the CA/CPR group exhibited increased locomotor behavior and dysregulation of the diurnal rhythm in activity, whereas locomotor activity and diurnal rhythmicity in activity did not vary throughout the study among the ischemic control mice. Data are collapsed across post-surgical days 1–7. The dark background denotes lights off (animal’s active period). Data are presented as mean ± SD.
See this image and copyright information in PMC

References

    1. American Heart Association (2002). Heart Disease and Stroke Statistics: 2003 Update. Dallas, TX: American Heart Association
    1. Berntson G. G., Bigger J. T., Jr., Eckberg D. L., Grossman P., Kaufmann P. G., Malik M., Nagaraja H. N., Porges S. W., Saul J. P., Stone P. H., van der Molen M. W. (1997). Heart rate variability: origins, methods, and interpretive caveats. Psychophysiology 34, 623–64810.1111/j.1469-8986.1997.tb02140.x - DOI - PubMed
    1. Berntson G. G., Cacioppo J. T., Binkley P. F., Uchino B. N., Quigley K. S., Fieldstone A. (1994). Autonomic cardiac control. III. Psychological stress and cardiac response in autonomic space as revealed by pharmacological blockades. Psychophysiology 31, 599–60810.1111/j.1469-8986.1994.tb02352.x - DOI - PubMed
    1. Berntson G. G., Norman G. J., Hawkley L. C., Cacioppo J. T. (2008). Cardiac autonomic balance versus cardiac regulatory capacity. Psychophysiology 45, 643–65210.1111/j.1469-8986.2008.00652.x - DOI - PMC - PubMed
    1. Bigger J. T., Jr., Kleiger R. E., Fleiss J. L., Rolnitzky L. M., Steinman R. C., Miller J. P. (1988). Components of heart rate variability measured during healing of acute myocardial infarction. Am. J. Cardiol. 61, 208–21510.1016/0002-9149(88)90917-4 - DOI - PubMed