PubMed · 8617408
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
I A Macdonald. 1995. How do we study autonomic function in humans?. https://doi.org/10.1111/j.1472-8206.1995.tb00519.x
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
In this study we present a computer model of a pacemaker cell subjected to vagal stimulation. This model allows us to investigate the entrainment phenomena of the pacemaker cell resulting from its dynamic interaction with a periodic train of vagal bursts. The possibility of entrainment depends mainly on the fact that a vagal stimulation discharge can "correct" the pacemaker rhythm by an amount that depends on its instantaneous relationship to the pacemaker cycle length. This very simple model, is based on the two most important functional properties of the cardiac pacemaker cells. The first property is the intrinsic pacemaker cycle length, which is an "internal" parameter of the cell, describing the most basic feature of a pacemaker cell. The second one is the phase response curve (PRC), which is an "overall collective" function, containing all the "information" about the possible interactions between the pacemaker cell and the outside world (i.e. its interaction with surrounding cells, external stimulus, etc.). A "collective" PRC was reconstructed from the resulting effects of all the pulses composing a burst. It appears that the PRC parameters as well as the vagal burst parameters are important factors in predicting the entrainment phenomena. Specifically, we found that the tendency of the pacemaker cell to become synchronized with bursts of vagal activity is greater, the larger the number of pulses per burst. However, increasing the number of pulses may also increase the tendency of the pacemaker towards instability, which was unveiled as changes in the configuration of the "collective" PRC. We applied the periodic train of vagal bursts so as to simulate the respiratory sinus arrhythmia (RSA) modulation on the pacemaker cell. We included also a modulation of sympathetic origin, represented as periodic changes in the intrinsic pacemaker cycle length. The frequency response of the pacemaker to "autonomic" modulations allowed us to demonstrate that the RSA dynamics can be interpreted in terms of the entrainment of the pacemaker cell by the respiratory modulation of vagal activity.
Ninety newlywed couples (mean age = 25), selected on the basis of extremely stringent mental and physical health criteria, were admitted to a hospital research unit for 24 hours to provide a detailed assessment of conflict-resolution behaviors and changes in autonomic, endocrine, and immune function. Among these newlyweds, negative or hostile behaviors during marital conflict (coded from videotaped interactions) were associated with increased levels of epinephrine, norepinephrine, growth hormone, and ACTH as well as greater immunological change over the subsequent 24 hours. Wives demonstrated greater and more persistent physiological changes related to marital conflict than husbands. To assess the generalizability of these physiological changes, a similar laboratory paradigm was used with 31 older couples (mean age = 67) who had been married an average of 42 years. Consistent with the data from newlyweds, both endocrinological and immunological data showed significant relationships to negative behavior during marital conflict in these older couples. These findings suggest that abrasive marital interactions have important endocrinological and immunological correlates.
We examined the effects of brief psychological stressors on cardiovascular, neuroendocrine, and cellular immune response in 22 older women to investigate the common effects of stress across systems. Results revealed that psychological stressors heightened cardiac sympathetic activation, elevated plasma catecholamine concentrations, and affected the cellular immune response (ps < 0.05). In a replication and extension, 27 women caring for a spouse with a progressive dementia (high chronic stress) and 37 controls category matched for age and family income (low chronic stress) performed the 12-min laboratory stressor. Measures were taken before (low acute stress) and immediately following (high acute stress) exposure to the laboratory stressors as well as 30 min after termination of the stressor (recovery period). Acute stress again heightened cardiac sympathetic activation, elevated plasma catecholamine concentrations, and affected cellular immune responses (ps < 0.05), whereas chronic stress was associated with higher reports of negative affect, enhanced cardiac sympathetic activation, elevated blood pressure and plasma levels of ACTH, and diminished production of interleukin-1 beta (ps < 0.05). Correlational analyses in both studies further suggested that individuals who showed the greatest stress-related changes in HPA activation also exhibited the greatest diminution in cellular immune response.