Secretory immunoglobulin A and cardiovascular reactions to mental arithmetic, cold pressor, and exercise: Effects of beta‐adrenergic blockade

Winzer, Alexandra; Ring, Christopher; Carroll, Douglas; Willemsen, Gonneke; Drayson, Mark T.; Kendall, M. J.

doi:10.1111/1469-8986.3650591

Cited by 99 publications

(62 citation statements)

References 21 publications

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“…PHA = phytohemagglutinin. , 1997, 1998 Van der Voort et al, Wang et al, 1998Weisse et al, 1990Willemsen et al, 1998Winzer et al, 1999Zakowski, 1995Zakowski et al, 1992Zeier et al, 1996 Note. CI = confidence interval; IgG = immunoglobulin G.…”

Section: Resultsmentioning

confidence: 99%

Psychological Stress and the Human Immune System: A Meta-Analytic Study of 30 Years of Inquiry.

Segerstrom

Miller

2004

Psychological Bulletin

2,647

1,845

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The present report meta-analyzes more than 300 empirical articles describing a relationship between psychological stress and parameters of the immune system in human participants. Acute stressors (lasting minutes) were associated with potentially adaptive upregulation of some parameters of natural immunity and downregulation of some functions of specific immunity. Brief naturalistic stressors (such as exams) tended to suppress cellular immunity while preserving humoral immunity. Chronic stressors were associated with suppression of both cellular and humoral measures. Effects of event sequences varied according to the kind of event (trauma vs. loss). Subjective reports of stress generally did not associate with immune change. In some cases, physical vulnerability as a function of age or disease also increased vulnerability to immune change during stressors.Since the dawn of time, organisms have been subject to evolutionary pressure from the environment. The ability to respond to environmental threats or stressors such as predation or natural disaster enhanced survival and therefore reproductive capacity, and physiological responses that supported such responses could be selected for. In mammals, these responses include changes that increase the delivery of oxygen and glucose to the heart and the large skeletal muscles. The result is physiological support for adaptive behaviors such as "fight or flight." Immune responses to stressful situations may be part of these adaptive responses because, in addition to the risk inherent in the situation (e.g., a predator), fighting and fleeing carries the risk of injury and subsequent entry of infectious agents into the bloodstream or skin. Any wound in the skin is likely to contain pathogens that could multiply and cause infection (Williams & Leaper, 1998). Stress-induced changes in the immune system that could accelerate wound repair and help prevent infections from taking hold would therefore be adaptive and selected along with other physiological changes that increased evolutionary fitness.Modern humans rarely encounter many of the stimuli that commonly evoked fight-or-flight responses for their ancestors, such as predation or inclement weather without protection. However, human physiological response continues to reflect the demands of earlier environments. Threats that do not require a physical response (e.g., academic exams) may therefore have physical consequences, including changes in the immune system. Indeed, over the past 30 years, more than 300 studies have been done on stress and immunity in humans, and together they have shown that psychological challenges are capable of modifying various features of the immune response. In this article we attempt to consolidate empirical knowledge about psychological stress and the human immune system through meta-analysis. Both the construct of stress and the human immune system are complex, and both could consume bookCorrespondence concerning this article should be addressed to Suzanne C. Segerstrom, Department of Ps...

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Section: Resultsmentioning

confidence: 99%

Psychological Stress and the Human Immune System: A Meta-Analytic Study of 30 Years of Inquiry.

Segerstrom

Miller

2004

Psychological Bulletin

2,647

1,845

View full text Add to dashboard Cite

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“…b-receptor blockade always prolongs PEP Sherwood et al, 1990;Winzer et al, 1999) whereas atropine leaves it unchanged ).…”

Section: Discussionmentioning

confidence: 99%

Comparing low frequency heart rate variability and preejection period: Two sides of a different coin

et al. 2008

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It has been hypothesized that the ratio of heart rate variability in the low-(LF) and high-(HF) frequency bands may capture variation in cardiac sympathetic control. Here we tested the temporal stability of the LF/HF ratio in 24-h ambulatory recordings and compared this ratio to the preejection period (PEP), an established measure of cardiac sympathetic control. Good temporal stability was found across a period of 3.3 years (.46oro.78), but the LF/HF ratio did not show the expected negative correlation to PEP, either between or within subjects. We conclude that the evidence to support the LF/HF ratio as a potential marker of cardiac sympathetic control in epidemiology-scaled research is currently insufficient.

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“…To measure cardiac sympathetic activity, we use non-invasive thoracic impedance cardiography to derive the PEP as the time interval between the onset of ventricular depolarization and the opening of the semilunar valves (Sherwood et al, 1990). Changes in PEP reliably index changes in b-adrenergic inotropic drive to the left ventricle as shown in laboratory studies manipulating b-adrenergic tone by EPI infusion (Mezzacappa et al, 1999;Schachinger et al, 2001;Svedenhag et al, 1986), amyl nitrite inhalation (Nelesen et al, 1999), adrenoceptor blockade (Harris et al, 1967;Schachinger et al, 2001;Winzer et al, 1999;Cacioppo et al, 1994), exercise (Krzeminski et al, 2000;Miyamoto et al, 1983;Smith et al, 1989), or emotional stress Newlin and Levenson, 1979;Sherwood et al, 1986). PEP is an indirect measure of cardiac sympathetic activity as the sympathetic effects on the left ventricle are not just determined by changes in cardiac NE release but also by adrenoceptor status and circulating catecholamines.…”

Section: Introductionmentioning

confidence: 92%

Effects of Antidepressants, but not Psychopathology, on Cardiac Sympathetic Control: A Longitudinal Study

Licht

Penninx

Geus³

2012

Neuropsychopharmacol

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Increased sympathetic activity has been hypothesized to have a role in the elevated somatic disease risk in persons with depressive or anxiety disorders. However, it remains unclear whether increased sympathetic activity reflects a direct effect of anxiety or depression or an indirect effect of antidepressant medication. The aim of this study was to test longitudinally whether cardiac sympathetic control, measured by pre-ejection period (PEP), was increased by depression/anxiety status and by antidepressant use. Cross-sectional and longitudinal data were from a depression and anxiety cohort: the Netherlands Study of Depression and Anxiety (NESDA). Baseline data of 2838 NESDA subjects (mean age 41.7 years, 66.7% female) and 2-year follow-up data of 2226 subjects were available for analyses. Included were subjects with and without depressive/anxiety disorders, using or not using different antidepressants at baseline or followup. The PEP was measured non-invasively by 1.5 h of ambulatory impedance cardiography. Cross-sectional analyses compared PEP across psychopathology and antidepressant groups. Longitudinal analyses compared 2-year changes in PEP in relation to changes in psychopathology and antidepressant use. Cross-sectional analyses showed that antidepressant-naïve depressive/anxious subjects had comparable PEP as controls, whereas subjects using tricyclic (TCA) or combined serotonergic/noradrenergic antidepressants (SNRI) had significantly shorter PEP compared with controls. In contrast, subjects using selective serotonin re-uptake inhibitors (SSRIs) had longer PEP than controls. Longitudinal results confirmed these findings: compared with 2-year change in PEP in continuous non-users ( + 2 ms), subjects who started TCA or SNRI treatment showed significantly shortened PEP (À11 ms, p ¼ 0.005 and po0.001), whereas subjects who started SSRI treatment showed significant prolongation of PEP ( + 9 ms, p ¼ 0.002). Reversed findings were observed among those who stopped antidepressant use. These findings suggest that depressive and anxiety disorders are not associated with increased cardiac sympathetic control. However, results pose that TCA and SNRI use increases sympathetic control, whereas SSRI use decreases sympathetic control.

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Secretory immunoglobulin A and cardiovascular reactions to mental arithmetic, cold pressor, and exercise: Effects of beta‐adrenergic blockade

Cited by 99 publications

References 21 publications

Psychological Stress and the Human Immune System: A Meta-Analytic Study of 30 Years of Inquiry.

Psychological Stress and the Human Immune System: A Meta-Analytic Study of 30 Years of Inquiry.

Comparing low frequency heart rate variability and preejection period: Two sides of a different coin

Effects of Antidepressants, but not Psychopathology, on Cardiac Sympathetic Control: A Longitudinal Study

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