Autonomic function in panic disorder: cardiorespiratory and plasma catecholamine responsivity to multiple challenges of the autonomic nervous system

1994 ◽  
Vol 36 (8) ◽  
pp. 548-558 ◽  
Author(s):  
Murray B. Stein ◽  
Gordon J.C. Asmundson
2010 ◽  
Vol 72 (5) ◽  
pp. 442-449 ◽  
Author(s):  
Jose M. Martinez ◽  
Amir Garakani ◽  
Horacio Kaufmann ◽  
Cindy J. Aaronson ◽  
Jack M. Gorman

Author(s):  
Jennifer Weggen ◽  
Ashley Darling ◽  
Aaron Autler ◽  
Austin C Hogwood ◽  
Kevin Decker ◽  
...  

PURPOSE: Posttraumatic stress disorder (PTSD) has been associated with an increase in risk of cardiovascular disease (CVD). The goal of the study was to determine if peripheral vascular dysfunction, a precursor to CVD, was present in young adults with PTSD, and if an acute antioxidant (AO) supplementation could modify this potential PTSD-induced vascular dysfunction. METHODS: Thirteen individuals with PTSD were recruited for this investigation and were compared to 35 age- and sex-matched controls (CTRL). The PTSD group participated in two visits, consuming either a placebo (PTSD-PL) or antioxidants (PTSD-AO; Vitamins C and E; Alpha Lipoic Acid) prior to their visits, while the CRTL subjects only participated in one visit. Upper and lower limb vascular function were assessed via flow-mediated dilation and passive leg movement technique. Heart rate variability was utilized to assess autonomic nervous system modulation. RESULTS: The PTSD-PL condition, when compared to the CTRL group, reported lower arm and leg microvascular function as well as sympathetic nervous system (SNS) predominance. Following acute AO supplementation, arm, but not leg, microvascular function was improved and SNS predominance was lowered to which the prior difference between PTSD group and CTRL was no longer significant. CONCLUSION: Young individuals with PTSD demonstrated lower arm and leg microvascular function as well as greater SNS predominance when compared to age- and sex-matched controls. Furthermore, this lower vascular/autonomic function was augmented by an acute AO supplementation to the level of the healthy controls, potentially implicating oxidative stress as a contributor to this blunted vascular/autonomic function.


2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Anna Mazzeo ◽  
Claudia Stancanelli ◽  
Rita Di Leo ◽  
Giuseppe Vita

Autonomic function can be impaired in many disorders in which sympathetic, parasympathetic, and enteric arms of the autonomic nervous system are affected. Signs and symptoms of autonomic involvement are related to impairment of cardiovascular, gastrointestinal, urogenital, thermoregulatory, sudomotor, and pupillomotor autonomic functions. Availability of noninvasive, sensitive, and reproducible tests can help to recognize these disorders and to better understand specific mechanisms of some, potentially treatable, immune-mediated autonomic neuropathies. This paper describes autonomic involvement in immune-mediated neuropathies with a subacute or chronic course.


2003 ◽  
Vol 94 (2) ◽  
pp. 709-715 ◽  
Author(s):  
Amy L. Hakeman ◽  
Don D. Sheriff

Tolerance to +Gzstress is reduced by preceding exposure to −Gz (push-pull effect). The mechanism(s) responsible for this effect are not fully understood, although the arterial baroreceptor reflexes have been implicated. We investigated the integrative response of the autonomic nervous system by studying responses to gravitational stress before and after autonomic function was inhibited by hexamethonium in 10 isoflurane-anesthetized male and female Sprague-Dawley rats. Animals were restrained supine and subjected to two rotations imposed about the x-axis: 1) a control G profile consisting of rotation from 0 Gz (+1 Gy) to 90° head-up tilt (+1 Gz) for 10 s and 2) a push-pull G profile consisting of rotation from 0 Gz to 90° head-down tilt (−1 Gz) for 2 s immediately preceding 10 s of +1 Gz stress. Eight G profiles consisting of equal numbers of control and push-pull trials were imposed by using a counterbalanced design. We found that hexamethonium lowered baseline arterial pressure and abolished the push-pull effect. The lack of a push-pull effect after autonomic blockade persisted when arterial pressure was restored to baseline levels by phenylephrine infusion. Lowering baseline arterial pressure by sodium nitroprusside infusion or by hemorrhage when autonomic function was intact also abolished the push-pull effect. We conclude that intact autonomic function and a normal baseline arterial pressure are needed for expression of the push-pull effect in anesthetized rats subjected to tilting.


1991 ◽  
Vol 261 (2) ◽  
pp. H493-H499 ◽  
Author(s):  
D. S. Martin ◽  
J. R. McNeill

Effects of intravenous infusions of arginine vasopressin (AVP) on whole body vascular capacitance were determined in anesthetized cats when autonomic nervous system function was intact and, in other cats, when reflexes were blocked by the ganglionic blocking agent pentolinium. With the use of the constant cardiac output-reservoir technique, changes in reservoir volume were assumed to reflect reciprocal changes in whole body vascular capacitance. Relationships between the dose of AVP and the plasma concentration of the peptide achieved during infusions were not significantly different in the two groups of animals. Blood pressure responses to AVP were greater, whereas heart rate responses to the peptide were abolished in ganglion-blocked cats. In cats with intact autonomic function, reservoir volume decreased by 1.6, 4.2, and 7.8 ml/kg at AVP doses of 1, 10, and 100 ng.kg-1.min-1, respectively. In contrast, in ganglion-blocked cats, reservoir volume did not change significantly at 1.0 and 10 ng.kg-1.min-1 of AVP, and the highest dose caused a much smaller change in volume (3 ml/kg) than that observed in cats with intact autonomic function (7.8 ml/kg). Systemic compliance was unchanged by AVP in both groups of animals, suggesting that the increases in whole body vascular capacitance were likely due to changes in unstressed volume. The results suggest that reflexively mediated changes in autonomic function increase whole body vascular capacitance during elevations in the circulating levels of AVP to plasma concentrations that are biologically relevant. These findings may explain how AVP decreases cardiac output in animals with an intact autonomic nervous system.


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