Effect of prolonged catecholamine infusion on immunoregulatory function: Implications in congestive heart failure

Harris, Tamara J.; Waltman, Thomas J.; Carter, Steve M.; Maisel, Alan S.

doi:10.1016/0735-1097(95)00123-h

Cited by 42 publications

(22 citation statements)

References 45 publications

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“…Also, corticosteroids and catecholamine-induced increased accumulation of lymphocytes in the spleen, lymph nodes and mucosal sites which decrease in lymphocytes in the blood (Viswanathan and Dhabhar, 2005). In contrast, some studies have shown that stress increased blood WBCs numbers in rats (Harris et al, 1995) and humans (Bosch et al, 2003).…”

Section: Discussionmentioning

confidence: 98%

Behavioral Activities, Physiological Body Reactions, Hematological Parameters and Hormonal Profiles for Bucks of New Zealand White and Baladi Red Rabbits Exposed to Short Term of High Temperature

Khalil¹,

Yaseen²,

Hamdy³

2015

Asian J. of Poultry Science

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This study was conducted to investigate the effect of acute short term heat exposure on behavioral activities, physiological body reactions, hematological parameters and hormonal profiles of New Zealand White (NZW) and Baladi Red (BR) bucks. Twenty male NZW and BR bucks were divided into two groups; natural winter climate of 19±1°C and 55±5%, Relative Humidity (RH) (control group) and the bucks in the other group were exposed to short term heat stress for 1 h at 37±0.5°C and 20±2% RH. The results indicated that, heat stress decreased (p#0.001) standing and walking behavior and increased (p#0.001) sitting behavior compared with these recorded under control temperature. Moreover, Respiration Rate (RR), Rectal Temperatures (RT) and Time of Sexual Libido (TSL) were significantly increased (p#0.001) following stress. Concentration of plasma testosterone and T 3 were significantly reduced (p#0.001) and cortisol were significantly increased after submission to stress. The RBCs, WBCs, Hb, PCV values were insignificantly reduced and lymphocyte was significantly reduced after stress. In contrast, neutrophils, Neutrophils/Lymphocytes (N/L) ratio were increased (p#0.05) and monocytes were insignificantly increased after the end of heat stress. On the other hand, breeds of rabbit had significant effects on most of the studied traits, especially after heat exposure. The BR bucks were significantly superior; RBCs, WBCs, neutrophils, N/L ratio and monocytes than those recorded in NZW bucks after heat stress. Also, plasma concentration of testosterone were significantly higher but cortisol and T 3 were significantly lower (p#0.05) in BR bucks than those estimated in NZW bucks. Moreover, BR bucks had insignificantly higher walking and lower standing behavior than those recorded in NZW bucks. Also, RR was significantly higher (p#0.001), but RT and TSL were significantly lower (p#0.001) in BR bucks than those recorded in the NZW bucks. Furthermore, the results showed that there were prevalent significant (p#0.05) negative correlation between plasma level of cortisol and each of plasma level of testosterone, RBCs, WBCs counts, standing and walking behavior and significant (p#0.001) positive with RR, RT, TSL and time of sitting behavior. Current results explained that acute short term heat stress, negatively affected of internal environment of rabbit bucks which were reflected in their performance. Also, behavioral traits, sexual libido, hematological parameters and hormonal profile in BR bucks seem to be better than those recorded by NZW bucks after exposed heat stress, which may be explained, why BR breed had more tolerate to heat stress compared to exotic breeds.

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Section: Discussionmentioning

confidence: 98%

Behavioral Activities, Physiological Body Reactions, Hematological Parameters and Hormonal Profiles for Bucks of New Zealand White and Baladi Red Rabbits Exposed to Short Term of High Temperature

Khalil¹,

Yaseen²,

Hamdy³

2015

Asian J. of Poultry Science

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“…4A,B). Since elevated concentrations of catecholamines can trigger lymphocyte cell death (Harris et al, 1995;Gu et al, 2000;Stevenson et al, 2001;Wahle et al, 2002;del Rey et al, 2003), we tested whether the reduction in spleen size and splenocyte number after T3 SCI was a result of increased immune cell apoptosis. Western blot analyses of homogenized spleen showed elevated levels of activated caspase-3 (a primary effecter of apoptosis) only after T3 SCI; thereby confirming our initial hypothesis (p<0.05; Fig.…”

Section: T3 Sci Induces Splenocyte Cell Death and B Cell Apoptosismentioning

confidence: 99%

“…This deficit is overcome by activating B cells in the presence of β2-adrenergic receptor (β2AR) agonists (e.g., terbutaline) (Podojil and Sanders, 2003). However, repeated or prolonged exposure of B cells to NE or other β2AR agonists is immunosuppressive (Melmon et al, 1974;Keller et al, 1983;Maisel, 1994;Harris et al, 1995;Woiciechowsky et al, 1998;Prass et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Impaired antibody synthesis after spinal cord injury is level dependent and is due to sympathetic nervous system dysregulation

Lucin

Sanders

Jones

et al. 2007

Experimental Neurology

173

217

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Individuals with spinal cord injury (SCI) are highly susceptible to infection. This post-traumatic immune suppression is thought to occur via alterations in sympathetic nervous system (SNS) or hypothalamic-pituitary-adrenal (HPA) axis function. Normally, the HPA axis and SNS help coordinate proper immune function. After SCI, the HPA axis becomes activated and descending input to sympathetic preganglionic neurons (SPNs) is impaired. Because lymphoid organs are innervated by SPNs distributed throughout the thoracolumbar spinal cord, we predicted leveldependent immune suppression after SCI due to activation of the HPA axis and loss of descending input to SPNs. We tested this hypothesis by measuring indices of HPA (circulating corticosterone; CORT) and SNS function (norepinephrine (NE) in spleen) as well as antigen-specific antibody synthesis against an exogenous non-self protein following high or low level SCI. Using a midthoracic (T9) spinal contusion injury model, we found that CORT was elevated after SCI with aberrant patterns of diurnal CORT synthesis evident through at least the first 24 hours post-injury. However, splenic NE and antibody synthesis were similar to uninjured controls. Injury severity did not change these parameters. Indeed, CORT, NE and antibody synthesis were similar after T9 contusion or transection SCI. In contrast, high level SCI (T3) caused sustained increases in CORT and splenic NE along with impaired antibody synthesis and elevated splenocyte apoptosis. The immunosuppressive effects of T3 SCI were caused by NE acting at β2-adrenergic receptors (β2AR) and could be reversed using β2AR blockers. Interestingly, impaired antibody after T3 SCI could be Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript mimicked after T9 SCI with a β2AR agonist. These data illustrate the immunosuppressive effects of the SNS after high-level SCI and indicate that immune deficits may be overcome using β-blockers.

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“…Thus, infusion of catecholamines in pharmacological doses was found to evoke a transient leukocytosis [2,3] in a biphasic manner: within the initial 30 minutes, predominantly lymphocytes are mobilized, while later on an increased number of granulocytes was conspicuous in the peripheral blood stream [3]. Upon physiological stimuli, like acute psychological stress [1], lymphocyte subpopulations, particularly natural killer cells [1,5], expand, most probably due to adrenergic mechanisms, since betablockers can prevent these alterations in lymphocyte subsets. The lymphocytic adrenoceptors moreover are subject to dynamic regulation by their agonists [6], indicative of functional feedback loops.…”

Section: Schlüsselwörter: Herzinsuffizienz · Katecholamine · Zytokinementioning

confidence: 99%

Immune Modulation by Catecholamines - a Potential Mechanism of Cytokine Release in Heart Failure?

Müller‐Werdan¹,

Werdan

2000

Herz

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Cytokine blood levels are found to be moderately elevated in chronic heart failure, as a function of severity of disease. The source of these cytokines and the trigger mechanisms stimulating cytokine release are a matter of intense research. Potential players include bacterial endotoxin from intestinal translocation, a neurohumoral dysbalance with an enhanced sympathetic tone or an overspill of cytokines from the failing heart itself. We present arguments in favor of a direct link between the chronically enhanced sympathetic tone in heart failure and the clinically overt activation of the immune system, particularly interleukin 6 release.

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Effect of prolonged catecholamine infusion on immunoregulatory function: Implications in congestive heart failure

Cited by 42 publications

References 45 publications

Behavioral Activities, Physiological Body Reactions, Hematological Parameters and Hormonal Profiles for Bucks of New Zealand White and Baladi Red Rabbits Exposed to Short Term of High Temperature

Behavioral Activities, Physiological Body Reactions, Hematological Parameters and Hormonal Profiles for Bucks of New Zealand White and Baladi Red Rabbits Exposed to Short Term of High Temperature

Impaired antibody synthesis after spinal cord injury is level dependent and is due to sympathetic nervous system dysregulation

Immune Modulation by Catecholamines - a Potential Mechanism of Cytokine Release in Heart Failure?

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