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Stephen M Patterson - One of the best experts on this subject based on the ideXlab platform.
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stress Hemoconcentration plasma volume changes or splenic contraction a reply to engan and schagatay
Annals of Behavioral Medicine, 2015Co-Authors: Anthony W. Austin, Stephen M Patterson, Roland KänelAbstract:In their recent letter regarding our 2011 review article [1], Engan and Schagatay [2] suggest that spleen-induced increases in erythrocyte concentration may be partly responsible for stress-Hemoconcentration. They rightly state that, due to a release of erythrocytes into the blood, Hemoconcentration occurs as a result of spleen contraction during physiological stressors such as exercise [3] or apneic diving [3, 4]. Moreover, the spleen is sympathetically innervated [3] and catecholamine infusion results in spleen contraction and subsequent release of erythrocytes [5–8]. Although there is much research on this topic in animals, we did not mention animal research in our review because we limited our review to humans. We [9, 10] and others [11] have shown that erythrocytes increase during acute mental stress. After correcting for plasma volume changes, erythrocytes were no longer different from baseline [10] or they even decreased [9]. This suggests that the increase in erythrocytes is a passive by-product of plasma volume shifts as opposed to a result of active release from the spleen. If the release of erythrocytes from the spleen and plasma volume reduction occur simultaneously, it seems unlikely that correcting for plasma volume changes would result in a decrease in erythrocytes. Instead, one would expect that the increase in erythrocytes and the decrease in plasma volume to offset. Moreover, HDL cholesterol, LDL cholesterol [10, 12–14], plasma proteins [13], and immune cells/messengers [15] are affected by Hemoconcentration. However, erythrocyte concentration does not change during stress to the same extent that these substances change, suggesting that an increase in erythrocytes is not responsible for these increases. Nevertheless, this does not completely preclude the possibility that the spleen releases erythrocytes during acute mental stress. The next step in this line of research would be to concurrently measure splenic contraction, erythrocyte concentration, and plasma volume before, during, and after stress in order to disentangle how these mechanisms may work together to produce a state of stress-Hemoconcentration.
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comparison of stress Hemoconcentration correction techniques for stress induced coagulation
BioMed Research International, 2013Co-Authors: Anthony W. Austin, Stephen M PattersonAbstract:When examining stress effects on coagulation, arithmetic correction is typically used to adjust for concomitant Hemoconcentration but may be inappropriate for coagulation activity assays. We examined a new physiologically relevant method of correcting for stress-Hemoconcentration. Blood was drawn from healthy men (N = 40) during baseline, mental stress, and recovery, and factor VII activity (FVII:C), factor VIII activity (FVIII:C), activated partial thromboplastin time (APTT), prothrombin time (PT%), fibrinogen, D-dimer, and plasma volume were determined. Three Hemoconcentration correction techniques were assessed: arithmetic correction and two reconstitution techniques using baseline plasma or physiological saline. Area-under-the-curve (AUC) was computed for each technique. For FVII:C, uncorrected AUC was significantly greater than AUC corrected arithmetically. For PT%, uncorrected AUC was significantly greater than AUC corrected with saline or arithmetically. For APTT, uncorrected AUC was significantly less than AUC corrected with saline and greater than AUC corrected arithmetically. For fibrinogen, uncorrected AUC was significantly greater than AUC corrected with saline or arithmetically. For D-dimer, uncorrected AUC was significantly greater than AUC corrected arithmetically. No differences in AUC were observed for FVIII:C. Saline reconstitution seems most appropriate when adjusting for Hemoconcentration effects on clotting time and activity. Stress-Hemoconcentration accounted for the majority of coagulation changes.
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abstract 112 reconstitution with saline is more appropriate than arithmetic correction when examining stress Hemoconcentration effects on coagulation
Arteriosclerosis Thrombosis and Vascular Biology, 2012Co-Authors: Anthony W. Austin, Stephen M PattersonAbstract:Introduction: The goal of this study was to examine a new physiologically relevant method of correcting for Hemoconcentration effects on stress-induced changes in coagulation parameters (i.e., acti...
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stress induced alterations in coagulation assessment of a new Hemoconcentration correction technique
Psychosomatic Medicine, 2012Co-Authors: Anthony W. Austin, Stephen M Patterson, Monika Stutz, Petra H Wirtz, Roland KänelAbstract:OBJECTIVE: For the examination of psychological stress effects on coagulation, the Dill and Costill correction (DCC) for Hemoconcentration effects has been used to adjust for stress-induced plasma volume changes. Although the correction is appropriate for adjusting concentrations of various large blood constituents, it may be inappropriate for time-dependent or functional coagulation assays. Two new plasma reconstitution techniques for correcting Hemoconcentration effects on stress-induced changes in coagulation were compared with the DCC. METHODS: Blood was collected from 31 men during baseline, the Trier Social Stress Test (TSST), and after 20-minute recovery. For the reconstitution techniques, TSST plasma samples were reconstituted with either baseline plasma or physiological saline equal to the amount of plasma lost during stress. RESULTS: Uncorrected activated partial thromboplastin time (APTT) decreased, whereas fibrinogen, factor VIII clotting activity (FVIII:C), D-dimer and prothrombin time (PT%) increased significantly during the TSST. The DCC produced a significantly greater decrease in APTT during stress compared to uncorrected APTT, a significant decrease in PT% compared to uncorrected PT%, and stress D-dimer and fibrinogen and FVIII:C being no different than baseline. APTT, fibrinogen, D-dimer and PT% after saline reconstitution were not different from baseline, whereas FVIII:C after saline reconstitution remained elevated. APTT, PT%, fibrinogen and D-dimer after plasma reconstitution were no different from uncorrected values, whereas FVIII:C remained significantly elevated. CONCLUSIONS: The observed changes in coagulation are likely in part a consequence of stress and Hemoconcentration, but the DCC seems to be an inappropriate Hemoconcentration correction technique of time-dependent assays. The saline reconstitution technique may be more biologically relevant when examining stress-Hemoconcentration effects on coagulation.
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Hemoconcentration and Hemostasis During Acute Stress: Interacting and Independent Effects
Annals of Behavioral Medicine, 2011Co-Authors: Anthony W. Austin, Stephen M Patterson, Roland KänelAbstract:Background Acute psychological stress can produce significant Hemoconcentration as well as prothrombotic changes in blood, both of which may have potentially harmful effects on the cardiovascular system. It is unclear whether these effects are independent or have influence on each other. Purpose This review discusses research investigating the effects of acute psychological stress on Hemoconcentration and hemostasis and explores future directions for psychohematology research. Physiology, associations with cardiovascular disease, and relationships between acute psychological stress are discussed independently for Hemoconcentration and hemostasis, followed by an examination of the effects of stress-Hemoconcentration on hemostasis. Conclusions Traditional methods of adjusting for stress-Hemoconcentration effects (e.g., calculated plasma volume or hematocrit level corrections) may not be appropriate when examining stress-induced changes in hemostasis. The effects of acute stress on hemostasis should be examined in conjunction with Hemoconcentration.
Philip R Greipp - One of the best experts on this subject based on the ideXlab platform.
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narrative review the systemic capillary leak syndrome
Annals of Internal Medicine, 2010Co-Authors: Kirk M Druey, Philip R GreippAbstract:First described in 1960, the systemic capillary leak syndrome (SCLS) is a rare disease of reversible plasma extravasation and vascular collapse accompanied by Hemoconcentration and hypoalbuminemia ...
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control of systemic capillary leak syndrome with aminophylline and terbutaline
The American Journal of Medicine, 1992Co-Authors: Robert M Droder, Robert A Kyle, Philip R GreippAbstract:Abstract purpose: Patients with systemic capillary leak syndrome have a characteristic triad of hypotension, Hemoconcentration, and monoclonal gammopathy. They have frequent and severe attacks of Hemoconcentration and hypotension accompanied by marked plasma shifts. The exact role of this monoclonal protein is unknown, but it probably leads, in some way, to an increase in capillary permeability. Despite efforts to resuscitate the patients during an acute attack, the syndrome is often fatal. Some success has been obtained in preventing the attacks with the β-adrenergic-stimulating agent terbutaline. The purpose of this study was to determine the effectiveness of aminophylline and terbutaline in the treatment of systemic capillary leak syndrome. methods: Over a decade, three patients with systemic capillary leak syndrome presented at our institution. All three patients were treated with terbutaline and aminophylline. Prednisone was used during the course of treatment in each of the three patients. results: In contrast to previous reports of partial or temporary control of episodes, all three patients are alive with almost complete resolution of their recurrent attacks and have been able to return to their normal lifestyles. conclusion: The regimen of terbutaline and aminophylline effectively prevents the attacks of hypotension and Hemoconcentration that occur in systemic capillary leak syndrome. The role of prednisone is not clear. Until more is known about the pathophysiology of the disorder, treatment must remain empiric and supportive.
Roland Känel - One of the best experts on this subject based on the ideXlab platform.
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stress Hemoconcentration plasma volume changes or splenic contraction a reply to engan and schagatay
Annals of Behavioral Medicine, 2015Co-Authors: Anthony W. Austin, Stephen M Patterson, Roland KänelAbstract:In their recent letter regarding our 2011 review article [1], Engan and Schagatay [2] suggest that spleen-induced increases in erythrocyte concentration may be partly responsible for stress-Hemoconcentration. They rightly state that, due to a release of erythrocytes into the blood, Hemoconcentration occurs as a result of spleen contraction during physiological stressors such as exercise [3] or apneic diving [3, 4]. Moreover, the spleen is sympathetically innervated [3] and catecholamine infusion results in spleen contraction and subsequent release of erythrocytes [5–8]. Although there is much research on this topic in animals, we did not mention animal research in our review because we limited our review to humans. We [9, 10] and others [11] have shown that erythrocytes increase during acute mental stress. After correcting for plasma volume changes, erythrocytes were no longer different from baseline [10] or they even decreased [9]. This suggests that the increase in erythrocytes is a passive by-product of plasma volume shifts as opposed to a result of active release from the spleen. If the release of erythrocytes from the spleen and plasma volume reduction occur simultaneously, it seems unlikely that correcting for plasma volume changes would result in a decrease in erythrocytes. Instead, one would expect that the increase in erythrocytes and the decrease in plasma volume to offset. Moreover, HDL cholesterol, LDL cholesterol [10, 12–14], plasma proteins [13], and immune cells/messengers [15] are affected by Hemoconcentration. However, erythrocyte concentration does not change during stress to the same extent that these substances change, suggesting that an increase in erythrocytes is not responsible for these increases. Nevertheless, this does not completely preclude the possibility that the spleen releases erythrocytes during acute mental stress. The next step in this line of research would be to concurrently measure splenic contraction, erythrocyte concentration, and plasma volume before, during, and after stress in order to disentangle how these mechanisms may work together to produce a state of stress-Hemoconcentration.
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stress induced alterations in coagulation assessment of a new Hemoconcentration correction technique
Psychosomatic Medicine, 2012Co-Authors: Anthony W. Austin, Stephen M Patterson, Monika Stutz, Petra H Wirtz, Roland KänelAbstract:OBJECTIVE: For the examination of psychological stress effects on coagulation, the Dill and Costill correction (DCC) for Hemoconcentration effects has been used to adjust for stress-induced plasma volume changes. Although the correction is appropriate for adjusting concentrations of various large blood constituents, it may be inappropriate for time-dependent or functional coagulation assays. Two new plasma reconstitution techniques for correcting Hemoconcentration effects on stress-induced changes in coagulation were compared with the DCC. METHODS: Blood was collected from 31 men during baseline, the Trier Social Stress Test (TSST), and after 20-minute recovery. For the reconstitution techniques, TSST plasma samples were reconstituted with either baseline plasma or physiological saline equal to the amount of plasma lost during stress. RESULTS: Uncorrected activated partial thromboplastin time (APTT) decreased, whereas fibrinogen, factor VIII clotting activity (FVIII:C), D-dimer and prothrombin time (PT%) increased significantly during the TSST. The DCC produced a significantly greater decrease in APTT during stress compared to uncorrected APTT, a significant decrease in PT% compared to uncorrected PT%, and stress D-dimer and fibrinogen and FVIII:C being no different than baseline. APTT, fibrinogen, D-dimer and PT% after saline reconstitution were not different from baseline, whereas FVIII:C after saline reconstitution remained elevated. APTT, PT%, fibrinogen and D-dimer after plasma reconstitution were no different from uncorrected values, whereas FVIII:C remained significantly elevated. CONCLUSIONS: The observed changes in coagulation are likely in part a consequence of stress and Hemoconcentration, but the DCC seems to be an inappropriate Hemoconcentration correction technique of time-dependent assays. The saline reconstitution technique may be more biologically relevant when examining stress-Hemoconcentration effects on coagulation.
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Hemoconcentration and Hemostasis During Acute Stress: Interacting and Independent Effects
Annals of Behavioral Medicine, 2011Co-Authors: Anthony W. Austin, Stephen M Patterson, Roland KänelAbstract:Background Acute psychological stress can produce significant Hemoconcentration as well as prothrombotic changes in blood, both of which may have potentially harmful effects on the cardiovascular system. It is unclear whether these effects are independent or have influence on each other. Purpose This review discusses research investigating the effects of acute psychological stress on Hemoconcentration and hemostasis and explores future directions for psychohematology research. Physiology, associations with cardiovascular disease, and relationships between acute psychological stress are discussed independently for Hemoconcentration and hemostasis, followed by an examination of the effects of stress-Hemoconcentration on hemostasis. Conclusions Traditional methods of adjusting for stress-Hemoconcentration effects (e.g., calculated plasma volume or hematocrit level corrections) may not be appropriate when examining stress-induced changes in hemostasis. The effects of acute stress on hemostasis should be examined in conjunction with Hemoconcentration.
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Hemoconcentration and hemostasis during acute stress interacting and independent effects
Annals of Behavioral Medicine, 2011Co-Authors: Anthony W. Austin, Stephen M Patterson, Roland KänelAbstract:Background Acute psychological stress can produce significant Hemoconcentration as well as prothrombotic changes in blood, both of which may have potentially harmful effects on the cardiovascular system. It is unclear whether these effects are independent or have influence on each other.
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prothrombotic changes with acute psychological stress combined effect of Hemoconcentration and genuine coagulation activation
Thrombosis Research, 2009Co-Authors: Roland Känel, Brigitte M Kudielka, Andre Haeberli, Monika Stutz, Joachim E Fischer, Stephen M PattersonAbstract:INTRODUCTION: Acute psychosocial stress accelerates blood coagulation and elicits Hemoconcentration which mechanisms are implicated in acute coronary thrombotic events. We investigated the extent to which the change in prothrombotic measures with acute stress reflects Hemoconcentration and genuine activation of coagulation. MATERIAL AND METHODS: Twenty-one middle-aged healthy men underwent three sessions of a combined speech and mental arithmetic task with one-week intervals. Coagulation and plasma volume were assessed at baseline, immediately post-stress, and 45 min post-stress at sessions one and three. Measures of both visits were aggregated to enhance robustness of individual biological stress responses. Changes in eight coagulation measures with and without adjustment for simultaneous plasma volume shift were compared. RESULTS: From baseline to immediately post-stress, unadjusted levels of fibrinogen (p=0.028), clotting factor VII activity (FVII:C) (p=0.001), FVIII:C (p<0.001), FXII:C (p<0.001), and von Willebrand factor (VWF) (p=0.008) all increased. Taking into account Hemoconcentration, fibrinogen (p=0.020) and FVII:C levels (p=0.001) decreased, activated partial prothrombin time (APPT) shortened (p<0.001) and prothrombin time (PT) was prolonged (p<0.001). Between baseline and 45 min post-stress, unadjusted (p=0.050) and adjusted (p=0.001) FVIII:C levels increased, adjusted APTT was prolonged (p=0.017), and adjusted PT was shortened (p=0.033). D-dimer levels did not significantly change over time. CONCLUSIONS: Adjustment for stress-Hemoconcentration altered the course of unadjusted levels of several prothrombotic factors. After adjustment for Hemoconcentration, APPT was shortened immediately post-stress, whereas 45 min post-stress, FVIII:C was increased and PT was shortened. Procoagulant changes to acute stress may reflect both Hemoconcentration and genuine activation of coagulation molecules and pathways.
Douglas Carroll - One of the best experts on this subject based on the ideXlab platform.
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Hemoconcentration during a prolonged stress task associations with hemodynamic reactivity and microvascular permeability
Biological Psychology, 2009Co-Authors: Jet Veldhuijzen J C S Van Zanten, Christopher Ring, Douglas Carroll, David Mcintyre, Margaret D BrownAbstract:This study explored the association between stress-induced Hemoconcentration and plasma colloid osmotic pressure, hemodynamic reactivity, and microvascular permeability during a protracted stress task in 26 healthy, young participants. Microvascular permeability was measured during rest using venous congestion plethysmography in a subsample of 13 participants. The task increased hematocrit, colloid osmotic pressure, blood pressure, and heart rate and decreased R-wave to pulse interval. Resting microvascular permeability was not correlated with Hemoconcentration. Colloid osmotic pressure and diastolic blood pressure were associated with stress-induced Hemoconcentration throughout the task. The association with systolic blood pressure as well as heart rate, however, was more evident during the initial 8 min of the task than throughout the total task duration. These findings suggest that factors associated with Hemoconcentration vary with task duration.
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mental stress induced Hemoconcentration and its recovery a controlled study of time course and mechanisms
Psychophysiology, 2007Co-Authors: Dolf De Boer, Christopher Ring, Alexander C Curlett, Matt Ridley, Douglas CarrollAbstract:: Hemoconcentration to mental stress has been implicated in acute cardiovascular events. Participants were exposed to a 30-min baseline, a 4-min stress task, and a 40-min recovery; they also undertook a 74-min no-stress control session. Hemodynamic activity was recorded and blood sampled regularly and analyzed for hematocrit, colloid osmotic pressure, and coagulation time. Hematocrit increased with stress and fully recovered after 20 min. Colloid osmotic pressure showed a similar time course. No such changes occurred in the control session. Coagulation time was not perturbed by stress. The pattern of increase in hematocrit correlated with contemporary colloid osmotic pressure and blood pressure. In recovery, only colloid osmotic pressure was strongly associated with hematocrit. The mechanisms of stress-induced Hemoconcentration may differ from those responsible for recovery, which may depend primarily on colloid osmotic pressure.
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time course and mechanisms of Hemoconcentration in response to mental stress
Biological Psychology, 2006Co-Authors: Dolf De Boer, Christopher Ring, Douglas CarrollAbstract:Abstract Hemoconcentration with mental stress exposure may be involved in the triggering of acute cardiovascular events. In the present study, hematocrit was measured repeatedly at baseline, during a 4 min mental stress task and during 20 min of recovery. Blood was sampled every 1–2 min throughout. Blood pressure, heart rate and R-wave to pulse interval, a measure of cardiac contractility, were measured with the same periodicity. The stress task elicited a 1.3% increase in hematocrit, which was sustained with full return to baseline level occurring only after 16 min of recovery. Between-subject correlations between hematocrit and hemodynamic activity were low. Aggregate within-subject coefficients were more impressive; the temporal profile of hematocrit correlated significantly with all hemodynamic variables. Similar within-subject analyses indicated that whereas cardiac contractility was correlated with hematocrit both during stress-related increase and subsequent recovery, blood pressure was related to hematocrit only during the increase. This suggests that stress-induced Hemoconcentration may driven by different mechanisms than those which underlie its recovery.
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mental stress induced Hemoconcentration sex differences and mechanisms
Psychophysiology, 2004Co-Authors: Jet Veldhuijzen J C S Van Zanten, Christopher Ring, Victoria E Burns, Kate M Edwards, Mark Drayson, Douglas CarrollAbstract:Given the possible role of Hemoconcentration in myocardial infarction and apparent sex differences in susceptibility, three studies examined sex differences in mental stress-induced Hemoconcentration, and explored possible underlying mechanisms. Blood pressure, heart rate, and hematocrit were monitored at rest and in response to a mental stress task that was contrived to be increasingly provocative across the three studies. This was confirmed by self-report, performance, and cardiovascular reactivity data. The most convincing evidence for Hemoconcentration effects and sex differences in Hemoconcentration emerged from exposure to the more provocative of the stress tasks, with men also showing greater Hemoconcentration than women. Blood pressure reactivity was a strong and consistent predictor of stress-induced Hemoconcentration. These findings may help to explain sex differences in susceptibility to myocardial infarction.
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Mental stress‐induced Hemoconcentration: Sex differences and mechanisms
Psychophysiology, 2004Co-Authors: Jet Veldhuijzen J C S Van Zanten, Christopher Ring, Victoria E Burns, Kate M Edwards, Mark Drayson, Douglas CarrollAbstract:Given the possible role of Hemoconcentration in myocardial infarction and apparent sex differences in susceptibility, three studies examined sex differences in mental stress-induced Hemoconcentration, and explored possible underlying mechanisms. Blood pressure, heart rate, and hematocrit were monitored at rest and in response to a mental stress task that was contrived to be increasingly provocative across the three studies. This was confirmed by self-report, performance, and cardiovascular reactivity data. The most convincing evidence for Hemoconcentration effects and sex differences in Hemoconcentration emerged from exposure to the more provocative of the stress tasks, with men also showing greater Hemoconcentration than women. Blood pressure reactivity was a strong and consistent predictor of stress-induced Hemoconcentration. These findings may help to explain sex differences in susceptibility to myocardial infarction.
Anthony W. Austin - One of the best experts on this subject based on the ideXlab platform.
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stress Hemoconcentration plasma volume changes or splenic contraction a reply to engan and schagatay
Annals of Behavioral Medicine, 2015Co-Authors: Anthony W. Austin, Stephen M Patterson, Roland KänelAbstract:In their recent letter regarding our 2011 review article [1], Engan and Schagatay [2] suggest that spleen-induced increases in erythrocyte concentration may be partly responsible for stress-Hemoconcentration. They rightly state that, due to a release of erythrocytes into the blood, Hemoconcentration occurs as a result of spleen contraction during physiological stressors such as exercise [3] or apneic diving [3, 4]. Moreover, the spleen is sympathetically innervated [3] and catecholamine infusion results in spleen contraction and subsequent release of erythrocytes [5–8]. Although there is much research on this topic in animals, we did not mention animal research in our review because we limited our review to humans. We [9, 10] and others [11] have shown that erythrocytes increase during acute mental stress. After correcting for plasma volume changes, erythrocytes were no longer different from baseline [10] or they even decreased [9]. This suggests that the increase in erythrocytes is a passive by-product of plasma volume shifts as opposed to a result of active release from the spleen. If the release of erythrocytes from the spleen and plasma volume reduction occur simultaneously, it seems unlikely that correcting for plasma volume changes would result in a decrease in erythrocytes. Instead, one would expect that the increase in erythrocytes and the decrease in plasma volume to offset. Moreover, HDL cholesterol, LDL cholesterol [10, 12–14], plasma proteins [13], and immune cells/messengers [15] are affected by Hemoconcentration. However, erythrocyte concentration does not change during stress to the same extent that these substances change, suggesting that an increase in erythrocytes is not responsible for these increases. Nevertheless, this does not completely preclude the possibility that the spleen releases erythrocytes during acute mental stress. The next step in this line of research would be to concurrently measure splenic contraction, erythrocyte concentration, and plasma volume before, during, and after stress in order to disentangle how these mechanisms may work together to produce a state of stress-Hemoconcentration.
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comparison of stress Hemoconcentration correction techniques for stress induced coagulation
BioMed Research International, 2013Co-Authors: Anthony W. Austin, Stephen M PattersonAbstract:When examining stress effects on coagulation, arithmetic correction is typically used to adjust for concomitant Hemoconcentration but may be inappropriate for coagulation activity assays. We examined a new physiologically relevant method of correcting for stress-Hemoconcentration. Blood was drawn from healthy men (N = 40) during baseline, mental stress, and recovery, and factor VII activity (FVII:C), factor VIII activity (FVIII:C), activated partial thromboplastin time (APTT), prothrombin time (PT%), fibrinogen, D-dimer, and plasma volume were determined. Three Hemoconcentration correction techniques were assessed: arithmetic correction and two reconstitution techniques using baseline plasma or physiological saline. Area-under-the-curve (AUC) was computed for each technique. For FVII:C, uncorrected AUC was significantly greater than AUC corrected arithmetically. For PT%, uncorrected AUC was significantly greater than AUC corrected with saline or arithmetically. For APTT, uncorrected AUC was significantly less than AUC corrected with saline and greater than AUC corrected arithmetically. For fibrinogen, uncorrected AUC was significantly greater than AUC corrected with saline or arithmetically. For D-dimer, uncorrected AUC was significantly greater than AUC corrected arithmetically. No differences in AUC were observed for FVIII:C. Saline reconstitution seems most appropriate when adjusting for Hemoconcentration effects on clotting time and activity. Stress-Hemoconcentration accounted for the majority of coagulation changes.
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abstract 112 reconstitution with saline is more appropriate than arithmetic correction when examining stress Hemoconcentration effects on coagulation
Arteriosclerosis Thrombosis and Vascular Biology, 2012Co-Authors: Anthony W. Austin, Stephen M PattersonAbstract:Introduction: The goal of this study was to examine a new physiologically relevant method of correcting for Hemoconcentration effects on stress-induced changes in coagulation parameters (i.e., acti...
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stress induced alterations in coagulation assessment of a new Hemoconcentration correction technique
Psychosomatic Medicine, 2012Co-Authors: Anthony W. Austin, Stephen M Patterson, Monika Stutz, Petra H Wirtz, Roland KänelAbstract:OBJECTIVE: For the examination of psychological stress effects on coagulation, the Dill and Costill correction (DCC) for Hemoconcentration effects has been used to adjust for stress-induced plasma volume changes. Although the correction is appropriate for adjusting concentrations of various large blood constituents, it may be inappropriate for time-dependent or functional coagulation assays. Two new plasma reconstitution techniques for correcting Hemoconcentration effects on stress-induced changes in coagulation were compared with the DCC. METHODS: Blood was collected from 31 men during baseline, the Trier Social Stress Test (TSST), and after 20-minute recovery. For the reconstitution techniques, TSST plasma samples were reconstituted with either baseline plasma or physiological saline equal to the amount of plasma lost during stress. RESULTS: Uncorrected activated partial thromboplastin time (APTT) decreased, whereas fibrinogen, factor VIII clotting activity (FVIII:C), D-dimer and prothrombin time (PT%) increased significantly during the TSST. The DCC produced a significantly greater decrease in APTT during stress compared to uncorrected APTT, a significant decrease in PT% compared to uncorrected PT%, and stress D-dimer and fibrinogen and FVIII:C being no different than baseline. APTT, fibrinogen, D-dimer and PT% after saline reconstitution were not different from baseline, whereas FVIII:C after saline reconstitution remained elevated. APTT, PT%, fibrinogen and D-dimer after plasma reconstitution were no different from uncorrected values, whereas FVIII:C remained significantly elevated. CONCLUSIONS: The observed changes in coagulation are likely in part a consequence of stress and Hemoconcentration, but the DCC seems to be an inappropriate Hemoconcentration correction technique of time-dependent assays. The saline reconstitution technique may be more biologically relevant when examining stress-Hemoconcentration effects on coagulation.
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Hemoconcentration and Hemostasis During Acute Stress: Interacting and Independent Effects
Annals of Behavioral Medicine, 2011Co-Authors: Anthony W. Austin, Stephen M Patterson, Roland KänelAbstract:Background Acute psychological stress can produce significant Hemoconcentration as well as prothrombotic changes in blood, both of which may have potentially harmful effects on the cardiovascular system. It is unclear whether these effects are independent or have influence on each other. Purpose This review discusses research investigating the effects of acute psychological stress on Hemoconcentration and hemostasis and explores future directions for psychohematology research. Physiology, associations with cardiovascular disease, and relationships between acute psychological stress are discussed independently for Hemoconcentration and hemostasis, followed by an examination of the effects of stress-Hemoconcentration on hemostasis. Conclusions Traditional methods of adjusting for stress-Hemoconcentration effects (e.g., calculated plasma volume or hematocrit level corrections) may not be appropriate when examining stress-induced changes in hemostasis. The effects of acute stress on hemostasis should be examined in conjunction with Hemoconcentration.