2011
DOI: 10.1007/s12160-011-9274-0
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Hemoconcentration and Hemostasis During Acute Stress: Interacting and Independent Effects

Abstract: 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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Cited by 44 publications
(46 citation statements)
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References 160 publications
(270 reference statements)
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“…The resultant hyperviscosity increases shear stress and raises the probability of rupturing of atherosclerotic plaques (8). Activation of the sympathetic nervous system is once again implicated as major cause, since the increased systolic and diastolic blood pressure following sympathetic overactivity causes plasma to move from the intravascular space, while there is retention of blood cells and proteins in the vascular lumen (14). This phenomenon could occur during stress-induced hypercoagulopathy, although de novo synthesis or activation of coagulation factors cannot be ruled out (14).…”
Section: Hematologic Consequences Of Stressmentioning
confidence: 99%
“…The resultant hyperviscosity increases shear stress and raises the probability of rupturing of atherosclerotic plaques (8). Activation of the sympathetic nervous system is once again implicated as major cause, since the increased systolic and diastolic blood pressure following sympathetic overactivity causes plasma to move from the intravascular space, while there is retention of blood cells and proteins in the vascular lumen (14). This phenomenon could occur during stress-induced hypercoagulopathy, although de novo synthesis or activation of coagulation factors cannot be ruled out (14).…”
Section: Hematologic Consequences Of Stressmentioning
confidence: 99%
“…It is unlikely that the observed Hcy increase is a concomitant phenomenon of stresshemoconcentration (Austin et al, 2011) as the molecular weight of Hcy (0.135 kDa) is substantially smaller than the critical molecular weight of 69 kDa. We can only speculate that underlying mechanisms may include altered Hcy metabolism regulation (Williams and Schalinske, 2007) or altered sensitivity to stress hormone release (Rohleder et al, 2002) with age.…”
Section: Discussionmentioning
confidence: 96%
“…It is reasonable to assume that an increase in the concentration of red blood cells, a situation in which Ht level is also increased, will lead to thrombosis. In practice, an increase in the concentration of red blood cells from the movement or shift of plasma from the vascular compartment into interstitial spaces is believed to be a cause of polycythemia rather than an increase in red blood cell production in the bone marrow as in stress-induced polycythemia (Emery et al, 1974, Patterson et al, 1998, de Boer et al, 2007, Austin et al, 2011). In contrast to PV, polycythemia in which only red blood cells increase has been referred to as relative polycythemia (Lawrence and Berlin, 1952) or stress polycythemia (Dameshek, 1953).…”
Section: Discussionmentioning
confidence: 99%