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Mental stress-induced hemoconcentration and its recovery: a controlled study of time course and mechanisms
Dolf de Boer1, Christopher Ring, Alexander C Curlett
1Behavioural Medicine Group, School of Sport and Exercise Sciences, University of Birmingham, B15 2TT, Birmingham, UK. DXD033@bham.ac.uk
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.
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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