Stephen M. Patterson

Hemoconcentration and stress: A review of physiological mechanisms and relevance for cardiovascular disease risk.

Elevated levels of hematocrit and hemoglobin have been identified as an independent risk factor for the development of a number of diseases, including hypertension, coronary heart disease, and stroke. A growing body of evidence also indicates that elevations in hematocrit and hemoglobin are present in situations involving both physical and mental stressors. This paper reviews the evidence linking decreases in plasma volume causing hemoconcentration with hemodynamic adjustments associated with activation of the sympathetic nervous system, and the potential relevance of stress-induced hemoconcentration in triggering deleterious cardiovascular events. The importance of blood viscosity in understanding the effects of hemoconcentration is discussed, along with the need to evaluate the degree of hemoconcentration during stress for accurate interpretation of changes in certain blood constituents.

Effects of acute mental stress on serum lipids: mediating effects of plasma volume.

&NA; The present study assessed the acute effects of mental stress (mental arithmetic) on serum cholesterol, triglycerides, high‐density lipoprotein‐cholesterol (HDL‐C), and low‐density lipoprotein‐cholesterol (LDL‐C), and the extent to which stress‐induced changes are attributable to decreases in plasma volume. Total cholesterol, triglycerides, HDL‐C, and LDL‐C were assessed in 18 healthy men (35 +/‐ 7 years) during a resting baseline (30 minutes), challenging mental arithmetic (math; 10 minutes), and recovery (30 minutes). Five additional subjects served as controls receiving no stress intervention. An indirect estimation of the change in plasma volume was computed from hematocrit and hemoglobin at each time point. Results indicated significant (p < .001) increases in cholesterol, triglycerides, LDL‐C, and HDL‐C levels during mental arithmetic. Changes in lipid levels during stress were not related to plasma epinephrine levels or changes. Significant (p < .002) increases in hematocrit and hemoglobin levels reflected a 9.23% decrease in plasma volume during mental arithmetic. Correcting for this decreased plasma volume, changes in cholesterol, triglycerides, HDL‐C, and LDL‐C levels during math were no longer significant (p > .16, p > .23, p > .27, and p > .42, respectively). These results indicate that acute psychological stress can cause a rapid and substantial decrease in plasma volume, producing hemoconcentration. Thus, stress‐mediated increases in circulating lipid concentrations are a secondary result of decreased plasma volume, perhaps due to vascular fluid shifts. Methodologically, stress‐induced hemoconcentration during mental stress suggests that acute plasma volume decreases may need to be evaluated in studies of the biochemical effects of stress on high molecular weight substances.

PROTHROMBOTIC EFFECTS OF ENVIRONMENTAL STRESS : CHANGES IN PLATELET FUNCTION, HEMATOCRIT, AND TOTAL PLASMA PROTEIN

Mental stress can affect a range of variables relevant to hemostasis and thrombosis.However, research has not clarified whether these effects occur as part of a generalized sympathodrenal response or whether stress-induced increases in catecholamines and blood pressure have selective and independent effects on hematologic variables. This study assessed the effects of mental and cold pressor stress on platelet activation, hematocrit, and total plasma protein and the relationship of these changes to sympathoadrenal and hemodynamic mechanisms. Platelet factor 4, beta-thromboglobulin, total plasma protein, hematocrit values, and hemoglobin were measured in 22 healthy men (32 +/- 7 years) during rest, mental arithmetic, and cold pressor task. A no-stress control group of five male subjects was used to rule out the possible effects of blood withdrawal in producing these changes. Significant increases to mental arithmetic and cold pressor (p <.001) were observed in platelet factor 4 and beta-thromboglobulin. Increases (p <.002) in hematocrit values and total plasma protein also occurred with mental arithmetic and cold pressor. Correlational analyses revealed that changes in hematocrit and total plasma protein concentrations were related to increased mean arterial pressure during stress, and platelet activation correlated positively with norepinephrine and negatively with epinephrine. The present results indicate that acute psychologic and cold stress cause concurrent changes in several hemostatic factors (increased platelet activation, hematocrit, and total plasma protein) that may play key roles in thrombosis and ischemia. The relationships of hematocrit and total plasma protein to blood pressure increases and the associations between platelet activation and catecholamines support the notion that stress-induced increases in catecholamines and blood pressure have selective effects on specific hemostatic variables.

Stress-induced hemoconcentration of blood cells and lipids in healthy women during acute psychological stress.

This study examined the effects of psychological stress on hemoconcentration in women. Hematologic and hemodynamic variables were assessed in 17 women before and after a 3-min speech task. Significant changes in hematocrit, hemoglobin levels, red and white blood cell (WBC) count, and calculated plasma volume occurred during psychological stress (all ps < .05). Significant increases were also observed for total cholesterol, triglycerides, high density lipoprotein cholesterol, low density lipoprotein cholesterol, and free fatty acid (FFA; all ps < .05) during stress. After statistically correcting for the hemoconcentration effects of decreased plasma volume during stress, only WBC count and FFA concentration remained significantly elevated during the stress task (p < .006 and p < .05, respectively). In sum, acute stress alters hemoconcentration in women, which in turn can account for most stress-induced changes in lipids.

Use of bioelectrical impedance in hydration status assessment: reliability of a new tool in psychophysiology research

Adequate hydration is crucial in maintaining optimal physical and mental functioning and the need for a fast and reliable hydration status assessment in behavioral medicine research has become increasingly important. The goal of this study was to determine the reliability of bioelectrical impedance assessment (BIA) in assessing total body water (TBW), extracellular water (ECW) and intracellular water (ICW) and to assess whether individuals can be reliably classified as being hypohydrated or hyperhydrated using lower and upper quartiles, respectively. TBW, ECW and ICW were assessed via BIA (Bodystat, Isle of Man, UK) in 52 male and 48 female college students on 2 separate days within 1 week. Results revealed strong test-retest reliability for TBW (r=0.983), ECW (r=0.972) and ICW (r=0.988) (all Ps<0.001). Following the initial and follow-up assessments, participants were then classified as being either hypohydrated or hyperhydrated based on the percentage of body weight accounted for by TBW. Test-retest reliability of hydration status within classifications was then assessed by gender. Test-retest reliability was found for TBW, ECW and ICW among hypohydrated (r=0.985, r=0.972 and r=0.99, respectively) and hyperhydrated (r=0.994, r=0.989 and r=0.994, respectively) males (all Ps<0.001). Significant test-retest correlations were also found for females classified as being hypohydrated (r=0.97, r=0.956 and r=0.976, respectively) and hyperhydrated (r=0.973, r=0.976 and r=0.976, respectively) (all Ps<0.001). These findings suggest that hydration status, as indexed by bioelectrical impedance technique, is reliable across time and is also reliable within individuals who are chronically hyperhydrated or hypohydrated.

Racial Differences in Hemodynamic Responses to Environmental Thermal Stress Among Adolescents

BACKGROUND Previous studies by our laboratory and others have shown that blood pressure (BP) responses to many short-term laboratory stressors are greater in black than in white children. We sought to determine the cardiac and vascular contributions to these differences in BP reactivity and whether racial differences in vascular reactivity involve excessive vasoconstriction or deficient vasodilation. METHODS AND RESULTS We evaluated BP, heart rate, and impedance cardiographic measures of preejection period (PEP) and total peripheral resistance (TPR) in healthy black (n=76) and white (n=60) adolescents (mean age, 14.8 years) during passive exposure to a vasoconstrictive cold chamber (8 degrees C to 10 degrees C) and a vasodilatory heat chamber (40 degrees C to 42 degrees C). Results indicated greater decreases in PEP and increases in TPR in blacks than whites during cold exposure (P<0.05) but no group differences during heat exposure. Covariance analyses indicated that the racial differences during cold exposure probably reflected greater beta-adrenergic cardiac reactivity and alpha-adrenergic vasoconstrictive reactivity in blacks than whites. CONCLUSIONS Blacks and whites exhibited comparable myocardial and vasodilatory responses to heat stress, but blacks exhibited heightened myocardial and vasoconstrictive reactivity to cold stress. These results suggest that the locus of racial differences in vascular reactivity involves vasoconstrictive rather than vasodilatory function. The pattern of racial differences during cold stress raises the possibility that both myocardial and vasoconstrictive mechanisms may contribute to the increased risk of hypertension in blacks.

Lymphocyte Subset Redistribution During Acute Laboratory Stress in Young Adults: Mediating Effects of Hemoconcentration

Acute psychological stress is known to alter the distribution of circulating lymphocyte subsets and also to cause a reduction of plasma volume. Data were reanalyzed from 4 previously reported studies (E. A. Bachen et al., 1995; T. B. Herbert et al., 1994; A. L. Marsland, S. B. Manuck, T. V. Fazzari, C. J. Stewart, & B. S. Rabin, 1995; A. L. Marsland, S. B. Manuck, P. Wood, et al., 1995) to determine the extent to which changes in the concentration of lymphocyte subsets are attributable to such hemoconcentration. Meta-analytic procedures showed circulating concentrations of T-suppressor/cytotoxic (CD8) and natural killer (NK) cells to increase following acute laboratory challenge, whereas T-helper (CD4) and B- (CD19) cell populations did not change. Adjustments for concomitant hemoconcentration reduced the magnitude of stress-related increases in CD8 and NK cells significantly and revealed a decrease in CD4 and CD19 cell concentrations from baseline to stress measurements. These data provide evidence (a) that increases in circulating numbers of CD8 and NK cells following acute stress are partially attributable to hemoconcentration and (b) that CD4 and CD19 cell concentrations decrease during acute stress when hemoconcentration is taken into account.

Hemoconcentration and hemostasis during acute stress: interacting and independent effects

BackgroundAcute 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.PurposeThis 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.ConclusionsTraditional 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.

Prothrombotic changes with acute psychological stress: Combined effect of hemoconcentration and genuine coagulation activation

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.

Blood pressure and cerebral oxygenation responses to skeletal muscle tension: a comparison of two physical maneuvers to prevent vasovagal reactions

Aim:  The present study compared blood pressure, heart rate, and cerebral oxygenation responses to two manipulations used to prevent vasovagal reaction – skeletal muscle tensing alone and skeletal muscle tensing with leg crossing.