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Observational data have suggested that increased water intake decreases the risk of CHD. A postulated mechanism is that increased water ingestion reduces blood viscosity. The aim of the present study was to assess the effect of increased fluid intake on blood viscosity. Men (n 67) and postmenopausal women (n 27) with one or more risk factors for CVD who reported intake of < or =0.5 litres water daily were randomised to a control group (n 31), an intervention group (n 32) that increased their daily water intake by 1 litre/d and an intervention group (n 31) that ingested 1 litre blueberry juice/d. All were encouraged to continue their usual diet and lifestyle. Whole-blood viscosity and blood and urine chemistries were measured by standard techniques after 2 and 4 weeks. Urine volume increased (by a median of 872 and 725 ml in the water and blueberry juice groups, respectively, v. 10 ml in the control group; P< or =0.002), confirming the subjects' adherence to the protocol. Urine osmolality and urinary levels of Na, K and creatinine decreased in the water and blueberry juice groups v. the controls (P<0.05). No change was seen in whole-blood viscosity or in levels of fibrinogen, total protein, lipids, glucose, insulin, C-peptide or other chemistry and haematology variables. In conclusion, a postulated protective effect of increased water or fluid intake is not explained by a change in blood viscosity and increased fluid intake does not influence CVD risk factors in the short term.

We studied effects of mental stress on whole-blood viscosity (WBV) and blood pressure (BP), and relations between WBV and autonomic nervous system activity and insulin sensitivity. We measured WBV (rotational rheometer), plasma noradrenaline (NA), finger BP, heart rate variability (HRV) and baroreflex sensitivity (BRS; transfer technique) during hyperinsulinaemic glucose clamp and mental arithmetic stress test (MST) in 20 men with high ( > or =140/90 mmHg) and 21 men with normal (< or =115/75 mmHg) screening BP, and 10 women regardless of screening BP (all normotensive). WBV and NA increased during the MST, while HRV and BRS decreased. During the MST, WBV (all shear rates) and the response ((delta)WBV) (low shear) were higher in men with high compared to normal screening BP (p<0.05). In men, WBV correlated positively with NA and negatively with HRV, BRS and insulin sensitivity. The diastolic BP response ((delta)DBP) was independently explained by high-shear (delta)WBV (p<0.05) and (delta)NA (p<0.0001), and (delta)WBV independently by (delta)DBP (p<0.05). WBV is related to increased sympathetic activity, impaired vagal cardiac control and low insulin sensitivity in young adults. The haemorheological effect of mental stress is increased in young men with high screening BP and may be mediated by the acute increase in BP.

The Carvedilol Acute Myocardial Infarction Study (CAMIS) investigates cardiac remodeling in patients (n = 250) randomized to carvedilol vs atenolol and treated for 12 months after acute myocardial infarction. In a sub-study, we compared sympathetic, hemorrheological and vascular effects in small but particularly well-matched groups of participants who had been on reasonably equipotent but unchanged doses of carvedilol (n = 10) or atenolol (n = 10) for at least 4 weeks. Blood pressures (p < 0.05), plasma adrenaline (p = 0.034), plasma vasopressin (p = 0.022) and whole blood viscosity at shear rate 0.5 cp (p = 0.050), 1.1 cp (p = 0.023), 5.8 cp (p = 0.049) and 201 cp (p = 0.060) taken in the laboratory at baseline before 2 h of using the hyperinsulinemic, isoglycemic glucose clamp were lower on carvedilol. Plasma noradrenaline was lower on carvedilol at baseline and throughout the clamp (p < 0.0005). Forearm vascular resistance as measured by plethysmography during the clamp tended to be lower on carvedilol (p = 0.074). No significant difference was found between the groups in glucose disposal rate measured by clamp, maximal forearm blood flow and minimal forearm vascular resistance after 10 min of ischemia, or in ambulatory blood pressure and heart rate taken a few days later. Thus, potential benefits of carvedilol vs atenolol were seen in these post-infarction patients in a laboratory setting. These findings suggest that the inhibitory effects on the sympathetic nervous system and related blood viscosity are stronger with carvedilol than with atenolol.

Objective - Activation of the sympathetic nervous system may increase hematocrit (Hct), whole blood viscosity (WBV), and possibly cardiovascular risk. The aim was to study gender specific differences of mental stress on sympathetic reactivity and blood rheology. Methods - Responses in blood pressure, heart rate (HR), Hct, WBV (Bohlin rotational viscosimeter), and plasma catecholamines to a mental arithmetic stress test (MST) were measured in male (n = 10, 23 ± 3 years, BMI 23 ± 2 kg/m2) and female (n = 10, 21 ± 4 years, BMI 24 ± 2 kg/m2) students. Results - Systolic blood pressure (SBP), diastolic blood pressure (DBP), and HR increased during MST in men and women, and declined to baseline levels after 15 min of recovery. In men, plasma adrenaline increased by 217% during MST (p < 0.01, ANOVA), and plasma noradrenaline increased by 68% (p < 0.05). Hct and WBV at low shear rates (0.5 and 1.1 l/s) increased as well (p < 0.01, p < 0.05, and p < 0.05, respectively). In women, the increase in plasma adrenaline averaged 118% during MST (p < 0.05) while plasma noradrenaline (-3%, p = 0.38), Hct, and WBV at all shear rates remained unchanged. Men and women differed in Δ adrenaline (p < 0.05), Δ noradrenaline (p = 0.01), Δ Hct (p < 0.05), and Δ WBV (p < 0.05). Δ Hct tended to correlate with Δ SBP (r = 0.60, p = 0.07), Δ DBP (r = 0.57, p = 0.09), and Δ HR (r = 0.50, p = 0.14), and correlated significantly with Δ noradrenaline (r = 0.66, p < 0.05) in men only. Multiple regression analysis showed that gender independently explained 22% of the change in Hct during mental stress. Conclusion - Data suggest gender specific differences in sympathetic and hemorrheological responses to mental stress in healthy young subjects. In men, sympathetic responses were related to hemorrheological responses, but not in women. It may be speculated whether such differences in stress responses may contribute to lower cardiovascular risk in premenopausal women than in men. [ABSTRACT FROM AUTHOR]

We have seen relationships between whole blood viscosity (WBV) and components of the metabolic cardiovascular syndrome in borderline hypertensive young men and suggested that sympathetic nervous system (SNS) activity may be a mediator. In the present study we aimed to test this hypothesis in established hypertension and to investigate the relationship between WBV and cardiac dimensions. Unmedicated patients (n = 42) with stage II-III hypertension and electrocardiographic left ventricular hypertrophy (LVH) underwent hyperinsulinemic isoglycemic glucose clamp to assess glucose disposal rate (GDR) and echocardiographic studies. WBV, plasma catecholamines and insulin were measured in arterialized venous blood. WBV at high shear rate correlated with baseline plasma adrenaline (r = 0.33, p = 0.04) and fasting insulin (r = 0.34, p = 0.04) while there was a negative trend for GDR (r = -0.21, p = 0.2). WBV at low shear rate correlated with plasma adrenaline (r = 0.49, p = 0.002) and resting heart rate (r = 0.36, p = 0.02). WBV was higher in smokers than in non-smokers (p = 0.02) and in males than in females (p = 0.02). Fasting insulin independently explained 12% of the variation in WBV at high shear, while baseline adrenaline independently explained 17% of the variation in WBV at low shear. Systolic blood pressure explained 31% of the variation in LV mass index. Thus, we demonstrate positive relationships between blood viscosity versus plasma adrenaline and fasting insulin in hypertensive patients with LVH. We suggest that adrenergic activity may increase hematocrit and viscosity and hence reduce insulin sensitivity. [ABSTRACT FROM AUTHOR]