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In chronic hypoxemia blood flow and oxygen supply to vital organs are maintained, but to nonvital organs they are decreased. We measured organ blood flows (microspheres) and whole blood viscosity in 10 chronically hypoxemic lambs, with an atrial septal defect and pulmonary stenosis, and in 8 control lambs. Vascular hindrance (resistance/viscosity) was calculated to determine to what extent the effect of increased blood viscosity on organ blood flow was compensated for by a decrease in vascular tone. Arterial oxygen saturation was decreased (68 +/- 10 vs. 91 +/- 3%, P < 0.001), and both hemoglobin concentration (145 +/- 10 vs. 109 +/- 9 g/l, P < 0.05) and blood viscosity (4.4 +/- 0.6 vs. 3.6 +/- 0.6 mPa.s, P < 0.05) were increased in hypoxemic lambs. Systemic blood flow, oxygen supply, oxygen uptake, and blood pressures were not significantly different between hypoxemic and control lambs. Myocardial and cerebral blood flow was maintained in hypoxemic lambs, whereas renal, gastrointestinal, splenic, and thyroidal blood flows were at least 30% lower. Vascular hindrance was significantly decreased in the myocardium and tended to be lower in the brain of hypoxemic lambs, but in all other organs it was similar to that in control lambs. It is concluded that blood flow is redistributed in chronic hypoxemia in lambs; myocardial and cerebral blood flow is maintained, whereas blood flow to splanchnic organs, the kidneys, and the thyroids is decreased. The decreased blood flow to organs is a consequence of the increased whole blood viscosity.
The effects of intravenous oxpentifylline on blood viscosity and cerebral blood flow were studied in eight patients with cerebrovascular disease using a double-blind placebo controlled design. A single dose of 200 mg oxpentifylline in 10 ml saline was given by intravenous injection over 10 min and compared with 10 ml saline alone. Whole blood and plasma viscosity were measured in a Contraves LS 30 coaxial viscometer at shear rates of 0.7 and 94.5 s-1. Cerebral blood flow was measured by the non-invasive intravenous xenon133 clearance method. The measurements were made before and then 30 min after the start of the injection of drug or saline alone. Oxpentifylline was found to have no significant effect on blood viscosity or cerebral blood flow.
Peripheral blood flow and systolic blood pressure (strain-gauge plethysmograph), blood volume (Evans blue) and whole blood viscosity (cone-plate viscometer) have been measured in 66 premature and full-term infants 6 to 144h of age. Blood flow and blood volume were moderately decreased in the infants with respiratory distress. Highly significant (P less than 0.001) correlations were found between blood flow and blood volume (r = 0.77), blood pressure and blood volume (r = 0.50), peripheral resistance and blood volume (r = -0.44), blood flow and blood pressure (r = 0.50), blood flow and peripheral resistance (r = -0.67), peripheral resistance and blood viscosity (r = 0.45), and blood viscosity and haematocrit (r = 0.86). There was no correlation between peripheral blood flow and blood viscosity. However, at given blood volume, peripheral blood flow decreased with increasing blood viscosity. These results indicate that in newborn infants peripheral blood flow, blood pressure and peripheral resistance are influenced by blood volume, but also depend on blood viscosity.
Effects of high osmotic media on the shape and deformability of RBC were examined for determining increasing factors of blood viscosity. Dog blood and Urographin (a hypertonic contrast medium) were used; the plasma osmolality was changed by Urografin suspended in blood. The viscosity was measured for normal RBC and glutaraldehyde-treated RBC suspensions with a cell volume concentration. The RBC deformability was evaluated from the difference in viscosity between the two suspensions. It was shown that normal RBC suspension increased the viscosity with increase in osmolality at high shear rate; hardened RBC suspension decreased the viscosity with increase in osmolality. It was concluded that the RBC deformability decreased with increasing osmolality.
Cerebral blood flow (CBF) was measured by the non-invasive xenon-133 technique in patients with increased blood viscosity as a result of paraproteinaemia or leukaemia. A highly significant inverse relation was found between CBF and arterial oxygen content in 59 paraproteinaemic patients. There was no significant correlation between CBF and whole blood viscosity, and no significant difference between CBF in paraproteinaemic patients and a matched group of anaemic patients. 7 leukaemic patients with up to threefold increases in whole blood viscosity were also found to have CBF appropriate to their degree of anaemia. The effects of treatment to reduce blood viscosity were studied in 7 paraproteinaemic and 5 leukaemic patients; changes in CBF were significantly related to changes in arterial oxygen content but not to changes in blood viscosity. These studies confirm the importance of arterial oxygen content in the determination of CBF, and demonstrate that regulatory mechanisms can maintain normal cerebral oxygen transport despite increased plasma and whole blood viscosity.
Therapies including hyperventilation (HV) and hypothermia (HT) are currently simultaneously used in brain-injured children at risk for cerebral swelling to reduce cerebral blood flow (CBF) and alter cerebral metabolic rate for oxygen (CMRO2). Since HV and HT may contribute to significant patient morbidity, we evaluated the effects of these treatments in combination on CBF, CMRO2, and cross-brain oxygen extraction (CBO2) using the Kety-Schmidt technique before controlled bleeding to alter blood viscosity in 20 lightly anesthetized, paralyzed cats, and after bleeding in another 17 cats. The degree of HV (PaCO2 24 to 26 torr) and HT (32 degrees and 30 degrees C) used were representative of that employed in pediatric neurointensive care. HV at normothermia resulted in a significant decline in CBF (P less than .05) and an unchanged CMRO2. HV and HT together to 32 degrees C resulted in a further significant fall in CBF and CMRO2 (p less than .05), but an unchanged CBO2. Further cooling of the animal to 30 degrees C during HV, both before and after controlled bleeding, resulted in no further significant fall in CBF, CBO2, or CMRO2. This relationship was found despite a significant fall in Hgb (p less than .001), suggesting that blood viscosity did not significantly influence CBF at this temperature. Our data suggest that HT to 32 degrees C during HV may have therapeutic benefit by decreasing CBF and CMRO2, but further cooling to 30 degrees C may not result in further cerebral protective effects.
The effects of plasma exchange using a low viscosity plasma substitute on blood viscosity and cerebral blood flow were investigated in eight subjects with normal cerebral vasculature. Plasma exchange resulted in significant reductions in plasma viscosity, whole blood viscosity, globulin and fibrinogen concentration without affecting packed cell volume. The reduction in whole blood viscosity was more pronounced at low shear rates suggesting an additional effect on red cell aggregation. Despite the fall in viscosity there was no significant change in cerebral blood flow. The results support the metabolic theory of autoregulation. Although changes in blood viscosity appear not to alter the level of cerebral blood flow under these circumstances, plasma exchange could still be of benefit in the management of acute cerebrovascular disease.
The influence of multiple systemic factors upon the blood velocities obtained from the orbital circulations was investigated. The velocities obtained by colour Doppler imaging from the ophthalmic artery, central retinal artery, and vein from 95 ophthalmologically healthy volunteers were analyzed. The effects of age, systemic blood pressure, and smoking habit were examined. In 24 volunteers blood viscosity was also measured and its relation with blood velocity assessed. Age was weakly negatively correlated with the blood velocities in the ophthalmic artery and weakly positively correlated with resistance to flow in the retinal circulation. Systolic blood pressure showed a positive correlation with the peak systolic velocities in the arteries while cigarette smoking was associated with lower ophthalmic artery velocities. Increased haematocrit and viscosity were positively correlated with resistance to flow proximal to the ophthalmic artery and red cell rigidity negatively correlated with the pulsatility of flow in the retinal vein. These results help to identify the roles of systemic conditions in the ocular circulation. The influence of blood viscosity on retinal venous flow may be relevant to the pathogenetic mechanisms of conditions such as central retinal vein occlusion.
Nine patients with extensive peripheral arterial disease were treated with subcutaneous injections of ancrod (Arvin) for 10 to 21 days. Reduction in plasma fibrinogen was associated with a sustained reduction in plasma and blood viscosity, and a sustained increase in nutritional skin blood flow, measured by a Xenon-133 clearance technique (P less than 0.001). These findings may be relevant to the therapeutic effect of ancrod in ischemic rest pain.
Our finding of a decrease in blood viscosity in newborn infants compared with adults leads to analysis of this change by measuring blood viscosity, plasma fibrinogen concentration, plasma viscosity and mean corpuscular volume (MCV) of 24 adults and 16 newborn infants. Plasma proteins in newborn infants are synthesized to a lesser extent than in adults, therefore plasma fibrinogen concentration of newborn infants is less than that of adults. This causes decreased blood viscosity in newborn infants compared with adults. Secondly plasma viscosity of newborn infants is also less than that of adults. In the same situation this causes a decrease in blood viscosity in newborn. Thirdly. MCV of newborn infants is greater than that of adults because of young red cells. There is a negative correlation between blood viscosity and MCV. High MCV in newborns leads to low blood viscosity in newborn infants, compared with adults.
Whole blood viscosity (WBV) was measured in a normal population and was analyzed in relation to packed cell volume, (hematocrit, PCV), fibrinogen, white blood cell count (WBC), platelet count, and plasma lipids, including total cholesterol, triglycerides, high density lipoprotein cholesterol (HDLc) and low density lipoprotein cholesterol (LDLc). Conventional assays were used for all blood and lipid measurements. Whole blood viscosity was measured under disaggregating conditions with a disposable, porous bed viscometer. As expected, the strongest correlation was seen between WBV and PCV (r = 0.78, p < 0.001). Significant positive correlations also were demonstrated between WBV and cholesterol (r = 0.22, p < 0.001), triglycerides (r = 0.14, p < 0.001) and LDLc (r = 0.21, p < 0.001). A significant negative correlation was found between HDLc and WBV (r = -0.20, p < 0.001). Correlation analysis by sex showed only the correlation of LDLc was significant for both men and women. A stepwise multiple regression analysis of WBV indicated that LDLc, fibrinogen (Fbg) and platelet (Plt) counts correlated independently of PCV to WBV. The equation derived from multiple regression and partial correlation analysis was: WBV (mPa.sec) = -9.317 + 0.0047 (LDLc) + 0.381 (PCV) + 0.00152 (Plt) + 0.0021 (Fbg). The calculated mean specific contribution of PCV was 90.8 percent, LDLc 3.5 percent, and fibrinogen 3.3 percent to observed mean WBV. This study shows that LDLc is the principal lipoprotein independently influencing whole blood viscosity and its effect is similar in magnitude to fibrinogen. Further studies to elucidate the mechanism and clinical significance of the effects of LDLc on WBV are indicated.
BACKGROUND: Blood viscosity is correlated with cerebral blood flow and cardiac output, and increased viscosity may increase the risk of thrombosis or thromboembolic events. The relationship between hematocrit and viscosity is well-known, however, the relationships between white blood cell (WBC) or platelet count and viscosity were not fully studied. The aim of the present study was to determine the influences of platelet count and WBC count on blood viscosity. METHODS: One-hundred and 13 subjects with different hemoglobin, WBC and platelet count were enrolled into the study. The variables measured included serum fibrinogen, cholesterol, triglyceride, high-density lipoprotein (HDL), low-density lipoprotein (LDL), complete blood counts including hemoglobin, hematocrit, platelet count, red blood cell (RBC) count, WBC count, whole blood and plasma viscosity. The relationships of these variables with whole blood or plasma viscosity were analyzed. RESULTS: Serum fibrinogen, cholesterol, triglyceride, HDL and LDL did not correlate with whole blood viscosity. Not only hematocrit, hemoglobin and RBC, but also WBC and platelet count, could affect whole blood viscosity. On the other hand, none of the variables could affect plasma viscosity. CONCLUSIONS: All the blood cell components, but not the plasma proteins detected above, could affect whole blood viscosity. When patients are with high leukocytosis and thrombocytosis, impaired blood viscosity should also be considered to obtain appropriate clinical management.
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