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PubMed1993

Dichotomous response of whole blood viscosity in streptozotocin-diabetic rats.

Abnormalities of blood rheology may play an important role in the underlying mechanism of the development of diabetic complications. Although streptozotocin (STZ)-induced diabetic rats have been used extensively in the investigation of diabetic complications, blood rheological alterations in this model have not previously been assessed. To assess one aspect of blood rheology, we repeated whole blood viscosity (WBV) measurements at 4, 8, 12 and 16 weeks after the STZ injection in rats. Nine of fifteen diabetic rats showed increased WBV after the induction of diabetes. Although these rats had a higher haematocrit, the increase in WBV was maintained after correction to a standard haematocrit. Percentage changes of WBV were significantly greater in these diabetic rats than in control rats at low shear rates (0.1s-1 and 1.0s-1), but not at high shear rates. In contrast, WBV was lowered at all shear rates after the injection of STZ in the remaining six diabetic rats which had lower haematocrit, severe weight loss and high mortality; no rats survived for 16 weeks post-injection. Animals in this group may be implicated in the high mortality among STZ-diabetic rats. Although there was a clear distinction of rheological and clinical pictures between these two groups of STZ-diabetic rats, blood glucose and HbA1 concentrations did not differ significantly. This study demonstrates a dichotomy in blood viscosity response to STZ-induced diabetes.

Animals↗
PubMed1980

Effect of blood viscosity decrease on exercise ST segment depressions in hyperlipidemia.

In order to study the possible relation between blood viscosity and exercise ST segment depressions in hyperlipidemia the former was lowered by infusion of dextran and by treatment with clofibrate 1 g twice daily. Acute decrease of blood viscosity with dextran infusion in two cases increased the ST segment depressions during work. Nine subjects with asymptomatic hyperlipidemia, hyperfibrinogenemia and exercise ST segment depressions were treated with clofibrate in order to lower plasma fibrinogen and serum lipids. This did not influence the area of ST segment depression with either Frank leads or CH leads as determined by computer estimation. As the plasma fibrinogen level is of major importance for the blood viscosity it is concluded that the ischaemic ST segment depression seen in hyperlipidemia is not due to increased blood viscosity but more likely to a premature subclinical coronary atherosclerosis.

Blood Viscosity↗
PubMed1982

Increased blood viscosity in a patient with sickle cell anemia.

Although intracellular viscosity is greatly increased in deoxygenated sickle cells, the viscosity of blood is not, because patients' packed cell volumes (PCV) are usually extremely low (15-25%). A young women with sickle cell anemia was admitted with a typical painful crisis, and was found to have a PCV of 39% with a reticulocyte count of 3.6%. During a hospitalization of 48 h, the PCV rose to 46%; her pain subsided but her behavior became bizarre, cardiopulmonary arrest occurred, and she could not be resuscitated. At autopsy, no abnormalities were found except for congested blood vessels containing sickle cells. It was subsequently discovered that she and her family had been exposed to carbon monoxide for a week prior to admission. Blood samples from another patient studied with a PCV of 40% showed progressively decreased viscosity if they contained 13-20% carboxyhemoglobin. It is suggested that preexisting accelerated erythropoesis was further stimulated by CO, and caused "compensatory polycythemia", but that the CO prevented most of the newly formed cells from sickling and being destroyed. Admission to hospital caused a gradual disappearance of CO but the patient's PXV continued to rise. Her death may have been due to a rare form of hyperviscosity syndrome, when the level of carboxyhemoglobin in her blood fell to more normal levels and her cells regained the ability to sickle. Treatment of sickle cell anemia with an effective non-covalently bound agent could have a similar effect, if the agent were withdrawn abruptly.

Acute Disease↗
PubMed1983

Mannitol causes compensatory cerebral vasoconstriction and vasodilation in response to blood viscosity changes.

There is no proof that osmotic agents such as mannitol lower intracranial pressure (ICP) by decreasing brain water content. An alternative mechanism might be a reduction in cerebral blood volume through vasoconstriction. Mannitol, by decreasing blood viscosity, would tend to enhance cerebral blood flow (CBF), but the cerebral vessels would constrict to keep CBF relatively constant, analogous to pressure autoregulation. The cranial window technique was used in this study to measure the pial arteriolar diameter in cats, together with blood viscosity and ICP changes after an intravenous bolus of 1 gm/kg of mannitol. Blood viscosity decreased immediately; the greatest decrease (23%) occurred at 10 minutes, and at 75 minutes there was a "rebound" increase of 10%. Vessel diameters decreased concomitantly, the largest decrease being 12% at 10 minutes, which is exactly the same as the 12% decrease in diameter associated with pronounced hyperventilation (PaCO2 30 to 19 mm Hg) in the same vessels; at 75 minutes vessel diameter increased by 12%. With hyperventilation, ICP was decreased by 26%; 10 minutes after mannitol was given, ICP decreased by 28%, and at 75 minutes it showed a rebound increase of 40%. The correlation between blood viscosity and vessel diameter and between vessel diameter and ICP was very high. An alternative explanation is offered for the effect of mannitol on ICP, the time course of ICP changes, "rebound effect," and the absence of influence on CBF, all with one mechanism.

Animals↗
PubMed1992

Blood viscosity and optimal hematocrit in preterm and full-term neonates in 50- to 500-micrometer tubes.

Blood viscosity is an important determinant of blood flow resistance. Because a substantial part of flow resistance arises in small arteries and arterioles with diameters of 100 microns and less, rheologic properties of blood from preterm infants (24 to 36 wk of gestation), full-term neonates, and adults were measured in glass tubes with diameters of 50, 100, and 500 microns for a wide range of adjusted feed hematocrits (0.15-0.70). At each of the feed hematocrits, blood viscosity decreased when going from a 500-microns tube to a 50-microns tube. The viscosity reduction increased with increasing hematocrit. Moreover, the viscosity reduction was more pronounced in the neonates than in the adults. At a hematocrit of 0.70, the viscosity reduction averaged 56% in preterm infants, 50% in full-term neonates, and 39% in adults (p less than 0.005). However, the viscosity reductions at a hematocrit of 0.30 were only 35, 29, and 19%, respectively (p less than 0.05). In all four groups, blood viscosity increased exponentially with increasing hematocrit. The steepness of the hematocrit-viscosity curves decreased with decreasing tube diameter and with decreasing maturity of the infants. Erythrocyte transport efficiency (hematocrit/blood viscosity) was calculated to estimate the optimal hematocrit (i.e. hematocrit with maximum erythrocyte transport). In 500-microns tubes, the optimal hematocrit was about 0.40 in all of the groups. In 100-microns tubes, the optimal hematocrit was 0.44 +/- 0.05 in the adults and 0.52 +/- 0.04 in the neonates (p less than 0.05). In 50-microns tubes, the optimal hematocrit was 0.51 +/- 0.04 in adults and 0.60 +/- 0.05 in the neonates.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Effect of a reduction in blood viscosity on maximal myocardial oxygen delivery distal to a moderate coronary stenosis.

This study tested the hypothesis that a reduction in blood viscosity by means of isovolumetric hemodilution will permit an increase in maximal oxygen delivery to myocardium distal to a moderate coronary arterial stenosis. It is known that blood viscosity is a determinant of resistance to blood flow at both the stenotic and the arteriolar levels. Accordingly, a reduction in blood viscosity could exert a favorable influence on maximal myocardial oxygen delivery in the setting of stenosis, provided that the oxygen-carrying capacity of the blood is not compromised excessively. Closed-chest, sedated domestic swine (n = 8) were instrumented with an artificial coronary arterial stenosis that reduced vessel diameter by 64%. Measurements of hemodynamics, regional myocardial blood flow (microspheres), lactate and oxygen metabolism, and whole blood viscosity were made at control and after two successive 10 min intracoronary infusions of adenosine (400 and 800 micrograms/min) distal to the stenosis. Next, albumin/saline solution was given intravenously to reduce the animal's hematocrit by approximately 50%. Repeat measurements of all experimental variables were then made at a second control and again after two successive 10 min intracoronary infusions of adenosine (400 and 800 micrograms/min) distal to the stenosis. Myocardial blood flow (ml/min/g) distal to the stenosis increased from 1.52 +/- 0.21 (mean +/- 1 SD) to 4.10 +/- 0.86 in response to adenosine (peak dose) before hemodilution (p less than .01) and from 2.07 +/- 0.59 to 4.08 +/- 0.93 (p less than .01) after hemodilution.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed2000

In vivo effects of Hb solutions on blood viscosity and rheologic behavior of RBCs: comparison with clinically used volume expanders.

BACKGROUND: Hb-based oxygen carriers (HbOCs) have vasoactive effects that are still poorly understood. Factors known to have vasoactive effects, such as plasma, whole-blood viscosity, and the rheologic behavior of RBCs, are modulated by HbOCs in vitro, but few in vivo studies have been performed. STUDY DESIGN AND METHODS: Rabbits were phlebotomized (30%) and resuscitated with unmodified stroma-free Hb (SFHb), dextran-tetracarboxylate-Hb (Dex-BTC-Hb), O-raffinose-polymerized Hb (OrpHb), HSA, or hydroxyethyl starch 200 (HES). Plasma viscosity was assessed with a capillary viscometer and whole-blood viscosity with a rotational viscosimeter. RBC aggregation kinetics were determined by analysis of back-scattered light in a rotating device. RESULTS: As compared to that in the control RBC suspension, resuscitation with SFHb, OrpHb, or HSA decreased plasma and whole-blood viscosity as well as RBC aggregation; resuscitation with Dex-BTC-Hb increased whole-blood viscosity at low shear rates as well as RBC aggregation, whereas that with HES decreased whole-blood viscosity but increased RBC aggregation. CONCLUSION: HbOCs have different rheologic effects in vitro and in vivo. There are marked differences among the Hb solutions in their in vivo effects on viscosity and RBC rheologic behavior (especially at low shear rates encountered in the venous circulation and the microcirculation), which may be related to the chemical modifications applied to hemoprotein. These results could contribute to an understanding of the vasoactive effects of HbOCs.

Adult↗
PubMed1990

Reduction in blood viscosity by treatment with coenzyme Q10 in patients with ischemic heart disease.

The effects of coenzyme Q10 (CoQ10) on blood viscosity were studied in twelve patients (mean age 49 +/- 16 years) with ischemic heart disease. Twenty mg of CoQ10 was orally administered three times daily for two months (total dose 60 mg per day). Blood viscosity was measured with a cone-plate type viscometer at the shear rates of 37.5, 75, 150, and 375 s-1. Yield shear stress was calculated from Casson's plot. Blood viscosity decreased at each shear rate after the administration of CoQ10. Yield shear stress decreased significantly by the treatment with CoQ10. Hematocrit and fibrinogen were also measured, but showed no significant change. These results suggest that CoQ10 decreases the blood viscosity, i.e., improves the rheological properties of blood in ischemic heart disease.

Administration, Oral↗
PubMed2006

Blood viscosity maintains microvascular conditions during normovolemic anemia independent of blood oxygen-carrying capacity.

Responses to exchange transfusion with red blood cells (RBCs) containing methemoglobin (MetRBC) were studied in an acute isovolemic hemodiluted hamster window chamber model to determine whether oxygen content participates in the regulation of systemic and microvascular conditions during extreme hemodilution. Two isovolemic hemodilution steps were performed with 6% dextran 70 kDa (Dex70) until systemic hematocrit (Hct) was reduced to 18% (Level 2). A third-step hemodilution reduced the functional Hct to 75% of baseline by using either a plasma expander (Dex70) or blood adjusted to 18% Hct with all MetRBCs. In vivo functional capillary density (FCD), microvascular perfusion, and oxygen distribution in microvascular networks were measured by noninvasive methods. Methylene blue was administered intravenously to reduce methemoglobin (rRBC), which increased oxygen content with no change in Hct or viscosity from MetRBC. Final blood viscosities after the entire protocol were 2.1 cP for Dex70 and 2.8 cP for MetRBC (baseline, 4.2 cP). MetRBC had a greater mean arterial pressure (MAP) than did Dex70. FCD was substantially higher for MetRBC [82 (SD 6) of baseline] versus Dex70 [38 (SD 10) of baseline], and reduction of methemoglobin to oxyhemoglobin did not change FCD [84% (SD 5) of baseline]. P(O2) levels measured with palladium-meso-tetra(4-carboxyphenyl)porphyrin phosphorescence were significantly changed for Dex70 and MetRBC compared with Level 2 (Hct 18%). Reduction of methemoglobin to oxyhemoglobin partially restored P(O2) to Level 2. Wall shear rate and wall shear stress decreased in arterioles and venules for Dex70 and did not change for MetRBC or rRBC. Increased MAP and shear stress-mediated factors could be the possible mechanisms that improved perfusion flow and FCD after exchange for MetRBC. Thus the fall in systemic and microvascular conditions during extreme hemodilution with low-viscosity plasma expanders seems to be, in part, from the decrease in blood viscosity independent of the reduction in oxygen content.

Anemia↗
PubMed2004

Catheter-based impedance measurements in the right atrium for continuously monitoring hematocrit and estimating blood viscosity changes; an in vivo feasibility study in swine.

Hematocrit is the most important determinant of whole blood viscosity and it affects thrombosis. As hematocrit can be measured accurately in vitro by using an electrical impedance technique, aim of the present study is to investigate the diagnostic potential of using this technique in vivo to continuously monitor hematocrit. Characteristics of a special catheter for in vivo measurement of electrical resistivity in blood in the right atrium are described. In five anesthetized swine hematocrit is monitored continuously with this catheter while different levels of hemoconcentration are induced. In addition, blood viscosity is increased by inducing 'acute phase' reaction the day before surgery, resulting in variable degree of elevated fibrinogen levels in the five swine. Good reproducibility of the resistivity measurements (S.D < 0.01) and excellent correlation between resistivity data in vivo and hematocrit levels in each swine are found (r2 = 0.95-0.99). Furthermore, stepwise regression analysis of data from all swine shows a highly significant contribution also of other important parameters of blood viscosity, such as fibrinogen, total protein and temperature (cumulative r2 = 0.97). Determining hematocrit continuously in vivo by electrical resistivity measurements with a catheter in the right atrium is feasible and these measurements correlate significantly also with other important parameters of blood viscosity.

Animals↗
PubMed1986

Umbilical cord whole blood viscosity and the umbilical artery flow velocity time waveforms: a correlation.

The possibility was examined of an association between umbilical cord whole blood viscosity and umbilical artery flow velocity time waveforms obtained with continuous wave Doppler ultrasound. The cord blood viscosity was measured at both high (100 s-1) and low (0.1 s-1) shear rates with a concentric cylinder viscometer. Plasma viscosity and fibrinogen were also measured. An abnormal pattern in the umbilical artery flow velocity waveform (high A/B ratio) indicative of high resistance was associated with an increase in whole blood viscosity at high shear (which may reflect a change in red cell rigidity). Viscosity at low shear (reflecting red cell aggregation and rouleaux formation) did not differ. There was a significant association between the small-for-gestational age fetus and abnormal umbilical artery waveform study (P less than 0.002) but not abnormal whole blood viscosity at high (P = 0.09) or low (P = 0.08) shear.

Blood Flow Velocity↗
PubMed1979

Reduction of blood viscosity following plasma exchange.

The effect of plasma exchange with plasma protein fraction on blood viscosity was determined in seven hyperlipoproteinaemic patients with coronary or peripheral vascular disease. This resulted in decreases in whole blood viscosity of 83% and 30% respectively at the lowest and highest shear rates studied, and decreases of 21% and 59% in plasma viscosity and fibrinogen. Serum cholesterol and triglyceride were reduced by 66% and 48% respectively. Sequential studies in two patients showed that blood viscosity returned to near-basal values by the 6th day. These findings suggest that plasma exchange may result in short-term enhancement of blood flow in vessels where low shear rates predominate.

Adolescent↗
PubMed1981

Filterability and other methods of approaching red cell deformability. Determinants of blood viscosity and red cell deformability.

The major determinants of blood viscosity are RBC concentration, plasma viscosity, RBC aggregation and RBC deformation. RBC deformation is determined by the intrinsic deformability of the cell and the shear stress acting on the cell surface. In using filterability tests to assess RBC deformability, it is necessary to eliminate variations in other determinants of blood viscosity and to specify the rheological conditions of the test. Further theoretical and experimental work is needed for the interpretation of filterability tests in terms of cell geometry, internal viscosity and membrane properties.

Blood↗
PubMed2001

Blood viscosity, hemodynamics and vascular hindrance in a rat model of acute controlled bleeding and volume restitution with blood or Haemaccel.

BACKGROUND: Hemorrhage and volume restitution with commercially available solutions is followed by reduced blood viscosity. Consequent hemodynamic changes may arise not only from the reduced viscosity itself but also from changes in vascular geometry induced by autoregulation processes. Vascular hindrance reflects the contribution of vascular geometry to flow. Our aim was to explore the possible effects of blood volume restitution with Haemaccel or blood, on regional blood flow and vascular geometry. METHODS: Under ketamine anesthesia, blood was withdrawn at a rate of 0.3 ml/min for 15 min followed by 15 min of stabilization. The shed blood or Haemaccel was infused at the same rate and volume as used for withdrawal. Hemodynamic measurements were performed using radioactive microspheres. Blood viscosity was measured with an Ostwald viscometer. Vascular hindrance was calculated as the resistance/viscosity ratio. RESULTS: Volume replacement with Haemaccel (n=10), compared to blood (n=10), was followed by increased cardiac output and portal venous inflow (37.1 +/- 9.0 and 3.1 +/- 0.5 vs 25.9 +/- 6.8 and 2.2 +/- 0.9 ml x min(-1) x 100 g bw(-1), respectively; P<0.05), decreased viscosity (2.8 +/- 1.3 vs 3.7 +/- 1.3, respectively; P<0.01) and decreased peripheral and splanchnic arteriolar resistance (3.8 +/- 1.1 and 40.9 +/- 7.6 vs 5.2 +/- 1.7 and 61.1 +/- 29.5 mmHg x ml(-1) x min x 100 g bw, respectively; P<0.05). No significant differences between the groups were observed in vascular hindrance and cardiac output distribution. CONCLUSION: Volume replacement with Haemaccel, compared to blood, induced increase in systemic and splanchnic blood flows, reflecting mainly changes in viscosity and not in blood vessel geometry. These results suggest no significant difference in overall activation of autoregulation process between volume restitution with blood or Haemaccel.

Animals↗
PubMed1976

The effects of increased blood viscosity on pulmonary vascular resistance.

The isolated left lower lobes of 15 dogs' lungs were perfused by means of a roller pump with blood at hematocrit values ranging from 31 to 80 per cent. Pressure-flow curves were constructed at blood flow rates from one half to three times the normal flow for the left lower lobe at each hematocrit level. The perfusion pressure was normalized with reference to the normal hematocrit(38 to 48 per cent) and normal blood flow for the left lower lobe (20 ml. per kilogram per minute). From these normalized pressure-flow curves, normalized resistance-flow curves were constructed at different mean hematocrit levels. Regression lines were drawn relating normalized pulmonary vascular resistance to hematocrit at different rates of pulmonary blood flow which might be found in patients with congenital heart disease. It was found that pulmonary vascular resistance rose in an exponential fashion as the hematocrit was increased, and that the blood viscosity determined both the shape of the resistance-flow curve and magnitude of the increase in resistance to pulmonary blood flow, especially when the pulmonary blood flow was less than normal and the hematocrit was greater than 54 per cent. The family of regression lines relating pulmonary vascular resistance to hematocrit at different flow rates may be used clinically in patients with congenital heart disease and polycythemia to determine if an elevated pulmonary vascular resistance is due to increased blood viscosity or obstructive pulmonary vascular disease. It is concluded that an increased blood viscosity due to polycythemia significantly alters the pulmonary hemodynamics of patients with congenital heart disease with either increased or decreased pulmonary blood flow. Increased blood viscosity may play an important part in the early initiation and development of pulmonary arteriosclerosis in patients with transposition of the great arteries.

Animals↗
PubMed2003

Influence of propofol on erythrocyte morphology, blood viscosity and platelet function.

The intravenous anaesthetic propofol has been associated with cardiovascular side effects. We therefore studied its influence on blood viscosity, erythrocytes and platelet aggregation. Blood from healthy volunteers was incubated with propofol concentrations of 0, 5, 10, 20, 40, 80, 200, and 500 microg/ml plasma. Whole blood viscosity (shear rates 94.5 and 0.1 s(-1)), plasma viscosity, erythrocyte morphology and platelet aggregation (PFA-100 system) were determined. These parameters were also measured in vivo in 9 patients prior to anaesthesia, after induction, before the end and 1 h after the end of propofol anaesthesia. Propofol induced a slight, dose-dependent echinocytic shape transformation of erythrocytes in vitro, indicating a preferential intercalation of the drug in the outer hemileaflet of the membrane. Neither whole blood nor plasma viscosity were affected in vitro. In vivo, no change in erythrocytes shape was seen, but plasma and whole blood viscosity at high shear rate (94.5 s(-1)) were decreased at the end of anaesthesia, which may be due to some extent to plasma dilution. Platelet aggregation with epinephrine was decreased both in vitro and in vivo. We conclude that propofol interacts with the erythrocyte membrane without affecting blood and plasma viscosity and decreases platelet aggregation, which may have clinical implications.

Adult↗
PubMed1984

Whole blood viscosity as a determinant of cardiac hypertrophy in systemic hypertension.

The relationships among blood pressure (BP), blood viscosity and echocardiographic left ventricular (LV) muscle mass were evaluated in 24 patients with essential hypertension and in 13 normotensive control subjects. LV mass was greater in the hypertensive patients than in the control subjects (225 +/- 69 vs 170 +/- 31 g, p less than 0.02) as was blood viscosity at a shear rate of 104 sec-1 (4.7 +/- 0.1 vs 4.3 +/- 0.2 cp, p less than 0.005). Among the hypertensive patients, LV mass was most closely related to viscosity at 104 sec-1 (r = 0.80, p less than 0.001), whereas only weak correlations were found between LV mass and systolic or diastolic BP (r = 0.45, p less than 0.05 for both). The 14 hypertensive patients with normal LV mass had viscosity similar to that in control subjects (4.5 +/- 0.3 vs 4.3 +/- 0.2 cp), whereas viscosity was consistently increased (5.0 +/- 0.4 cp, p less than 0.02) in hypertensive patients with LV hypertrophy. Thus, increased blood viscosity may be a determinant of or a response to hypertensive cardiac hypertrophy.

Adult↗
PubMed1991

The effects of a hyperosmolar intravenous contrast medium on blood viscosity.

The effects of the hyperosmolar contrast medium, diatrizoate meglumine (Renografin-76) on blood viscosity and other metabolic parameters were measured in 20 immature piglets. Intravenous contrast medium caused a significant (P less than .5) increase in serum osmolality, cardiac output, and urine output, and a decrease in hematocrit. There was a fall in blood viscosity that was not statistically significant. These changes, which are attributed to an acute shift of fluid into the hyperosmolar vascular compartment, were greatest at 3 minutes following injection and subsequently returned towards baseline levels. We conclude that blood viscosity is not increased following intravenous injection of hyperosmolar radiocontrast media.

Animals↗