Reduction In Blood Viscosity Research Articles

Effects of Defibrination on Hemorheology, Cerebral Blood Flow Velocity, and CO 2 Reactivity During Hypocapnia in Normal Subjects

Plasma fibrinogen is reported to be an independent risk factor for stroke and cardiovascular diseases. The effects of defibrination on hemorheology, middle cerebral artery (MCA) blood flow velocity, and CO2 reactivity during hypocapnia were evaluated in normal subjects. Twenty-five healthy subjects (mean age, 31.8 +/- 5.7 years) were included in the study. Measurements were done at rest and repeated 24 hours after administration of 10 batroxobin units. Plasma fibrinogen, plasma viscosity, and whole blood viscosity were measured as hemorheological factors. MCA blood flow velocity was measured with a transcranial Doppler flowmeter. Blood flow velocity was corrected to 40 mm Hg of end-tidal CO2 partial pressure (PETCO2), and expressed as CV40. CO2 reactivity was measured as percent change in mean blood flow velocity per millimeter of mercury PETCO2. Plasma fibrinogen (from 7.04 to 2.29 mumol/L; P < .001), whole blood viscosity, and plasma viscosity decreased after administration of batroxobin. Mean MCA blood flow velocity at rest, CV40. and CO2 reactivity during hypocapnia increased significantly (from 67.4 to 73.6 cm/s, from 71.7 to 77.7 cm/s, and from 2.9%/mm Hg to 3.2%/mm Hg, respectively; P < .01) after defibrination. Mean arterial blood pressure and PETCO2 at rest were constant before and 24 hours after administration of batroxobin. There was a significant positive correlation between CV40 and CO2 reactivity (r = .623, P < .0001). The increase in MCA blood flow velocity was associated with improved CO2 reactivity and reduced blood viscosity after defibrination. The data may suggest that defibrination increases cerebral blood flow by reducing blood viscosity.

Effect of Oncotic Pressure of Diaspirin Cross-Linked Hemoglobin (DCLHb Trademark) on Brain Injury After Temporary Focal Cerebral Ischemia in Rats

Effect of Oncotic Pressure of Diaspirin Cross-Linked Hemoglobin (DCLHb Trademark) on Brain Injury After Temporary Focal Cerebral Ischemia in Rats

Fish oil and other nutritional adjuvants for treatment of congestive heart failure

Published clinical research, as well as various theoretical considerations, suggest that supplemental intakes of the ‘metavitamins’ taurine, coenzyme Q 10, and L-carnitine, as well as of the minerals magnesium, potassium, and chromium, may be of therapeutic benefit in congestive heart failure. High intakes of fish oil may likewise be beneficial in this syndrome. Fish oil may decrease cardiac afterload by an antivasopressor action and by reducing blood viscosity, may reduce arrhythmic risk despite supporting the heart's beta-adrenergic responsiveness, may decrease fibrotic cardiac remodeling by impeding the action of angiotensin II and, in patients with coronary disease, may reduce the risk of atherothrombotic ischemic complications. Since the measures recommended here are nutritional and carry little if any toxic risk, there is no reason why their joint application should not be studied as a comprehensive nutritional therapy for congestive heart failure.

Changes in rheological properties of the blood after irradiation with helium-neon laser

The effect of helium-neon (HNL) laser on the rheological properties of the blood is examinedin vitro and during the treatment of 22 patients with obliterating atherosclerosis of the leg. It is shown that irradiation with HNLin vivo induces negative changes in blood rheology which are proportional to the time of exposure. Intravascular and extracorporeal irradiation reduces blood viscosity in the body as a result of dilution of the blood, as is evidenced by the lowered hematocrit, plasma viscosity, and hemoglobin concentration. Presumably, the decrease in blood viscosity accounts for the positive clinical results of laser therapy of patients with chronic arterial insufficiency.

Exercise Training and Bleed Viscosity in Patients With Ischemic Heart Disease

Several studies have suggested that regular exercise in healthy persons improves blood viscosity. 1–5 Regular exercise and exercise training have been shown to have several beneficial effects, including the prevention and modification of hypertension, hypercholesterolemia, diabetes mellitus, and obesity, and to have a role in both the primary and secondary prevention of coronary vascular events. 6 Whether exercise training, as prescribed in standard cardiac rehabilitation programs, can improve blood rheology has not been previously investigated. This study assesses whether a standard 10-week program of moderate-intensity aerobic exercise training had beneficial effects on whole blood viscosity and the factors that influence it among consecutive patients with ischemic heart disease who enrolled in cardiac rehabilitation.

Evaluation of the tolerance to hemorrhagic shock — Comparison between hemodilution and non-hemodilution: Jpn. J. Anesthesiol. 1994; 43/11: 1680–1685

We induced various degrees of bleedings in adult mongrel dogs to determine their tolerance to bleedings. The dogs were divided into two groups: the hemodilution group (Group A: Hct 11.1 +/- 1.9%) and the non-hemodilution group (Group B: Hct 36.8 +/- 6.6%). The Group A tended to show higher tolerance to bleedings than the Group B, although the difference was not significant. Throughout the period of increasing degrees of bleedings, MAP remained higher in Group B than in Group A, but CI was higher in Group A than Group B. DO2I was kept higher in Group B than in Group A. Both PaO2 and PaCO2 showed no difference between the two groups. The results of our study indicate that hemodilution group tends to be more tolerant to bleeding than non-hemodilution group. The reason is probably that under hemodilution the oxygen delivery is maintained through an increase in cardiac output in the presence of decreased arterial oxygen content. In addition, it is considered that the safety is obtained through various factors such as preferential blood distribution to important organs (in particular to the myocardium), more efficient extraction of oxygen from the blood, and the decreased work load resulting from a reduced blood viscosity.

The Effects of KBT-3022, a New Anti-platelet Agent, on Hemorheological Properties in Guinea Pigs

Using guinea pigs, a study was conducted on the effects of KBT-3022, a new anti-platelet agent, on hemorheological properties in various tests including blood filterability, blood viscosity, shear stress-induced red blood cell (RBC) deformability and contents of ATP and 2,3-diphosphoglycerate (2,3-DPG). Oral administration of KBT-3022 at 1 and 10 mg/kg significantly increased blood filterability, and significantly reduced blood viscosity at 10 mg/kg without changing the hematocrit, plasma fibrinogen concentration or plasma viscosity. KBT-3022 (10 mg/kg, p.o.) improved RBC deformability in response to shear stress, which was evoked by passing the blood through a thin tube. This dose of KBT-3022 also increased the contents of ATP and 2,3-DPG in RBC. These findings indicate that KBT-3022 may reduce blood viscosity as a sequel to improvement of RBC deformability through direct action on RBC. The increase in the intracellular levels of ATP and 2,3-DPG was considered to be involved in this improvement of hemorheological properties. These hemorheological effects of KBT-3022 appear to be promising for the treatment of patients with ischemic vascular disease.

An experimental study on the disturbance of liver circulation and the change of hemorrheology in dogs with acute liver damage.

The changes of hepatic hemodynamics and hemorrheology were investigated in dogs with acute liver damage induced by acetaminophen. There were remarkable disturbance in liver circulation and hemorrheological abnormality occurring in both slight and severe liver damage. The study indicated that the degree of disturbance in liver circulation as well as in hemorheological change is positively correlated with the severity of liver damage. For example, marked increase in blood viscosity linked with elevated fibrinogen level appeared in slight liver damage, whereas reduced blood viscosity associated with decreased plasma fibrinogen level and hematocrit occurred in severe liver damage. This study also revealed that the increase of portal venous resistance (PVR) and the disturbance of liver circulation in slight liver damage were chiefly related to the increase of blood viscosity and the increase of PVR in severe liver damage was mainly associated with the reduction of the radius of portal vein.

Local cerebral blood flow and glucose utilization after blood exchange with a hemoglobin-based O2 carrier in conscious rats.

The effects of a blood exchange on cerebral blood flow and glucose utilization were studied. A near to total blood exchange (hematocrit < 3%) was achieved in conscious rats by isovolemic hemodilution. Ultrapurified, polymerized, bovine hemoglobin (UPBHB) served as a blood substitute. Local cerebral blood flow (LCBF) and local cerebral glucose utilization (LCGU) were measured in 34 brain structures of conscious rats by means of the ido[14C]antipyrine and the 2-[14C]-deoxy-D-glucose methods. A group of rats without blood exchange served as control. After blood exchange LCBF increased from 36 to 126% in the different brain structures resulting in a nearly doubled mean cerebral blood flow (+82%). LCGU increased only moderately by 0-24%. Significant increases in LCGU were observed in 16 brain structures. Mean cerebral glucose utilization slightly increased (+14%). The relationship between LCGU and LCBF was found to be tight both in the control group (r = 0.95) as well as after blood replacement (r = 0.94), although it was reset to a higher overall LCBF-to-LCGU ratio. The profound increases in LCBF observed after blood exchange, which were not paralleled by comparable increases in LCGU, might be explained by a reduction of blood viscosity after blood exchange. Additional effects of blood exchange observed in the present study were an increase of mean arterial blood pressure and a decline of heart rate. The results indicate that replacement of blood with the hemoglobin-based oxygen carrier UPBHB appears to meet the cerebral circulatory and metabolic demands of the brain tissue.

Effects of genetic hypertension and nutritional anaemia on ventricular remodelling and myocardial damage in rats

In order to determine whether alterations in cardiac function and structure occur early in life in spontaneously hypertensive rats (SHR) and whether the addition of a volume load would affect myocardial growth and haemodynamic performance, SHR were exposed to an iron and copper deficient diet for 12 weeks (SHR-A) and compared with untreated SHR and Wistar Kyoto controls (WKY). Systolic arterial blood pressure increased in SHR, whereas nutritional anaemia prevented the rise of blood pressure in SHR-A. The diet employed provoked a severe hypochromic microcytic anaemia with a marked reduction in blood viscosity and increased volume load on the heart in SHR-A. Genetically determined hypertension alone induced a 16% increase in left ventricular weight and an increase in left ventricular peak systolic pressure (LVPSP) and +dP/dt. The superimposition of anaemia resulted in a 43% expansion in left ventricular weight with a decrease in LVPSP and +dP/dt, and an increase in left ventricular end diastolic pressure. Wall thickening and a preservation of chamber volume occurred in SHR, while SHR-A had a degree of ventricular dilatation which exceeded the extent of wall thickening. However, genetic hypertension was accompanied by myocardial tissue injury which was fully prevented by the addition of nutritional anaemia. Moreover, the capillary volume was decreased in SHR and increased in SHR-A. Genetically determined hypertension in combination with anaemia results in eccentric ventricular hypertrophy and cardiac dysfunction in spite of an increase in capillary luminal volume and limited structural damage.

Hemodilution with Oxyhemoglobin Mechanism of Oxygen Delivery and Its Superaugmentation with a Nitric Oxide Donor (Sodium Nitroprusside)

Hemodilution (HD) with oxyhemoglobin colloid (oxyHb) provides a greater arterial oxygen content (CaO2) than HD with conventional colloids; however, oxygen delivery (DO2) is essentially the same, because, in contrast to conventional HD, cardiac output (CO) is not augmented. This study seeks to elucidate the mechanism that limits CO during oxyHb-HD and to test whether infusion of a nitric oxide (NO) donor would augment DO2, because oxyHb is known to inactivate in vitro endothelial-derived NO. Anesthetized dogs were isovolemically hemodiluted with 10% oxyHb, 8% albumin, or 10% methemoglobin (weak NO inactivator) to 20% hematocrit. After HD, sodium nitroprusside (SNP) was titrated intravenously until decreases (> 10 mmHg) in mean aortic pressure (Pao) indicated the presence of exogenous NO. Systemic hemodynamics and regional blood flows (microsphere method) were measured. Albumin-HD and metHb-HD produced typical HD-mediated responses: increased CO (63-65%), slight decreases (13-15%) in DO2, decreases in systemic vascular resistance (SVR) proportional to the decreases (49-52%) in blood viscosity of all three groups, and increased regional blood flows (RBF). Responses to oxyHb-HD were atypical: CO and its determinants were not changed, DO2 decreased (23%) proportional to CaO2, and SVR and most RBF were not changed except for a net redistribution of CO to myocardium and skeletal muscle. In albumin-HD or metHb-HD, SNP (2-5 micrograms.kg-1.min-1) induced comparable decreases in mean Pao (29-37%) and SVR (39-41%); however, CO, RBF, and DO2 were not affected. In oxyHb-HD, exceptionally large doses of SNP (54 +/- 5 micrograms.kg-1.min-1) decreased mean Pao only 19 +/- 1%; however, CO increased 78 +/- 5% and decreases (61 +/- 3%) in SVR were slightly greater than viscosity reductions. Other determinants of CO were not affected. Most RBF increased proportional to CO; there was, however, preferential distribution to myocardium and skeletal muscle. Consequently, the augmented CO, and CaO2 of oxyHb-HD, produced large increases in DO2, 77 +/- 5% from HD alone and 43 +/- 3% from prehemodilution values. This study indicates that the limited CO and DO2 of oxyHb-HD resulted from opposing changes in two determinants of flow, i.e., reduced blood viscosity and increased arterial resistance (vasoconstriction). The vasoconstriction was not evident with metHb-HD and was reversed by the SNP infusion, indicating that oxyHb inactivated in vivo endothelial-derived NO. The ability of the NO donor (SNP) to facilitate large viscosity-mediated increases in DO2 during oxyHb-HD is an important finding that could potentially render oxyHb colloids more useful than conventional colloids, particularly for the individual with a compromised circulation who would benefit from an increased oxygen supply.

Influence of hematocrit on tissue O2 extraction capabilities during acute hemorrhage.

This study was performed to test the hypothesis that tissue O2 extraction capabilities during hemorrhage may be greater when hematocrit (Hct) is initially reduced. Twenty-four anesthetized and splenectomized dogs were randomly assigned in three groups of eight dogs each: group 1 (Hct 40), 40-45% Hct; group 2 (Hct 30), 30-35% Hct; and group 3 (Hct 20), 20-25% Hct. In each animal, the desired Hct was obtained by normovolemic hemodilution using hydroxyethyl starch 450/0.7 and maintained throughout the experiment. O2 delivery (DO2) was progressively reduced by hemorrhage. At each step, DO2 and O2 consumption (VO2) were measured separately. Critical DO2 obtained from a plot of VO2 vs. DO2 was lower in the Hct 30 and Hct 20 groups than in the Hct 40 group [(in ml.min-1.kg-1) Hct 30, 7.9 +/- 2.2; Hct 20, 7.8 +/- 1.0; Hct 40, 10.4 +/- 1.1; P < 0.05]. Critical DO2 obtained from blood lactate levels was also significantly lower in the Hct 30 and Hct20 groups than in the Hct 40 group. Critical O2 extraction ratio was also greater in the Hct 30 and Hct 20 groups than in the Hct 40 group (Hct 30, 73.0 +/- 13.9%; Hct 20, 70.1 +/- 9.6%; Hct 40, 57.1 +/- 11.5%; P < 0.05). In the conditions of our study, moderate hemodilution was associated with an improvement of the O2 extraction capabilities of the body, probably related to the reduction in blood viscosity.

Clinical Assessment of Low Molecular Weight Heparin Effects in Peripheral Vascular Disease

This study was carried out, using the double-blind method vs placebo, on 36 patients suffering from stage II peripheral vascular disease (PVD) according to Leriche, to check the clinical and hemorrheologic effects of the administration of a new low molecular weight heparin (LMWH). After a one-month washout period, the patients were randomly assigned either to the group treated with the LMWH (15,000 aXaU/day sc) or to the group treated with indistinguishable placebo. At the start of the study and after three and six months of treatment, clinical, instrumental, and laboratory tests were performed to assess local and systemic efficacy and tolerance. The LMWH under study caused a statistically significant increase in claudication time, with a parallel increase in the absolute claudication distance and in the interval free of pain. The drug also led to a significant increase in activated partial thromboplastin time, the values of which, however, remained within the normal limits, and to a marked reduction in blood viscosity. No significant variation was observed in the tolerability parameters in the two treatment groups, and no local or systemic adverse reactions occurred.

Blood viscosity during thrombolytic therapy with anistreplase in acute myocardial infarction

It has been postulated that a reduction in blood viscosity due to degradation of plasma fibrinogen may be of benefit to patients with acute myocardial infarction (AMI), who are treated with thrombolytic agents. The aims of this study were to investigate the time course of rheologic parameters, to identify the principal factors determining blood viscosity, and to find possible correlations between viscosity and cardiac function during thrombolytic therapy with anistreplase. Therefore, the viscosity of whole blood and plasma and the hematocrit were measured before and at 10 time points after thrombolysis in 10 patients with AMI. In addition, plasma fibrinogen and fibrin(ogen) degradation products were determined. Immediately after the start of thrombolysis, the viscosity of blood (both at high and low shear rate) and plasma decreased significantly and continued to do so for 24 hours. The mean hematocrit also decreased markedly, and even after correction for these hematocrit changes, the reduction in blood viscosity remained significant: it decreased to 72% of pretreatment (measured at low shear rate), whereas the high-shear viscosity decreased to 95% of baseline. The viscosity of plasma significantly decreased from 1.39 ± 0.13 mPa · s (mean ± SD) before thrombolysis to 1.22 ± 0.08 mPa · s after 2 hours. There was a rapid, nearly complete depletion in fibrinogen, followed by a striking rebound after the second day. The decrease in blood viscosity tasted for 2 days after anistrepiase and was mainly accounted for by the reduction in hematocrit. The contribution of fibrinogen to blood viscosity appeared less prominent. Despite these rheologic changes, no improvement in cardiac output was noticed in the patients.

Stoffwechselwirkungen von ω‐3‐Fettsäuren

AbstractDie biologischen Effekte von ω‐3‐Fettsäuren beruhen auf ihren Eigenschaften als strukturelle Bestandteile von Zellmembranen, auf ihrer Rolle als Vorläufer von Eicosanoiden und auf ihrem Einfluß auf den Lipidstoffwechsel. Hieraus ergeben sich vielseitige Stoffwechselwirkungen, die in zahlreichen medizinischen Gebieten Interesse geweckt haben. Besonders im kardiovaskulären Bereich hat sich gezeigt, daß ω‐3‐Fettsäuren ein breites Feld von potentiell antiatherogenen Wirkungen ausüben können. Hierzu gehören die Hemmung von Thrombozytenaggregation, Verminderung von Blutviskosität, Blutdrucksenkung und die Unterdrückung entzündlicher Prozesse im arteriosklerotischen Plaque. Im Lipidstoffwechsel steht die Senkung der Serumtriglyceride und eine geringe Erhöhung von HDL2 im Vordergrund. Die Wirkung auf das LDL‐Cholesterin ist komplex, und bei bestimmten Fettstoffwechselstörungen muß mit einer unerwünschten LDL‐Erhöhung gerechnet werden.

Comparative studies of drotaverine-acephyllinate (Depogen) and pentoxifylline (Trental)

Pentoxifylline is an orally active agent for the treatment of peripherial and cerebral vascular diseases. Pentoxifylline increases the deformability of red blood cells in vitro, reduces blood viscosity and decreases platelet aggregation and thrombus formation. Depogen has shown antiaggregatory effect both in vitro and in ex vivo. The inhibitory effect of Pentoxifylline was about 3–5 times weaker than that of Depogen. IC 50=900/ug/ml for Depogen and 3600/ug/ml for Pentoxifylline on human platelet rich plasma. Depogen has shown ex vivo antiaggregatory effect on anaesthetised rabbits, ID 50=7 mg/kg in case of iv. administration, and ID 50=300 mg/kg in case of orally administration. Both compound inhibit the release of platelet precoagulation factor, but the effect of Pentoxifylline was slighter.

Haemorheological changes in the very short term after abstention from tobacco by cigarette smokers

A study was made of the haemorheological changes that took place in the days immediately following tobacco withdrawal from cigarette smokers. In both males and females substantial and persistent reductions in blood viscosity occurred within 2 d, the fall at high shear rate corresponding to about 8% while at low shear rate it was approximately twice as much. These changes were due partly to a fall in packed cell volume (PCV), but also to reductions in total plasma protein and fibrinogen concentrations which led to reductions in plasma viscosity and rouleaux formation. These plasma protein-related changes were less pronounced in the female group. The results indicate that, even in the very short-term, abstention from cigarettes leads to substantial improvements in the haemorheological profile of heavy smokers.

N-3 fatty acids reduce blood viscosity in hyperlipoproteinemia: Results of a double blind study

n-3 fatty acids reduce blood viscosity in hyperlipoproteinemia: Results of a double blind study

Comparison of crystalloids and colloids for hemodilution in a model of focal cerebral ischemia

Forty dogs were subjected to 6 hours of occlusion of the left internal carotid and middle cerebral arteries. They were divided into two "hemodilution groups" of 13 dogs each and a control "nonhemodiluted group" of 14 dogs. Thirty minutes after arterial occlusion, isovolemic hemodilution was performed by phlebotomy and infusions of low-molecular weight (MW) dextran in one group and of lactated Ringer's solution in the other group. The animals were sacrificed 1 week after temporary arterial occlusion. Hemodilution reduced the hematocrit to a level of 33% to 34%, which lasted throughout the week in both groups. After hemodilution there was a very significant reduction in blood viscosity, plasma total protein content, and fibrinogen levels in both groups in the acute stage; these levels gradually returned to baseline by the end of the week. In the group with lactated Ringer's solution hemodilution, both osmotic and oncotic pressures were decreased by hemodilution in the acute stage. In the control and low-MW dextran groups, osmotic and oncotic pressure remained unaltered throughout the week. Hemodilution resulted in a slight decrease in mean arterial blood pressure in all groups in the acute stage, but there were no significant changes in central venous, pulmonary arterial, or pulmonary wedge pressures. During the week of study, there were no differences in the cardiac index and total blood volume between the groups, and no significant changes in hematological parameters with the exception of a slight increase in bleeding time immediately after hemodilution with low-MW dextran. Daily neurological assessment showed consistently poorer condition during the first 5 days in the group with lactated Ringer's solution compared to either the control group or the group receiving low-MW dextran. Based on Mann-Whitney U-testing, the infarct volume of the lactated Ringer's solution recipients, expressed as a percentage of the total volume of that hemisphere (median 15.7%, range 6.6% to 25.2%) was significantly larger than that of the group receiving low-MW dextran (median 2.2%, range 0% to 15.8%) and that of the control group (median 11.9%, range 0% to 39.9%). The results indicate that, in this model, hemodilution with colloids was beneficial, whereas hemodilution with crystalloids was deleterious. It is likely that the decrease in oncotic pressure observed after hemodilution with lactated Ringer's solution is one of the most important reasons for its detrimental effect.

Therapeutic defibrinogenation by ancrod

Reduction of blood viscosity by venesection may improve peripheral blood flow but similar haemorheological changes have not been conclusively demonstrated following reduction of plasma viscosity by defibrinogenation. Ancrod is a defibrinogenating enzyme from the venom of the Malayan pit viper. We studied six male patients with severe intermittent claudication before, during and after treatment with ancrod for 48 h. Ancrod was given by initial infusion of 2 U/kg over 6 h and four subsequent bolus i.v. injections of 2 U/kg. Skin blood flow in feet and toes were measured repeatedly by laser Doppler velocimetry and calf blood flow by electronic plethysmography both before and after 2 min arterial occlusion. Plasma fibrinogen [median (range)] fell from 2.3(1.4-3.9) to 0.1(0.1-0.3) g/l and plasma viscosity from 1.81(1.61-1.90) to 1.49(1.45-1.72) cp. Dorsal foot and toe skin blood (resting or post-ischaemic) flows were not changed significantly by ancrod. Resting calf blood flow fell significantly after 49 h treatment with ancrod (P less than 0.04). Brachial and ankle blood pressures remained unchanged and haematocrit was not changed. Thus, treatment with ancrod for 48 h did not improve peripheral blood flow in patients with peripheral vascular disease. The fall observed in calf blood flow could be related to increased circulating fibrin/fibrinogen high-molecular-weight complexes and degradation products.