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Increases in platelet and red cell counts, blood viscosity, and arterial pressure during mild surface cooling: factors in mortality from coronary and cerebral thrombosis in winter.

Six hours of mild surface cooling in moving air at 24 degrees C with little fall in core temperature (0.4 degree C) increased the packed cell volume by 7% and increased the platelet count and usually the mean platelet volume to produce a 15% increase in the fraction of plasma volume occupied by platelets. Little of these increases occurred in the first hour. Whole blood viscosity increased by 21%; plasma viscosity usually increased, and arterial pressure rose on average from 126/69 to 138/87 mm Hg. Plasma cholesterol concentration increased, in both high and low density lipoprotein fractions, but values of total lipoprotein and lipoprotein fractions were unchanged. The increases in platelets, red cells, and viscosity associated with normal thermoregulatory adjustments to mild surface cooling provide a probable explanation for rapid increases in coronary and cerebral thrombosis in cold weather. The raised arterial pressure and possibly cholesterol concentration may contribute to slower components of the increased thrombosis.

Adolescent↗

[Blood viscosity is correlated with insulin resistance].

The insulin resistance syndrome (or syndrome X) is a cluster of symptoms (dyslipidemia, impaired glucose tolerance, overweight, hypertension) associated with a higher risk of atherosclerosis. It has been suggested that hemorheological abnormalities, often found in association with most of these symptoms, may be a part of this syndrome, and possibly play a role in the circulatory abnormalities. In 22 nondiabetic women (20-54 years) presenting a wide range of body mass index (from 20 to 48 kg/m2), insulin sensitivity was assessed with the minimal model procedure, over a 180 min intravenous glucose tolerance test with frequent sampling. The insulin sensitivity index SI (i.e. the slope of the dose-response relationship between insulin increased above baseline and glucose disposal) ranges between 0.1 and 20.1 x 10(-4) min-1/microU/ml) i.e all the range of insulin sensitivity. SI was negatively correlated with blood viscosity (r = -0.530 p < 0.02), body mass index (r = 0.563 p < 0.01) and baseline insulinemia (r = 0.489 p < 0.05). These correlations were independent of each other and were not explained by relationships between SI and fibrinogen or blood lipids. Thus, blood fluidity is correlated with insulin sensitivity when it is measured with an accurate technique, suggesting that blood hyperviscosity is a symptom of insulin resistance that might be involved in the cardiovascular risk of this syndrome.

Adult↗

Insulin secretory capacity, beta-thromboglobulin and blood viscosity in long standing, non-insulin dependent diabetics with and without microangiopathy.

A comparison was made of insulin secretion in response to i.v. glucose between noninsulin dependent diabetics with and without severe microangiopathy. During i.v. glucose tolerance testing those with complications had significantly lower serum insulin concentration (at 40 and 60 min 15.2 +/- 2.9 and 11.7 +/- 2.5 mU-1 respectively) than those without (26.1 +/- 4.7 and 24.3 +/- 3.6 mU-1, p less than 0.01). The differences were also significant when insulin increment above basal was determined. All subjects had raised plasma beta-thromboglobulin concentration (indicating increased tendency to platelet aggregation), but with no significant difference between the two groups. There was also no difference in fasting glucose, kg values, HbAl or blood viscosity. We conclude that non-insulin dependent diabetics with severe microangiopathy have significantly reduced insulin secretory capacity in response to i.v. glucose when compared with those without.

Adult↗

Mathematical model describing erythrocyte sedimentation rate. Implications for blood viscosity changes in traumatic shock and crush syndrome.

BACKGROUND: The erythrocyte sedimentation rate (ESR) is a simple and inexpensive laboratory test, which is widespread in clinical practice, for assessing the inflammatory or acute response. This work addresses the theoretical and experimental investigation of sedimentation a single and multiple particles in homogeneous and heterogeneous (multiphase) medium, as it relates to their internal structure (aggregation of solid or deformed particles). METHODS: The equation system has been solved numerically. To choose finite analogs of derivatives we used the schemes of directional differences. RESULTS: (1) Our model takes into account the influence of the vessel wall on group aggregation of particles in tubes as well as the effects of rotation of particles, the constraint coefficient, and viscosity of a mixture as a function of the volume fraction. (2) This model can describe ESR as a function of the velocity of adhesion of erythrocytes; (3) Determination of the ESR is best conducted at certain time intervals, i.e. in a series of periods not exceeding 5 minutes each; (4) Differential diagnosis of various diseases by means of ESR should be performed using the aforementioned timed measurement of ESR; (5) An increase in blood viscosity during trauma results from an increase in rouleaux formation and the time-course method of ESR will be useful in patients with trauma, in particular, with traumatic shock and crush syndrome. CONCLUSION: The mathematical model created in this study used the most fundamental differential equations that have ever been derived to estimate ESR. It may further our understanding of its complex mechanism.

Blood Physiological Phenomena↗

Increased platelet and red cell counts, blood viscosity, and plasma cholesterol levels during heat stress, and mortality from coronary and cerebral thrombosis.

Recorded deaths from coronary and cerebral thrombosis rise markedly in heat waves. In a British heat wave with little or no distortion due to air-conditioning, outside temperatures of 34.6 degrees C (maximum) and 20.8 degrees C (minimum) were followed by peak mortalities from coronary and cerebral thrombosis one to two days later. Experimental exposure of volunteers to moving air at 41 degrees C for six hours caused core temperature to rise 0.84 degree C, weight to fall 1.83 kg with sweating despite access to water, heart rate to increase 32 beats per minute, and arterial pressure to fall, particularly on standing. The red blood cell count increased 9 percent, and blood viscosity increased 24 percent, mostly after the first hour. The platelet count rose 18 percent, and the platelet volume fell, mostly in the first hour. The plasma cholesterol level increased 14 percent without a change in distribution among lipoprotein fractions. The changes seem able to explain the increased mortality from arterial thrombosis in hot weather.

Adult↗

Smoking and relation to other risk factors in postmenopausal women with coronary artery disease, with particular reference to whole blood viscosity and beta-cell function.

OBJECTIVES: To investigate possible associations between smoking habits and other coronary risk factors in postmenopausal women with known coronary heart disease (CHD). SETTING: The study was conducted at a university clinic. SUBJECTS: A total of 118 postmenopausal women with CHD verified with angiography, consecutively recruited. INTERVENTIONS: Conventional treatment for CHD. The women were randomized to hormone replacement therapy (HRT) with transdermal 17-beta oestradiol and medroxyprogesterone acetate, or to a control group. RESULTS: Smokers were younger (P = 0.005), had lower body mass index (P = 0.04) and lipoprotein Lp(a) levels (P = 0.02) compared with nonsmokers. Smokers had reduced beta-cell function (homeostasis model assessment, P = 0.006), whereas whole blood viscosity (WBV) was higher at all shear rates. WBV was not affected by HRT over a 12-month period. Oestrone levels were higher in smokers. CONCLUSIONS: Smoking adversely affects insulin secretion (beta-cell function) and WBV in postmenopausal women with established CHD, which could be of importance as a mechanism for the increased risk of CHD in smokers. The importance of smoking as a risk factor, overrides the effect of Lp(a), which is lower in smokers compared with nonsmokers.

Aged↗

Increase in blood viscosity in the sprinting horse: can it account for the high pulmonary arterial pressure?

Blood was taken from 49 Thoroughbred horses before and after racing at the track to determine if frusemide modified the apparent viscosity of the blood and to determine the effects of changes in shear rate and packed cell volume (PCV), associated with strenuous exercise, on apparent and relative viscosities. Small increases in apparent viscosity of the blood (at a specified PCV and shear rate) occurred in horses given frusemide compared to those receiving no frusemide; however, no differences were seen in relative viscosity. Although 2 groups of horses, those receiving frusemide before racing and those not receiving this drug were studied, the results suggest no influence of frusemide on any red blood cell variable that might modify apparent blood viscosity. Apparent viscosity of the blood was slightly (but significantly) higher after racing than before racing at any given PCV and shear rate, but relative viscosity was lower in the post race than in the prerace blood sample. The most important contributing factor to the increase in apparent viscosity in blood during racing is the increase in PCV, because the blood becomes nearly shear rate independent at shear rates likely to exist in the cardiovascular system during exercise. With an increase in PCV from 40 to 65% at shear rates above 225/s, apparent viscosity approximately doubled. However, this increase alone cannot account for the elevated pulmonary vascular pressure in the running horse, and additional factors, especially those causing the high left atrial pressure, must be considered. The cause of the elevated pressure may be multifactorial in nature.

Animals↗

The effects on lipids, blood viscosity and platelet aggregation of combined use of niceritrol (Perycit) and a low dose of acetylsalicylic acid.

Forty-six elderly patients (mean age 60 years) suffering from diabetes mellitus (DM), or essential or arteriosclerotic hypertension (HT) were divided into 4 groups. Group 1 served as a control, group 2 was administered 1500 mg niceritrol, group 3 was administered 162 mg acetylsalicylic acid (ASA), and group 4 was administered both 1500 mg niceritrol and 162 mg ASA/day for 8 weeks. Niceritrol lowered serum levels of beta-lipoprotein and total cholesterol and increased HDL cholesterol, usually in 8 weeks. ASA did not affect the lipid-lowering effects of niceritrol. Platelet aggregation induced by epinephrine (1 microgram/ml), collagen (1 microgram/ml), and ADP (2 microM) was depressed in groups 2, 3 and 4. Degrees of depression were higher in groups administered ASA (groups 3 and 4) than in the group administered niceritrol alone (group 2). Plasma fibrinogen levels were lowered in groups administered niceritrol (groups 2 and 4) in 8 weeks. Apparent whole blood viscosity measured at shear rates of 37.6/s and 376/s was improved only in group 4 in 8 weeks, while hematocrit did not change during the study. Because flushing, the most frequent side effect of niceritrol, can be easily controlled by a low dose of ASA, and because the combination of the 2 drugs has some beneficial effects on blood rheology, this combination is considered worthwhile for treatment and prevention of atherosclerosis.

Adult↗

Effects of ticlopidine on blood fibrinogen and blood viscosity in peripheral atherosclerotic disease.

Ten patients with peripheral atherosclerotic disease(PAD) treated with 750 mg/d of 5-(2-chlorophenylmethyl)-4,5,6,7-tetrahydrothieno (3,5-c-pyridine) hydrochloride (ticlopidine, Tiklid) were studied for three months. As control was studied a similar group of patients treated with a traditional vasodilator (nicotinate). The aim of our study was to evaluate the effect of ticlopidine both on the clinical evolution of the disease and on rheologic, coagulative and platelet parameters. A progressive increase of maximal walking distance was noted during the three months of therapy with ticlopidine and limited to the first 30 days of treatment with nicotinate. The fibrinogen levels resulted significantly lowered during 90 days of treatment with ticlopidine, while that was not evident in the nicotinate group. There was also a slight improvement of blood viscosity in the ticlopidine group (not evident in the nicotinate group), but it was not statistically significant. No further modifications of investigated data were found in the two groups of patients. The clinical benefit of ticlopidine in PAD without adverse reactions can be confirmed at least at the dosage of 750 mg/d instead of the usual dose of 500 mg/d. A direct or indirect action of ticlopidine on plasma fibrinogen is suggested. This observation may supply new clues for the understanding of the mechanism of action of this drug.

Aged↗

Correlation between Doppler flow velocity waveforms and cord blood viscosity.

The contribution of rheological factors to the impedance of blood flow in the umbilical artery as determined by continuous-wave Doppler ultrasound was investigated. Of the 51 pregnancies recruited, six were complicated by pre-eclampsia, 10 by intrauterine growth retardation, 15 by both pre-eclampsia and fetal growth retardation, and there were 20 controls. A significant correlation was demonstrated between both plasma viscosity and gestational age and the resistance index used to characterize the Doppler waveform. Multiple regression analysis demonstrated that changes in plasma viscosity explained 55% of the variance seen in the resistance index and that this was statistically significant. This finding is, however, unlikely to be of clinical significance as whole blood viscosity had an insignificant effect on the impedance in the umbilical artery. We postulate that vascular factors such as the number and calibre of the placental arterioles are a more important determinant of umbilical artery impedance.

Blood Flow Velocity↗

Blood viscosity, plasma proteins, and Raynaud syndrome.

The rheology of the blood was studied in 20 patients with Raynaud syndrome. Sixteen patients had scleroderma, two had nonspecific angiitis, one had systemic lupus erythematosus, and one had Raynaud disease. Viscosity measurements were performed on whole blood, plasma, and suspensions of 45% red blood cells (RBCs). In autologous plasma, over a wide range of shear rates. The relative viscosity, an index of RBC aggregation, was obtained by dividing the RBC viscosity in autologous plasma (at a hematocrit value of 45%) by the plasma viscosity. Concentrations of the plasma globulins and fibrinogen were also measured. The mean plasma viscosity was significantly (P less than .01) elevated over established normal controls. The mean RBC viscosity and the relative viscosity were significantly (P less than .01) elevated over normal controls, as were fibrinogen and the globulins. These studies demonstrate increased blood viscosity and red blood cell aggregation, which may constitute an important hindrance to flow.

Adolescent↗