Biorheology

Prediction of thrombus formation at intact arterial walls under low shear flow conditions is clinically important particularly for better prognoses of embolisation in cerebral aneurysms. Although a new mathematical model for this purpose is necessary, little quantitative information has been known about platelet adhesion to intact endothelial cells.

The objective of this study is to measure the number of platelets adhering to intact endothelial cells with a focus upon the influence of the shear rate.

Endothelial cells disseminated in μ-slides were exposed to swine whole blood at different shear rates. Adenosine diphosphate (ADP) was used as an agonist. Adherent platelets were counted by means of scanning electron microscopy.

At an ADP concentration of 1 µM, 20.8 ± 3.1 platelets per 900 µm² were observed after 30-minute perfusion at a shear rate of 0.8 s⁻¹ whereas only 3.0 ± 1.4 per 900 µm² at 16.8 s⁻¹.

The number of adherent platelets is determined by a balance between the shear and the degree of stimulation by the agonist. At an ADP concentration of 1 µM, a limit to the shear rate at which platelets can adhere to intact endothelial cells is considered to be slightly higher than 16.8 s⁻¹.

The rheological properties of sputum may influence lung function and become modified in disease.

This study aimed to correlate the viscoelastic properties of sputum with clinical data on the severity of disease in patients with chronic obstructive pulmonary disease (COPD).

Sputum samples from COPD patients were investigated using rheology, simple mathematical modelling and Scanning Electron Microscopy (SEM). The samples were all collected from patients within two days of their admission to Prince Philip Hospital due to an exacerbation of their COPD. Oscillatory and creep rheological techniques were used to measure changes in viscoelastic properties at different frequencies over time.

COPD sputum was observed to behave as a viscoelastic solid at all frequencies studied. Comparing the rheology of exacerbated COPD sputum with healthy sputum (not diagnosed with a respiratory disease) revealed significant differences in response to oscillatory shear and creep-recovery experiments, which highlights the potential clinical benefits of better understanding sputum viscoelasticity. A common power law model G ( t ) = G 0 ( t τ 0 ) − m was successfully fitted to experimental rheology data over the range of frequencies studied.

A comparison between clinical data and the power law index m obtained from rheology, suggested that an important possible future application of this parameter is as a potential biomarker for COPD severity.

Reperfusion injury often occurs with therapeutic intervention addressing the arterial occlusions causing acute myocardial infarction and stroke. The no-reflow phenomenon has been ascribed to leukocyte plugging and blood vessel constriction in the microcirculation.

To assess possible red cell contributions to post-thrombolytic no-reflow phenomenon.

Blood clots were formed by recalcifying 1 ml of citrated fresh human venous blood and then lysed by adding 1,000 units of streptokinase (SK) at several intervals within 1 hour. Red cell deformability was tested by both a microscopic photometric and a filtration technique, viscosity by a cone and plate viscometer, and erythrocyte aggregation by an optical aggregometer.

Two sampling methods were devised for the microscopic photometric test, both of which indicated increases of erythrocyte stiffness after being lysed from the clot by SK. In accompanying experiments, the viscosity, aggregation and filterability of the post-lytic erythrocytes were assessed. Results indicated increased viscosity in Ringer’s, decreased aggregation index and filterability through a 5 μm pore size Nuclepore membrane.

Findings demonstrated that post-lytic changes in red cell deformability do occur which could contribute to the no-reflow phenomenon.

Although many studies have shown that arteries change diameter in response to chronic change in blood flow (BF), keeping wall shear stress (WSS) at physiologically normal levels, relatively little is known about the effects of flow restoration after flow reduction and also the role of vascular smooth muscle (VSM) during such a remodeling process.

To elucidate the biomechanical responses of the arterial wall to the restoration of normal BF after flow reduction and compare the results with our previous results observed in response to decreased BF alone.

Carotid artery BF in the Wistar rat was decreased by ligation and then restored to normal levels by release of the ligation. The effects of BF changes on the biomechanical properties of the carotid arterial wall were determined from measurements of diameters and pressures of excised artery segments.

During BF reduction and restoration, WSS was maintained at physiological levels by changes in the internal diameter. No significant changes in the incremental elastic modulus were found in response to changes in BF. VSM tone was significantly enhanced during the changes in BF.

Arteries change diameters in response to BF reduction and also flow restoration to normal after flow reduction, keeping WSS at physiologically normal levels. The lack of changes in vascular elasticity suggests that there were no significant changes in major wall constituents, such as elastin and collagen. VSM may play the dominant role in observed arterial remodeling and adaptation.

Cartilage surface contact geometry influences the deformational behavior and stress distribution throughout the extracellular matrix (ECM) under load.

To test the correlation between the mechanical and cellular response of articular cartilage when loaded with two different-sized spherical indenters under dynamic reciprocating sliding motion.

Articular cartilage explants were subjected to a reciprocating sliding load using a 17.6 mm or 30.2 mm spherical ball for 2000 cycles at 10 mm/s and 4 kg axial load. Deformation of the cartilage was recorded and contact parameters were calculated according to Hertzian theory. After mechanical loading cartilage samples were collected and analyzed for ECM collagen damage, gene regulation and proteoglycan (PG) loss.

Significantly higher ECM deformation and strain and lower dynamic effective modulus were found for explants loaded with the smaller diameter indenter whereas contact radius and stress remained unaffected. Also, the 17.6 mm indenter increased PG loss and significantly upregulated genes for ECM proteins and enzymes as compared to the 30.2 mm indenter.

Sliding loads that increase ECM deformation/strain were found to induce enzyme-mediated catabolic processes in articular cartilage explants. These observations provide further understanding of how changes in cartilage contact mechanics under dynamic conditions can affect the cellular response.