Purchase individual online access for 1 year to this journal.
Price: EUR 90.00
Impact Factor 2021: 1.875
Biorheology is an international interdisciplinary journal that publishes research on the deformation and flow properties of biological systems or materials. It is the aim of the editors and publishers of
Biorheology to bring together contributions from those working in various fields of biorheological research from all over the world. A diverse editorial board with broad international representation provides guidance and expertise in wide-ranging applications of rheological methods to biological systems and materials.
The aim of biorheological research is to determine and characterize the dynamics of physiological processes at all levels of organization. Manuscripts should report original theoretical and/or experimental research promoting the scientific and technological advances in a broad field that ranges from the rheology of macromolecules and macromolecular arrays to cell, tissue and organ rheology. In all these areas, the interrelationships of rheological properties of the systems or materials investigated and their structural and functional aspects are stressed.
The scope of papers solicited by
Biorheology extends to systems at different levels of organization that have never been studied before, or, if studied previously, have either never been analyzed in terms of their rheological properties or have not been studied from the point of view of the rheological matching between their structural and functional properties. This biorheological approach applies in particular to molecular studies where changes of physical properties and conformation are investigated without reference to how the process actually takes place, how the forces generated are matched to the properties of the structures and environment concerned, proper time scales, or what structures or strength of structures are required.
Biorheology invites papers in which such 'molecular biorheological' aspects, whether in animal or plant systems, are examined and discussed. While we emphasize the biorheology of physiological function in organs and systems, the biorheology of disease is of equal interest. Biorheological analyses of pathological processes and their clinical implications are encouraged, including basic clinical research on hemodynamics and hemorheology.
In keeping with the rapidly developing fields of mechanobiology and regenerative medicine,
Biorheology aims to include studies of the rheological aspects of these fields by focusing on the dynamics of mechanical stress formation and the response of biological materials at the molecular and cellular level resulting from fluid-solid interactions. With increasing focus on new applications of nanotechnology to biological systems, rheological studies of the behavior of biological materials in therapeutic or diagnostic medical devices operating at the micro and nano scales are most welcome.
Abstract: To obtain insights into transmural myocardial perfusion during coronary artery stenosis, we evaluated the characteristics of septal arterial blood flow velocity using a 20 MHz multichannel pulsed Doppler velocimeter. Septal arterial blood flow velocity was characterized by the presence of a retrograde blood velocity component. Thus, a substantial amount of blood that entered the myocardium during diastole flows backward to the proximal coronary arteries. This is evidence of the coronary slosh phenomenon. With coronary artery stenosis, the systolic retrograde flow was enhanced, and was augmented further by coronary vasodilation. Since the component of blood moving backward in systole does…not contribute to the perfusion of the myocardial bed, an augmented coronary slosh phenomenon plays an important role in disturbing myocardial inflow in addition to the stenotic impeding effects on diastolic flow.
Abstract: Nonlinear mathematical techniques now make it possible to quantify the complexity of an irregular time series through calculation of a parameter known as fractal dimension. In the present study, we use such an analysis to provide evidence that histamine-induced pressure oscillations in an isolated rabbit ear resistance artery are generated by deterministic rather than stochastic mechanisms, and that a minimum of 3 independent control variables is necessary to account for the complexity of the dynamics of these oscillations. The fractal dimension of the responses was independent both of the concentration of histamine used to induce rhythmic behavior, and the level…of activity of the endogeneous nitrovasodilator, EDRF. While both superficially influenced the form of the oscillations, it follows that neither are key control variables involved in their genesis. Nonlinear analysis of data obtained in the presence of NG -nitro-L-arginine methyl ester (L-NAME), which blocks EDRF synthesis, provided insights into the intrinsic smooth muscle control mechanisms responsible for generating rhythmic activity. The oscillations exhibited distinct “fast” and “slow” components (periods of 5–20 secs and 1–5 min. respectively). The former involved ion movements at the cell membrane and was inhibited by low [Ca2+ ]o, verapamil (which blocks voltage-dependent Ca2+ influx) and tetraethylammonium (which blocks Ca2+ -activated outward K+ channels), whereas the latter involved Ca2+ -induced Ca2+ release from intracellular stores and was inhibited by ryanodine. All such interventions decreased the overall fractal dimension of the responses to a value <2, thus removing one degree of complexity (and hence control variable) from the dynamics. We conclude that the nonlinear interaction between a fast membrane oscillator and a slow intracellular oscillator generates chaos in vascular smooth muscle and that exogeneous constrictor agonists and EDRF may be regarded as permissive and modulatory influences, respectively.
Abstract: Myocardial contrast echocardiography was used to characterize changes in the regional and transmural myocardial blood flow distribution that were provoked by rapid atrial pacing stress in patients with coronary artery diseases. In patients with coronary organic stenosis, a decrease in the myocardial contrast-enhancement in the subendocardial half after rapid atrial pacing was associated with stress-induced chest pain and electrocardiographic ST-T changes. The decrease in the myocardial contrast-enhancement in the subendocardial half after rapid atrial pacing was not observed in patients without coronary stenosis or after coronary angioplasty. Thus, the finding was considered to reflect myocardial ischemia. Pacing-induced decreases in myocardial…contrast-enhancement were observed in some patients with old myocardial infarction and significant resting coronary collaterals. In these patients, myocardial ischemia was considered to have developed at rapid pacing because collateral function was good enough to perfuse the infarct myocardium at rest, but was not good enough to prevent myocardial ischemia at stress. Thus, myocardial contrast echocardiography seems to be particularly useful in assessing myocardial ischemia at stress due to coronary stenosis in patients with angina pectoris and due to poor dynamic collateral function in patients with old myocardial infarction.
Abstract: Oxygen-derived free radicals are thought to inactivate ectosolic enzymes that regulate myocardial cellular functions. One such enzyme is ecto-5’-nucleotidase, which is responsible for adenosine production during coronary hyperemic flow. In the present study, we measured both reactive and hyperemic flow and adenosine release during reperfusion with and without superoxide dismutase. In 10 open chest dogs, the left anterior descending coronary artery was perfused through an extracorporeal bypass tube from the carotid artery. In the control hearts, a five-minute occlusion of the coronary artery caused the hyperemic flow with increased release of adenosine. In the superoxide dismutase-treated hearts, although administration of…superoxide dismutase altered neither adenosine release nor coronary blood flow in the baseline, it augmented both peak coronary blood flow and repayment, and adenosine release during reperfusion. Therefore, we hypothesized that superoxide dismutase reduces generation of oxygen-derived free radicals during ischemia and reperfusion and attenuates the degradation of ecto-5’-nucleotidase. The administration of superoxide dismutase enhanced the increase in ecto-5’-nucleotidase activity at 10 minutes after reperfusion over the untreated group. Thus, we conclude that super oxide dismutase enhances reactive hyperemic flow and adenosine release during reperfusion following ischemia, which may be attributable to the protection of ecto-5’-nucleotidase by superoxide dismutase during ischemia and reperfusion.
Abstract: The ATP-sensitive potassium channel (K+ ATP channel) is known to exist in blood vessels and to regulate vascular tone. We examined the role of this channel in coronary arteriolar vasomotion during coronary autoregulation, ischemia, reactive hyperemia and endothelium-dependent response by acetylcholine in vivo . Experiments were performed with anesthetized open-chest dogs. Coronary arterioles were directly observed in situ by means of a floating objective system or a stroboscropic epi-illumination system synchronized with cardiac motion. Small arterioles less than 100 μ m in internal diameter dilated in response to reduction in perfusion pressure (perfusion pressure: 60, 40, 25 mm…Hg). Glibenclamide, a selective blocker of the K+ ATP channel, reversed the dilation. Reactive hyperemia produced by 20-second occlusion of the left anterior descending coronary artery resulted in arteriolar dilation, the magnitude of which was greater in smaller arterioles than in larger ones. Glibenclamide significantly inhibited the dilation in both large and small arterioles. Acetylcholine (ACh) produced dilation in arterioles of all sizes. NG-monomethyl L-arginine, a competitive inhibitor of nitric oxide synthesis, abolished the dilation of large arterioles, but failed to abolish the dilation in small arterioles. Glibenclamide, however, did not have any additional inhibitory effect on ACh-induced arteriolar dilation. Thus, we conclude that the K+ ATP channel plays an important role in coronary microvascular vasomotion during autoregulation, ischemia and reactive hyperemia, but not during endothelium-dependent vasodilation induced by ACh in vivo .