scholarly journals Shear Stress-Induced Total Blood Trauma in Multiple Species

2017 ◽  
Vol 41 (10) ◽  
pp. 934-947 ◽  
Author(s):  
Chris H. H. Chan ◽  
Ina Laura Pieper ◽  
Christian R. Robinson ◽  
Yasmin Friedmann ◽  
Venkateswarlu Kanamarlapudi ◽  
...  
2018 ◽  
Vol 57 (4) ◽  
pp. 807-818 ◽  
Author(s):  
Zengsheng Chen ◽  
Sofen K. Jena ◽  
Guruprasad A. Giridharan ◽  
Michael A. Sobieski ◽  
Steven C. Koenig ◽  
...  

2002 ◽  
Vol 282 (4) ◽  
pp. H1262-H1269 ◽  
Author(s):  
Robinson Joannides ◽  
Agathe Costentin ◽  
Michaela Iacob ◽  
Patricia Compagnon ◽  
Agnès Lahary ◽  
...  

To assess the influence of initial diameter on the gender difference in flow-dependent dilatation (FDD) of the conduit artery, we measured radial artery internal diameter (echotracking), flow (Doppler) and total blood viscosity in 24 healthy (25 ± 0.8 yr) men and women during reactive hyperemia (RH) and during a gradual hand skin heating (SH). At baseline, mean diameter (men, 2.76 ± 0.09 vs. women, 2.32 ± 0.07 mm, P < 0.05), flow (men, 21 ± 4 vs. women, 10 ± 1 ml/min, P < 0.05), and blood viscosity (men, 4.13 ± 0.07 vs. women, 3.92 ± 0.13 cP, P < 0.05) were higher in men but mean shear stress (MSS) was not different between groups. During RH, the percent increase in diameter was lower in men (men, 9 ± 1 vs. women, 13 ± 1%, P< 0.05). This difference was suppressed after correction for baseline diameter. During SH, the increase in diameter with flow was higher in women ( P < 0.01). However, the increase in MSS was higher in women because of their smaller diameter at each level of flow ( P < 0.01) and there was no difference between groups for the increase in diameter at each level of MSS. These results demonstrate in a direct manner that initial diameter influences the magnitude of FDD of conduit arteries in humans by modifying the value of the arterial wall shear stress at each level of flow and support the interest of the heating method in presence of heterogeneous groups.


2020 ◽  
Vol 134 (17) ◽  
pp. 2399-2418
Author(s):  
Yoshito Yamashiro ◽  
Hiromi Yanagisawa

Abstract Blood vessels are constantly exposed to mechanical stimuli such as shear stress due to flow and pulsatile stretch. The extracellular matrix maintains the structural integrity of the vessel wall and coordinates with a dynamic mechanical environment to provide cues to initiate intracellular signaling pathway(s), thereby changing cellular behaviors and functions. However, the precise role of matrix–cell interactions involved in mechanotransduction during vascular homeostasis and disease development remains to be fully determined. In this review, we introduce hemodynamics forces in blood vessels and the initial sensors of mechanical stimuli, including cell–cell junctional molecules, G-protein-coupled receptors (GPCRs), multiple ion channels, and a variety of small GTPases. We then highlight the molecular mechanotransduction events in the vessel wall triggered by laminar shear stress (LSS) and disturbed shear stress (DSS) on vascular endothelial cells (ECs), and cyclic stretch in ECs and vascular smooth muscle cells (SMCs)—both of which activate several key transcription factors. Finally, we provide a recent overview of matrix–cell interactions and mechanotransduction centered on fibronectin in ECs and thrombospondin-1 in SMCs. The results of this review suggest that abnormal mechanical cues or altered responses to mechanical stimuli in EC and SMCs serve as the molecular basis of vascular diseases such as atherosclerosis, hypertension and aortic aneurysms. Collecting evidence and advancing knowledge on the mechanotransduction in the vessel wall can lead to a new direction of therapeutic interventions for vascular diseases.


1998 ◽  
Vol 80 (09) ◽  
pp. 437-442 ◽  
Author(s):  
I. Hioki ◽  
K. Onoda ◽  
T. Shimono ◽  
H. Shimpo ◽  
K. Tanaka ◽  
...  

SummaryAlterations in platelet aggregability may play a role in the pathogenesis of qualitative platelet defects associated with cardiopulmonary bypass (CPB). We circulated fresh heparinized whole blood through tubing sets coated with heparin (C group, n = 10) and through non-coated sets (N group, n = 10) as a simulated CPB circuit. Shear stress (108 dyne/cm2)-induced platelet aggregation (hSIPA), plasma von Willebrand factor (vWF) activity and platelet glycoprotein (GP) Ib expression were measured, before, during, and after this in vitro set up of circulation. In the two groups, the extent of hSIPA significantly decreased during circulation and was partially restored after circulation. Decreases in the extent of hSIPA were significantly less with use of heparin-coated circuits. There was an equivalent reduction in plasma vWF activity, in the two groups. Expression of platelet surface GP Ib decreased significantly during circulation and recovered after circulation. Reduction of surface GP Ib expression during circulation was significantly less in the C group than that in the N group. Decrease in surface GP Ib expression correlated (r = 0.88 in either group) with the magnitude of hSIPA, in the two groups. The progressive removal of surface GP Ib was mainly attributed to redistribution of GP Ib from the membrane skeleton into the cytoskeleton. Our observations suggest that use of heparin-coated circuits partly blocks the reduction of hSIPA, as a result of a lesser degree of redistribution of GP Ib.


1962 ◽  
Vol 02 (02) ◽  
pp. 165-172
Author(s):  
C Miras ◽  
G Lewis ◽  
J Mantzos

Summary1. Separated leukocytes or total blood from normal subjects, untreated leukaemic patients and from leukaemic patients treated with cytostatic agents were incubated with CH3COONa-l-C14. Radioactivity of mixed lipids was measured at standard time intervals.2. The time incorporation curve observed with leukocytes from treated leukaemic patients showed after an initial linear part, a more rapid levelling off than the curves observed with leukocytes from untreated and normal subjects.3. Therefore, an indirect effect of treatment on leukocyte lipid synthesis seems to be present.4. Phospholipid and neutral lipid synthesis by leukaemic leukocytes was also studied. The results give no evidence that these fractions as a whole have any precursor-product relation.


1961 ◽  
Vol 1 (04) ◽  
pp. 353-379
Author(s):  
Jacques Lammerant ◽  
Norman Veall ◽  
Michel De Visscher

Summary1. The technique for the measurement of cardiac output by external recording of the intracardiac flow of 131I labelled human serum albumin has been extended to provide a measure of the mean circulation time from right to left heart and hence a new approach to the estimation of the pulmonary blood volume.2. Values for the basal cardiac output in normal subjects and its variations with age are in good agreement with the previously published data of other workers.3. The pulmonary blood volume in normal man in the basal state was found to be 28.2 ± 0.6% of the total blood volume.4. There was no correlation between cardiac output and pulmonary blood volume in a series of normal subjects in the basal state.5. The increase in cardiac output during digestion was associated with a decrease in pulmonary blood volume equal to 6.3 ± 1.2% of the total blood volume, that is, about 280 ml.6. The increase in cardiac output during exercise was associated with a decrease in pulmonary blood volume equal to 4.5 ± 1.0% of the total blood volume, that is, about 200 ml.7. The increase in cardiac output attributed to alarm is not associated with a decrease in pulmonary blood volume, the latter may in fact be increased.8. The total blood volume is advocated as a standard of reference for studies of this type in normal subjects in preference to body weight or surface area.9. The significance of these results and the validity of the method are discussed.


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