Hemodynamic stress

Cardiac hypertrophy appears to be mediated by HS proteins (Izumo et al., 1988). Cardiac myocytes exposed to a hemodynamic stress have been found to increase their levels of heat shock proteins (Delcayre et al., 1988). Although experiments involving interference with HS protein synthesis were not done in these studies. 

Knock-out Impaired cardiac contractility in response to (3-adrenergic stimulation and hemodynamic stress Reduced anxiety-related responses and increased exploratory drive in male KO mice Prolonged Q-T intervals, reduced Ca2+-induced Ca2+ release upon 3-adrenergic stimulation. 

Du XJ, Cole TJ, Tenis N, Gao XM, Kontgen F, Kemp BE, Heierhorst J. 2002. Impaired cardiac contractility response to hemodynamic stress in S100A1-deficient mice. Mol Cell Biol 22(8) 2821-2829. 

The FGF family consists of 23 proteins that are classified by their expression pattern, receptor-binding preference, and protein sequence (20,21). FGF is present in the normal myocardium (22). Its expression is stimulated by hypoxia (23) and hemodynamic stress (24). FGF-2 is a pluripotent molecule and modulates numerous cellular functions for multiple cell types. In the context of angiogenesis, it induces endothelial cell proliferation, survival, and differentiation, and is also involved in cell migration of endothelial cells, smooth muscle cells, macrophages, and fibroblasts (21). These effects are mediated through its interaction with the tyrosine kinase receptor FGFRI which also leads to the downstream release of NO (25). Additionally, FGF-2 stimulates endothelial cells to produce a... 

E-actin capping (CapZ) and other contractile saphenous vein smooth muscle proteins are altered by hemodynamic stress a proteonomic approach. Mol. Cell Proteomics 3,115-124. 

Collectively, these studies suggest that COX-2 plays a dominate role in the regulation of salt and water excretion in prostaglandin dependent patient, while the role of COX-1 seems to involve the regulation of renal hemodynamics, including GFR. The Swan et al. [127] study suggests that COX-2 may also play a role in regulating GFR however, the combination of elderly patients who are salt depleted may have provided a more severe hemodynamic stress than was present in the other three studies. 

NSAID induced nephrotic syndrome is suspected of being immunologically mediated and idiosyncratic. It has a distinct presentation when compared to that ascribed to acute interstitial nephritis. The nephrotic syndrome is not associated with hemodynamically stressed patients. Recently Radford etal. [%] published a retrospective study of NSAIDs induced membranous nephropathy using the Mayo Clinic biopsy registry. They reported that >10% of biopsy proven membranous glomerulonephritis [stage I/II] was attributable to NSAIDs. They summarized the clinical features of... 

Maitland et al. followed on this work with laser-activated foams for embolic aneurysm treatments [57]. In this study, the Tg of the foam was lowered to 45 °C and tested in an in vitro setup using 21 °C water, which is a 15°C shift in the Metcalfe conditions. Through proper laser power and absorption tuning, the foam devices were fully deployed under arterial flow conditions. In a parallel study, simulations were used to evaluate the performance of the device during deployment and after implantation [56]. Changes in blood flow patterns into the aneurysm, increases in hemodynamic stresses, and potential of thermal damage due to laser heating were all assessed. 

Approximately 1 in 856 people will undergo kidney dialysis, resulting in over 354,000 patients in the US alone [59], During the process, blood is transferred and processed at a rate of 350 mL min via arteriovenous fistulas, which act as a permanent access point to the vasculature [60], Complications due to the hemodynamic stress (wall shear stress) induced by the dialysis needle have been observed. The presence of the outflow needle has been shown to increase turbulence intensities dramatically [61], which in turn increases wall shear stresses, induces intimal hyperplasia, and causes stenosis [60],... 

An SMP dialysis needle adapter has been developed to reduce the hemodynamic stresses during dialysis [61], The adaptor has been proposed to pass through the dialysis needle, expand upon heating to body temperature, and be retracted when the procedure is completed. Computational fluid dynamics and in vitro visualizations showed that the wall shear stresses were reduced by the adapter s elimination of jet impingement (Fig. 6). 

The most plausible pathogenetic theory is that they are acquired due to hemodynamic stress on the relatively unsupported bifurcations of cerebral arteries (Timperman et al. 1995). This is supported by the clinical observation that many patients with an anterior communicating artery (Acorn) aneurysm do have one hypoplastic or absent Al segment and thus an increased hemodynamic stress on the AcomA. Other factors than hemodynamics and structural alterations of the vessel wall contributing to the development of saccular aneurysms may be genetic, infection, trauma, neoplasms, radiation or idiopathic. 

Ortega, J.M., Small, W., Wilson, T.S., Benett, W.J., Loge, J.M., Maitland, D.J., 2007. A shape memory polymer dialysis needle adapter for the reduction of hemodynamic stress within arteriovenous grafts. IEEE Transactions on Biomedical Engineering 54, 1722-1724. 

In patients with known chronic cerebral ischemia related to underlying carotid artery stenotic lesions, CBF is usually preserved, at least initially, because of the cerebrovascular reserve. The cerebrovascular reserve represents the vasodilatation ability of cerebral arteries to compensate for a CBF tending to decrease and maintain this CBF at a normal level. In patients with chronic cerebral vascular disorders, it is necessary to quantify the residual cerebrovascular reserve and to distinguish tissue that has used only a limited fraction of its vasodilatation ability and still has cerebrovascular reserve available as a bulfer from tissue that has exhausted its vasodilatation ability and cerebrovascular reserve. The latter is at risk of ischemia, which can be triggered by any hemodynamic stress, and requires intervention to increased CBF, usually through carotid stenosis surgery or endovascular treatment, or extracranial-intracranial artery bypass (Nariai et al. 1995). 

Hemodynamic stress can be mimicked by using a tolerance test such as acetazolamide administration in conjunction with quantitative measurement of CBF. Although the exact mechanism of action is uncertain, acetazolamide causes vasodilatation of normal cerebral arteries and an increase in CBF in the corresponding territory. Patients with impaired cerebrovascular reserve, however, are aheady maximally vasodilated due to the response of cerebral autoregulatory mechanisms, and thus cannot respond further to acetazolamide. CBF does not increase, but remains stable or even decreases, because of a steal phenomenon by the healthy arteries (Nariai et al. 1995). Acetazolamide is generally well tolerated, with the most common side effects being cir-cumoral numbness, paresthesias, and headache. One case of acetazolamide-associated reversible ischemia has been reported (Komiyama et al. 1997). 

Katayose D, Isoyama S, Fujita H, Shibahara S (1993) Separate regulation of heme oxygenase and heat shock protein 70 mRNA expression in the rat heart by hemodynamic stress. Biochem Biophys Res Commun 191 587-594 Kaufmann SHE (1990) Heat shock proteins and the immune response. Immunol Today 11 129-136... 

Patients with hypertension have increased common carotid artery IMT and lower mean shear stress with a negative correlation between shear stress and IMT in hypertensives. In the general population, decreased shear stress may contribute to atherosclerosis (16). It was suggested that the ubiquitous atherosclerotic changes in fetal and pediatric subjects when serum cholesterol levels are normal demonstrate the importance of repetitive hemodynamic stresses, rather than hypercholesterolemia, in atherosclerosis (reviewed in ref. 17). 

Davies, P.F. (1988). Endothelial Cells, Hemodynamic Stress, and the Localization of Atherosclerosis. CRC Press, Boca Raton. 

Color DUS (CDUS) provides accurate and reproducible data when used for access surveillance. It provides direct visualization of the stenosis and measurement of velocity changes indicative of hemodynamic stress at the stenosis [15]. CDUS can be performed in the dialysis units, though currently it is performed in hospital laboratories or clinic settings. 

Prolonging the patency of an access circuit is a key element for patient safety. It starts with optimal access planning utilizing DUS and surgical techniques that minimize hemodynamic stress responsible for the development of MIH. Monitoring, surveillance and timely interventions play a key role in prolonging the access patency. It is important that the access plan developed and communicated to the patient gets reinforced by all personnel involved in patient care activities. 

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