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Hypertension
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
Peripheral muscular arteries (e.g. femoral, brachial, radial) have been studied extensively by ultrasonic techniques, by Safar, Brunner, Hayoz, Hoeks, Mancia, Bank and colleagues in Paris, Lausanne, Maastricht, Milan and Minneapolis. Special problems, such as spontaneous arterial vasomotion (Hayoz et al., 1995) and pressure measurement, have been identified and largely overcome. Data have been consistent and quite different from data from the aorta, carotid and other central, predominantly elastic arteries. Stiffness is directly related to change in blood pressure but is less marked than in central arteries. Any increase in stiffness in hyper-tensive subjects usually returns to the normal range when pressure is reduced to the normal range; there is no residual increment in stiffness as often observed for central arteries. Furthermore, muscular arteries dilate in hypertensive subjects such that their compliance (expressed as absolute volume change with change in pressure) may appear to be normal or even increased (Simon et al., 1982, 1983a, 1983b, 1984; Safar et al., 1983; Levenson et al., 1984b; Boutouyrie et al., 1992, 1994; Hayoz et al., 1992; Levenson et al., 1992; Mulvany, 1992; Benetos et al., 1993b; Laurent et al., 1993, 1994; Zhang et al., 2013; Ye et al., 2016; Laucyte-Cibulskiene et al., 2018).
Prediction of Dynamic Transcapillary Pressure Difference in the Coronary Circulation
Published in Samuel Sideman, Rafael Beyar, Analysis and Simulation of the Cardiac System — Ischemia, 2020
Jos A. E. Spaan, Jenny Dankelman
In the first place I should have mentioned that this applies to the fully dilated coronary bed, because then, arteriolar pressure is related to coronary flow. In the second place, vasomotion is a very controversial issue and I am not sure it exists in the heart.
Malignant Tumors and the Microcirculation
Published in John H. Barker, Gary L. Anderson, Michael D. Menger, Clinically Applied Microcirculation Research, 2019
Bernhard Endrich, Peter Vaupel
For unknown reasons, malignant cells rarely invade vessels of the arterial tree. As a result of the well-maintained contractile and nervous apparatus, one would assume that these vessels might respond to physical, pharmacological, and chemical stimuli, and may reveal the phenomenon of vasomotion.
The protective effect of tanshinone IIa on endothelial cells: a generalist among clinical therapeutics
Published in Expert Review of Clinical Pharmacology, 2021
Jun Feng, Lina Liu, Fangfang Yao, Daixing Zhou, Yang He, Junshuai Wang
The endothelium is a single layer of cells that overlays the lumen of blood vessels and plays an important physiological role in vascular homeostasis. The endothelial cells integrate and modulate the fundamental functions of the vascular wall, which controls inflammation, coagulation, and thrombosis, as well as regulates vasomotion. Many of these functions are mediated through the release of nitric oxide (NO). Endothelial injury involves a complex pathophysiological process that includes both increased activation of endothelial cells and the initiation of endothelial dysfunction, leading to vascular damage in both metabolic and atherosclerotic diseases, including cardiovascular diseases, neurodegenerative disorders, pulmonary diseases, hypertension, renal diseases, cancer, and metabolic diseases (such as hyperglycemia or diabetes and hyperlipidemia) [10–12]. Taken together, endothelial cells mediate important physiological functions, including the maintenance of blood fluidity, modulation of vascular tone, regulation of inflammation and immune response, and management of oxidative stress and neovascularization.
Bio-Electro-Magnetic-Energy-Regulation (BEMER) for the treatment of type I complex regional pain syndrome: A pilot study
Published in Physiotherapy Theory and Practice, 2020
Maria Grazia Benedetti, Lorenzo Cavazzuti, Massimiliano Mosca, Isabella Fusaro, Alessandro Zati
The present study applied the BEMER therapy for the treatment of CRPS-I. This system uses a low-frequency, pulsed magnetic field with a series of half-wave shaped sinusoidal intensity variations with characteristics similar to SPs. This has been shown to increase vasomotion and microcirculation with consequent improved organ blood flow, supply of nutrients, and removal of metabolites (Storch et al., 2016). Previous studies have demonstrated the benefits of this therapy in multiple sclerosis for fatigue (Piatkowski, Kern, and Ziemssen, 2009; Ziemssen, Piatkowski, and Haase, 2011), human mesenchymal stem cells, and chondrocytes (Walther, Mayer, Kafka, and Schütze, 2007) as well as in tumoral lymphoma cells (Ríhová et al., 2011); and in knee osteoarthritis and chronic low backpain (Gyulai et al., 2015).
Role of P38 mitogen-activated protein kinase on Cx43 phosphorylation in cerebral vasospasm after subarachnoid hemorrhage
Published in International Journal of Neuroscience, 2019
Chao Lei, Yutian Ruan, Changcheng Cai, Bao He, Dong Zhao
It is widely accepted that CVS is a pathologic delayed and prolonged contraction of cerebral arteries which have been regarded as the disorder of cerebrovascular vasomotion, induced by a cascade activated by factors released into the subarachnoid space after SAH. Some data showed that vasomotion, the regular oscillations of vascular tone or diameter, require intercellular communication, and gap junction (GJ) channels are of key importance [7]. Gap junctions, through which signaling spreads along the cells in the vascular wall to coordinates the synchronized vasomotion of cerebrovascular, are known to clusters of intercellular channels consisting of connexins, with connexin 43 (Cx43) being the most abundant Cx within the vasculature and expressed in both endothelial and smooth muscle cells [8]. In our previous studies, we demonstrated that the alteration of Cx43 expression is closely related to CVS [9], and some studies showed that Cx43 expression upregulates CVS after SAH through a gap junctional intercellular communication (GJIC) dependent mechanism [10].