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Contour of Pressure and Flow Waves in Arteries
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
Secondary flow fluctuations are more apparent in the brachiocephalic artery than in the descending thoracic aorta, partly because the former has a narrower caliber. The relationship between the brachiocephalic flow contour and the contour of the arterial pressure wave in humans has been examined by O'Rourke and Avolio (1980), by Hirata et al. (2006, 2008a) and by Hashimoto et al. (2018) and Hashimoto and Ito (2010, 2013, 2015). When the diastolic pressure wave was prominent, there was a prominent diastolic flow wave as well. When the pressure wave showed no diastolic wave, the flow wave usually showed a late systolic shoulder. Differences in the flow waves and in the pressure waves were studied in humans and in a model of the systemic arterial tree and were explained by O'Rourke (1967, 1971) and O'Rourke and Avolio (1980) on the basis of differences in the timing of wave reflection from the lower part of the body relative to that from the upper body. These studies on arterial models have been verified and extended by Karamanoglu et al. (1994, 1995). Implications to cerebrovascular disease are discussed in Chapter 14.
Cardiovascular disease
Published in Sally Robinson, Priorities for Health Promotion and Public Health, 2021
Cerebrovascular disease refers to several conditions that affect the blood vessels in the brain. A cerebrovascular accident (CVA), or a stroke, means that the blood supply to part of the brain has been interrupted. Most strokes are ischaemic, meaning they are caused because of a blood clot, often due to atherosclerosis. Some are the result of a haemorrhage, meaning a blood vessel burst. The symptoms of a stroke include the face may drop on one side, the individual may be unable to smilean inability to lift both arms and keep them thereslurred or garbled speech(NHS, 2019a)
Cerebrovascular Diseases
Published in Amy J. Litterini, Christopher M. Wilson, Physical Activity and Rehabilitation in Life-threatening Illness, 2021
Amy J. Litterini, Christopher M. Wilson
Cerebrovascular diseases include diagnoses in which the blood vessels to the brain are deformed or damaged, affecting cerebral circulation. Cerebrovascular accidents (CVA), also commonly referred to as strokes, are life-threatening diagnoses affecting arteries that lead to the brain causing them to rupture or occlude (see Figure 12.1).1
Highly-expressed circ_0129657 inhibits proliferation as well as promotes apoptosis and inflammation in HBMECs after oxygen-glucose deprivation via miR-194-5p/GMFB axis
Published in Autoimmunity, 2023
Yun Qian, Bo Tang, Hao Zhang, Hui Yang
Stroke, also known as cerebral stroke, is an acute cerebrovascular disease with a wide range of causes [1–4]. It is mainly caused by the sudden rupture of blood vessels in the brain or blockage of blood vessels [2], further causing brain tissue damage or brain blood circulation disorders of the disease [2, 5]. Insufficient blood supply to the brain is followed by neurological dysfunction, which can lead to disability or loss of autonomic consciousness [3, 6, 7]. Due to the rapid onset of the disease, the optimal treatment time is very short, resulting in a high mortality rate in addition to a high morbidity rate. Therefore, stroke has been a serious health problem for people all around the world [7]. It also imposes a huge economic burden on families and countries [8]. Therefore, it is of utmost importance to prevent the onset of the disease or to save the life of the patients within the best resuscitation time. Here, we aimed to investigate bio-diagnostic markers that could be used as valid markers for stroke and provide a theoretical basis for the early onset of the disease.
Gallic acid attenuates cerebral ischemia/re-perfusion-induced blood–brain barrier injury by modifying polarization of microglia
Published in Journal of Immunotoxicology, 2022
Yang Qu, Lin Wang, Yanfang Mao
Cerebrovascular disease is a common frequently-occurring pathology. The complexity of the pathologies present, and the underlying mechanisms for their development after cerebral ischemia determines the difficulty of treatment. Finding new and effective drugs that could block or reduce the cerebral ischemic cascade are an intense focus of research. Studies have shown that within a few hours after cerebral ischemia, an inflammatory response occurs immediately, and microglia are activated (Xu et al. 2020). The role of microglia in this response to cerebral ischemia is complex; it is believed that microglial activation leads to increased release of nitric oxide, oxygen free radicals, and other toxic substances, all which act to damage neurons (Jiang et al. 2020). As activation of microglia continues for a few weeks after ischemia, it would seem that interventions against this second type of brain injury (i.e., caused by inflammatory reactions) should become an additional target for the developers of neuroprotective drugs.
Curcumin inhibits cerebral ischaemia–reperfusion injury and cell apoptosis in rats through the ERK–CHOP–caspase-11 pathway
Published in Pharmaceutical Biology, 2022
Yue Chen, Lixia Zhang, Zengtai Yang, Jie Yu
Cerebrovascular disease is one of the major diseases that seriously endanger human life and health. Ischaemic injury occurs in 60–80% of patients with cerebrovascular disease, and it mainly causes temporary or permanent slowdown of blood flow, which leads to structural and functional damage in large areas of brain tissue (Wu et al. 2018; Jin et al. 2019). In addition to the ischaemic injury, the damage caused by reperfusion is more serious (He et al. 2015). Cerebral ischaemia–reperfusion injury (CIRI) is accompanied by a series of complex pathophysiological mechanisms, such as excitotoxicity, oxidative stress, inflammation and apoptosis (Xing et al. 2012; Yang et al. 2017). Neuroinflammation is an important and complex pathophysiological process in cerebral ischaemia, which is involved in the process from early injury to tissue repair after ischaemia (Palencia et al. 2015). So far, the exact molecular signalling pathways involved in cerebral ischaemia have not been fully elucidated, leading to difficulties in clinical treatment.