According to the classical Windkessel model, the heart is the only power source for blood flow, while the arterial system is assumed to be an elastic chamber that acts as a channel and buffer for blood circulation. In this paper we show that in addition to the power provided by the heart for blood circulation, strain energy stored in deformed arterial vessels in vivo can be transformed into mechanical work to propel blood flow. A quantitative relationship between the strain energy increment and functional (systolic, diastolic, mean and pulse blood pressure) and structural (stiffness, diameter and wall thickness) parameters of the aorta is described. In addition, details of blood flow across the aorta remain unclear due to changes in functional and other physiological parameters. Based on the arterial strain energy and fluid-structure interaction theory, the relationship between physiological parameters and blood supply to organs was studied, and a corresponding mathematical model was developed. The findings provided a new understanding about blood-flow circulation, that is, cardiac output allows blood to enter the aorta at an initial rate, and then strain energy stored in the elastic arteries pushes blood toward distal organs and tissues. Organ blood supply is a key factor in cardio-cerebrovascular diseases (CCVD), which are caused by changes in blood supply in combination with multiple physiological parameters. Also, some physiological parameters are affected by changes in blood supply, and vice versa. The model can explain the pathophysiological mechanisms of chronic diseases such as CCVD and hypertension among others, and the results are in good agreement with epidemiological studies of CCVD.

Heat treatment is one method to improve mechanical properties of metal, but each heat treatment method has its advantages and disadvantages, therefore, different requirements regarding size, shape, and properties with respect to different heat treatment processes should be considered. The traditional liquid quenchant are clear water and quench oil. Gas quenching is a relatively new process with several important advantages, such as minimal environmental impact, clean products, and ability to control the cooling locally and temporally for best product properties. To meet the high cooling rates required for quenching, the cooling gas must flow at very high velocities, but still the cooling capacity of gas is weakness. In order to increase the cooling capacity of gas, the spray water is added during gas quenching. In this paper, the GCr15 steel is as the research object, the cooling capacity of clear water, quench oil, nitrogen and nitrogen-spray water are studied through comparison of temperature difference and cooling velocity of the specimen

Postural Orthostatic Tachycardia Syndrome is characterized by an excessive increase in heart rate during postural changes without significant blood pressure alterations, often accompanied by symptoms such as dizziness, fatigue, and palpitations. While prior studies have explored potential mechanisms, the precise etiology and pathological basis of Postural Orthostatic Tachycardia Syndrome remain unclear, leading to treatments focused on symptom management rather than addressing root causes. This study employs a hemodynamic fluid-structure interaction model (using existing clinical data) to investigate the roles of hypovolemia, vascular dysfunction, and autonomic nervous system dysregulation in Postural Orthostatic Tachycardia Syndrome pathogenesis. Computational results revealed that hypovolemia reduces cerebral blood flow by approximately 100 mL/min due to a 30% decrease in blood volume, while vascular dysfunction—marked by a 50–100% increase in arterial stiffness—further diminishes cardiac output and cerebral perfusion. These conditions trigger compensatory tachycardia through autonomic feedback mechanisms. Our findings demonstrate that an insufficient cerebral blood supply, driven by hypovolemia and impaired vascular compliance, combined with autonomic dysregulation, underlies the hallmark tachycardia in Postural Orthostatic Tachycardia Syndrome. This mechanistic insight provides a foundation for targeted therapeutic strategies, emphasizing the need to address blood volume management, vascular elasticity, and autonomic balance to improve clinical outcomes.

Introduction: Orthostatic hypotension (OH) is common among the older population. The mechanism hypothesized by OH as a risk factor for cognitive decline and dementia is repeated transient cerebral blood flow deficiency. However, to our knowledge, quantitative evaluation of cardiac output and cerebral blood flow due to acute blood pressure changes resulting from postural changes is rare.Methods: We report a new fluid-structure interaction model to analyze the quantitative relationship of cerebral blood flow during OH episodes. A device was designed to simulate the aging of blood vessels.Results and Discussion: The results showed that OH was associated with decreased transient cerebral blood flow. With the arterial aging, lesions, the reduction in cerebral blood flow is accelerated. These findings suggest that systolic blood pressure regulation is more strongly associated with cerebral blood flow than diastolic blood pressure, and that more severe OH carries a greater risk of dementia. The model containing multiple risk factors could apply to analyze and predict for individual patients. This study could explain the hypothesis that transient cerebral blood flow deficiency in recurrent OH is associated with cognitive decline and dementia.

It is an indisputable physiological phenomenon that the arterial axial pre-stretch ratio (AAPSR) decreases with age, but little attention has been paid to the effect of this reduction on chronic diseases during aging. Here we reported an experimental method to simulate arteries aging, developed a fluid-structure interaction model with the effect of AAPSR changes, and compared it with the anatomy data and structural parameters of the human thoracic aorta. We showed that with the process of aging, the decrease of AAPSR leads to a decline of arterial elasticity, a decrease of arterial elastic strain energy, which weakens the ability to promote blood circulation, the corresponding decrease in cardiac output (CO) and cerebral blood flow (CBF) causes distal organ and body tissue ischemia, which is one of the main causes of increased blood pressure and decreased cerebral perfusion in the elderly. Thus, reduced AAPSR is the one of main manifestation of arteries aging and has an important impact on hypertension and hypoperfusion of the brain in the process of human aging. The research contributes to a better understanding of the physiological and pathological mechanisms of aging-related diseases.