Aim: The mechanism underlying the stiffness of the aorta and iliofemoral artery that is required to maintain blood pressure (BP) is unclear. A new stiffness index of the aorta (aBeta) and iliac-femoral arteries (ifBeta) was defined by applying the cardio-ankle vascular index (CAVI). We compared changes in stiffness of the two arteries in response to reduced BP, due to the non-selective α adrenergic blocker phentolamine and the β adrenergic blocker atenolol, in rabbits.
Methods: Pressure waves at the origin (oA) and distal ends of the aorta (dA) and the distal end of the left femoral artery (fA) were recorded simultaneously using three pressure sensors in 25 anesthetized rabbits. Phentolamine (50 µg/kg/min) and atenolol (10 mg/kg/min) were infused for 2 min. The pulse wave velocity (PWV) in each artery was determined; aBeta, ifBeta, and whole Beta (aifBeta) were calculated by the following formula; Beta=2ρ/PP×ln(SBP/DBP)×PWV (ρ: blood density; SBP, SBP, and PP: systolic, diastolic, and pulse pressures, respectively).
Results: SBP and DBP at oA, dA, and fA decreased by the administration of phentolamine and atenolol, with and without decreased total peripheral vascular resistance. After phentramine infusion, cardiac output (CO), aBeta, and aifBeta increased, while ifBeta decreased. After infusion of atenolol, CO decreased, while aBeta, ifBeta, and aifBeta remained unchanged.
Conclusion: The contradictory reactions of aBeta and ifBeta to phentolamine suggest that the stiffness of the aorta and ilio-femoral artery is regulated separately during decreased BP induced by phentolamine, but not by atenolol.
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http://dx.doi.org/10.5551/jat.57364 | DOI Listing |
Int J Cardiol
January 2025
Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN 55905, United States of America. Electronic address:
Background: We hypothesized that patients with coarctation of aorta (COA) and obesity would have more advanced cardiovascular remodeling and impaired aerobic capacity compared to COA patients without obesity. The purpose of this study was to assess the relationship between obesity, cardiovascular remodeling, and aerobic capacity in adults with repaired COA.
Method: The study comprised of 3 groups: (1) Obese COA group (n=177) (COA patients with body mass index [BMI] >30 kg/m); (2) Non-obese COA group (n=572) (COA patients with BMI ≤30 kg/m); (3) Control group (n=59) (subjects without structural heart disease and BMI ≤30 kg/m).
J Hypertens
December 2024
Division of Internal Medicine, Candiolo Cancer Institutute FPO - IRCCS, Candiolo.
Background: Heart failure with preserved ejection fraction (HFpEF) is a high prevalence condition, with high rates of hospitalization and mortality. Arterial hypertension is the main risk factor for HFpEF. Among hypertensive patients, alterations in cardiac and vascular morphology identify hypertension-mediated organ damage (HMOD).
View Article and Find Full Text PDFSci Rep
January 2025
Department of Engineering Mechanics, KTH Royal Institute of Technology, Stockholm, Sweden.
Aneurysm rupture is a life-threatening event, yet its underlying mechanisms remain largely unclear. This study investigated the fracture properties of the thoracic aneurysmatic aorta (TAA) using the symmetry-constraint Compact Tension (symconCT) test and compared results to native and enzymatic-treated porcine aortas' tests. With age, the aortic stiffness increased, and tissues ruptured at lower fracture energy [Formula: see text].
View Article and Find Full Text PDFActa Biochim Biophys Sin (Shanghai)
December 2024
Fibrosis is the main pathological feature of aortic stiffness, which is a common extracardiac comorbidity of heart failure with preserved ejection fraction (HFpEF) and a contributor to left ventricular (LV) diastolic dysfunction. Systemic low-grade inflammation plays a crucial role in the pathogenesis of HFpEF and the development of vascular fibrosis. In this study, we investigate the inflammatory mechanism of aortic fibrosis in HFpEF using a novel mouse model.
View Article and Find Full Text PDFPulse (Basel)
November 2024
Department of Biomedical Engineering, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.
Introduction: Arterial stiffening is a hallmark of vascular ageing, and unravelling its underlying mechanisms has become a central theme in the field of cardiovascular disease. While various techniques and experimental setups are accessible for investigating biomechanics of blood vessels both in vivo and ex vivo, comparing findings across diverse methodologies is challenging.
Methods: Arterial stiffness in the aorta of adult (5 months) and aged (24 months) wild-type C57Bl/6J mice was measured in vivo, after which ex vivo biomechanical evaluation was performed using the Rodent Oscillatory Tension Setup to study Arterial Compliance (ROTSAC; University of Antwerp, Belgium) and the DynamX setup (Maastricht University, The Netherlands).
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