Here, we assessed the histological changes in myocardial structure in old rats against the background of persistent arterial hypertension. This study was aimed to investigate the structural organization of tissues and vessels of animal myocardium to days 3, 7 and 30 after development of stress-induced arterial hypertension. The experiments were performed in 28-30-month-old white outbred male rats. The pathological state was simulated according to the patented technique under specialized cage conditions with a combined impact of stimuli (light, sound, electricity). Histological and histochemical assessments of the myocardium within these research terms showed the development of destructive and dystrophic disorders in myocardial tissues and vessels, the progression of interstitial and perivascular oedema, the occurrence of diapedetic hemorrhages. Significant differences in morphological structure of the myocardium in hypertensive old rats as compared with the control normotensive animals were established. These findings make it possible to clarify the pathogenesis of the stress-induced arterial hypertension development, which is a key element in designing the current anti-stress and antihypertensive therapy.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Mast Cells and Arteriogenesis: A Systematic Review.
Cardiovasc Pathol
January 2025
Department of Anatomical Sciences, St. George's University, School of Medicine, Grenada, West Indies; Department of Pathology, St. George's University, School of Medicine, Grenada, West Indies; Department of Clinical Anatomy, Mayo Clinic, Rochester, Minnesota; Nicolaus Copernicus Superior School, College of Medical Sciences, Olsztyn, Poland. Electronic address:
Vascular occlusive diseases remain a major health burden worldwide, necessitating a deeper understanding of the adaptive responses that mitigate their impact. Arteriogenesis, the growth and remodeling of collateral vessels in response to arterial occlusion, is a vital defense mechanism that counteracts fluid shear stress-induced vascular stenosis or occlusion. While physical factors driving arteriogenesis have been extensively studied, the specific cellular mediators involved are poorly understood.
View Article and Find Full Text PDFFear of Fragility: A Case of Osteoporosis-Triggered Takotsubo Cardiomyopathy.
Cureus
December 2024
Cardiology, St. Luke's Hospital, Chesterfield, USA.
We present a case of a 73-year-old woman with a medical history significant for hyperlipidemia, on pravastatin, who developed Takotsubo cardiomyopathy following a diagnosis of osteoporosis. She presented to the Emergency Department with acute transient left arm pain that resolved spontaneously. Investigations revealed elevated troponin levels, non-specific electrocardiographic changes, no significant coronary artery disease on angiography, and left ventricular systolic dysfunction, findings consistent with Takotsubo cardiomyopathy.
View Article and Find Full Text PDFLncRNA LUCAT1 offers protection against human coronary artery endothelial cellular oxidative stress injury through modulating hsa-miR-6776-5p/LRRC25 axis and activating autophagy flux.
J Transl Med
December 2024
Department of Cardiovascular Medicine, The First Affiliated Hospital of Nanjing Medical University, Guangzhou Road 300, Nanjing, 210029, Jiangsu, China.
Background: Coronary artery disease (CAD) has become a dominant economic and health burden worldwide, and the role of autophagy in CAD requires further clarification. In this study, we comprehensively revealed the association between autophagy flux and CAD from multiple hierarchies. We explored autophagy-associated long noncoding RNA (lncRNA) and the mechanisms underlying oxidative stress-induced human coronary artery endothelial cells (HCAECs) injury.
View Article and Find Full Text PDFEndothelial Cell-Selective Adhesion Molecule Deficiency Exhibit Increased Pulmonary Vascular Resistance Due to Impaired Endothelial Nitric Oxide Signaling.
Am J Physiol Heart Circ Physiol
December 2024
Department of Physiology.
Endothelial cell-selective adhesion molecule (ESAM) is a member of tight junction molecules, highly abundant in the heart and the lung, and plays a role in regulating endothelial cell permeability. We previously reported that mice with genetic ESAM deficiency (ESAM) exhibit coronary microvascular dysfunction leading to the development of left ventricular diastolic dysfunction. Here, we hypothesize that ESAM mice display impairments in the pulmonary vasculature, affecting the overall pulmonary vascular resistance (PVR).
View Article and Find Full Text PDFHydrogen gas inhalation therapy may not work sufficiently to mitigate oxidative stress induced with REBOA.
Sci Rep
December 2024
Department of Emergency and Critical Care Medicine, Jichi Medical University, Shimotsuke City, Tochigi, Japan.
Hemorrhagic shock is a significant cause of trauma-related mortality. Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a less-invasive aortic occlusion maneuver for severe hemorrhagic shock but potentially inducing oxidative stress injuries. In an animal model, this study investigated hydrogen gas inhalation therapy's potential to mitigate post-REBOA ischemia-reperfusion injuries (IRIs).
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!