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Filename: controllers/Detail.php
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File: /var/www/html/index.php
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Function: _error_handler
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Filename: models/Detail_model.php
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Over the past few decades, isometric contraction studies of isolated thoracic aorta segments have significantly contributed to our overall understanding of the active, contractile properties of aortic vascular smooth muscle cells (VSMCs) and their cross-talk with endothelial cells. However, the physiological role of VSMC contraction or relaxation in the healthy aorta and its contribution to the pulse-smoothening capacity of the aorta is currently unclear. Therefore, we investigated the acute effects of VSMC contraction and relaxation on the isobaric biomechanical properties of healthy mouse aorta. An in-house developed set-up was used to measure isobaric stiffness parameters of periodically stretched (10 Hz) aortic segments at an extended pressure range, while pharmacologically modulating VSMC tone and endothelial cell function. We found that the effects of α1-adrenergic stimulation with phenylephrine on the pressure-stiffness relationship varied in sensitivity, magnitude and direction, with the basal, unstimulated NO production by the endothelium playing a pivotal role. We also investigated how arterial disease affected this system by using the angiotensin-II-treated mouse. Our results show that isobaric stiffness was increased and that the aortic segments demonstrated a reduced capacity for modulating the pressure-stiffness relationship. This suggests that not only increased isobaric stiffness at normal pressure, but also a reduced capacity of the VSMCs to limit the pressure-associated increase in aortic stiffness, may contribute to the pathogenesis of this mouse model. Overall, this study provides more insight in how aortic VSMC tone affects the pressure-dependency of aortic biomechanics at different physiological and pathological conditions.
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http://dx.doi.org/10.14814/phy2.13934 | DOI Listing |
Cureus
November 2024
Physical Medicine and Rehabilitation, Centro Hospitalar Universitário de Santo António, Porto, PRT.
This literature review explores the role of biofeedback therapy (BFT) in managing functional fecal incontinence (FFI) in children - a common condition with a substantial impact on the quality of life. FFI diagnosis relies primarily on medical history and thorough physical examination and is categorized by the Rome IV criteria into functional constipation (FC) and functional nonretentive fecal incontinence (FNRFI). Treatment options for FFI remain limited, particularly for FNRFI.
View Article and Find Full Text PDFAm J Physiol Cell Physiol
December 2024
Department of Pharmacology, School of Basic Medical Sciences, Anhui Medical University, Hefei, China.
As a gas molecule, hydrogen sulfide (HS) exerts neuroprotective effects. Despite its recognized importance, there remains a need for a deeper understanding of HS's impact on vascular smooth muscle cells and its role in ischemic brain injury. This study employs encompassing cultured primary cerebral vascular smooth muscle cells, oxygen-glucose deprivation/reoxygenation model, in vitro vascular tone assessments, in vivo middle cerebral artery occlusion and reperfusion experimentation in male rats, and the utilization of ROCK knockout, to unravel the intricate relationship between H2S and cerebrovascular diastolic function.
View Article and Find Full Text PDFPLoS One
December 2024
Division of Pharmacology, National Institute of Health Sciences, Kawasaki, Kanagawa, Japan.
Cardiotoxicity associated with hepatic metabolism and drug-drug interactions is a serious concern. Predicting drug toxicity using animals remains challenging due to species and ethical concerns, necessitating the need to develop alternative approaches. Drug cardiotoxicity associated with hepatic metabolism cannot be detected using a cardiomyocyte-only evaluation system.
View Article and Find Full Text PDFFront Genet
December 2024
Dino Ferrari Center, Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy.
Myotonia congenita, both in a dominant (Thomsen disease) and recessive form (Becker disease), is caused by molecular defects in that encodes the major skeletal muscle chloride channel, ClC-1. This channel is important for the normal repolarization of muscle action potentials and consequent relaxation of the muscle, and its dysfunction leads to impaired muscle relaxation after voluntary or evoked contraction and muscle stiffness. More than 300 pathogenic variants have been found in association with congenital myotonia, inherited as recessive or dominant traits (with complete or incomplete penetrance).
View Article and Find Full Text PDFStructure
December 2024
Department of Physiology and Biophysics, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298, USA. Electronic address:
Mutations in the skeletal isoform of the ryanodine receptor 1 (RyR1) pose grave risks during anesthesia or treatment with succinylcholine muscle relaxants. These can trigger a potentially lethal malignant hyperthermia (MH) episode via intracellular calcium increase mainly from RyR1 channel leakage. Dantrolene is the only known treatment option to prevent death.
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