A method is presented for permanent catheterization of the aorta and the pulmonary artery in dogs. The preparation of single vessel catheters and double catheters for simultaneous arterial and venous sampling is described. The catheters, made of S-50-HL Tygon tubing, are introduced into the aorta and the pulmonary artery through the omocervical vessels, leaving the cerebral circulation intact. Removal of the catheter by the dog, thrombophlebitis and vascular embolism have not been observed. The catheters have remained functional for up to one year.
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http://dx.doi.org/10.1007/BF00583648 | DOI Listing |
Arterioscler Thromb Vasc Biol
January 2025
Department of Cardiovascular Medicine, The University of Tokyo, Bunkyo-ku, Japan. (H. Yagi, H.A., Q.L., A.S.-K., M.U., H.K., R.M., A.S., S.O., H.T., Norifumi Takeda, I.K.).
Background: Marfan syndrome (MFS) is an inherited disorder caused by mutations in the gene encoding fibrillin-1, a matrix component of extracellular microfibrils. The main cause of morbidity and mortality in MFS is thoracic aortic aneurysm and dissection, but the underlying mechanisms remain undetermined.
Methods: To elucidate the role of endothelial XOR (xanthine oxidoreductase)-derived reactive oxygen species in aortic aneurysm progression, we inhibited in vivo function of XOR either by endothelial cell (EC)-specific disruption of the gene or by systemic administration of an XOR inhibitor febuxostat in MFS mice harboring the missense mutation p.
Ann Thorac Cardiovasc Surg
January 2025
Division of Thoracic Surgery, Department of Surgery, Kobe University Hospital and Graduate School of Medicine, Kobe, Hyogo, Japan.
Purpose: The underlying mechanism why segmentectomy has demonstrated the non-inferiority to lobectomy in several randomized trials remains unclear. Computed tomography (CT)-measured pulmonary artery (PA) enlargement reflects PA pressure and predicts the prognosis of certain respiratory diseases. We compared the preoperative and postoperative PA diameter to the ascending aorta diameter (PA/A) ratio, investigating its impact on right ventricular function in lung resection.
View Article and Find Full Text PDFDrug Deliv Transl Res
January 2025
Center for Coronary Heart Disease, Department of Cardiology, National Center for Cardiovascular Diseases of China, State Key Laboratory of Cardiovascular Disease, Fu Wai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 167 Beilishi Rd, Beijing, 100037, China.
Atherosclerosis is one of the leading causes of ischemic cardiovascular disease worldwide. Recent studies indicated that vascular smooth muscle cells (VSMCs) play an indispensable role in the progression of atherosclerosis. Exosomes derived from mesenchymal stem cells (MSCs) have demonstrated promising clinical applications in the treatment of atherosclerosis.
View Article and Find Full Text PDFLife Metab
February 2025
Shanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism and Integrative Biology, Institutes of Biomedical Sciences, Fudan University, Shanghai 200438, China.
Abdominal aortic aneurysm (AAA) is strongly correlated with obesity, partially due to the abnormal expansion of abdominal perivascular adipose tissue (PVAT). Cell death-inducing DNA fragmentation factor-like effector C (CIDEC), also known as fat-specific protein 27 (FSP27) in rodents, is specifically expressed in adipose tissue where it mediates lipid droplet fusion and adipose tissue expansion. Whether and how CIDEC/FSP27 plays a role in AAA pathology remains elusive.
View Article and Find Full Text PDFAging Cell
January 2025
Departamento de Genética y Biología Molecular, Centro de Investigación y de Estudios Avanzados, Ciudad de México, Mexico.
Hutchinson-Gilford progeria syndrome (HGPS) is a premature aging disease caused by progerin, a mutant variant of lamin A. Progerin anchors aberrantly to the nuclear envelope disrupting a plethora of cellular processes, which in turn elicits senescence. We previously showed that the chromosomal region maintenance 1 (CRM1)-driven nuclear export pathway is abnormally enhanced in patient-derived fibroblasts, due to overexpression of CRM1.
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