PubMed Health⌕ Search

PubMed · 9914745

[Curriculum vitae aortae].

Abstract

The Greek word aorta means lifter. The vessel was so termed because Aristotle, who first described it, assumed that the heart was lifted by/hanging in aorta. Leonardo da Vinci described the detailed anatomy of aorta. During the 17th century our present understanding of the aorta and the circulation of blood took form due to the descriptions given by William Harvey. The first known operation for abdominal aortic aneurysm was performed in London in 1817 by Sir Astley Cooper who ligated the infrarenal aorta above the aneurysm. Puncture with needles and application of electricity were later tried in order to induce thromboses in the aneurysm. In 1948 Albert Einstein was operated with wrapping of his abdominal aneurysm with cellophane. In 1955 he suffered rupture and died after having refused operation. In 1951 the first successful operation for abdominal aortic aneurysm was performed in Paris by Charles Dubost. With slight modifications, the same operative technique is used today.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

S Solberg. 1998-12-10. [Curriculum vitae aortae].. https://pubmed.ncbi.nlm.nih.gov/9914745/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Critical role of NADPH oxidase-derived reactive oxygen species in generating Ca2+ oscillations in human aortic endothelial cells stimulated by histamine.

There is increasing evidence that intracellular reactive oxygen species (ROS) play a role in cell signaling and that the NADPH oxidase is a major source of ROS in endothelial cells. At low concentrations, agonist stimulation of membrane receptors generates intracellular ROS and repetitive oscillations of intracellular Ca(2+) concentration ([Ca(2+)](i)) in human endothelial cells. The present study was performed to examine whether ROS are important in the generation or maintenance of [Ca(2+)](i) oscillations in human aortic endothelial cells (HAEC) stimulated by histamine. Histamine (1 microm) increased the fluorescence of 2',7'-dihydrodichlorofluorescin diacetate in HAEC, an indicator of ROS production. This was partially inhibited by the NADPH oxidase inhibitor diphenyleneiodonium (DPI, 10 microm), by the farnesyltransferase inhibitor H-Ampamb-Phe-Met-OH (2 microm), and in HAEC transiently expressing Rac1(N17), a dominant negative allele of the protein Rac1, which is essential for NADPH oxidase activity. In indo 1-loaded HAEC, 1 microm histamine triggered [Ca(2+)](i) oscillations that were blocked by DPI or H-Ampamb-Phe-Met-OH. Histamine-stimulated [Ca(2+)](i) oscillations were not observed in HAEC lacking functional Rac1 protein but were observed when transfected cells were simultaneously exposed to a low concentration of hydrogen peroxide (10 microm), which by itself did not alter either [Ca(2+)](i) or levels of inositol 1,4,5-trisphosphate (Ins-1,4,5-P(3)). Thus, histamine generates ROS in HAEC at least partially via NADPH oxidase activation. NADPH oxidase-derived ROS are critical to the generation of [Ca(2+)](i) oscillations in HAEC during histamine stimulation, perhaps by increasing the sensitivity of the endoplasmic reticulum to Ins-1,4,5-P(3).

Aorta↗

Midkine, a heparin-binding growth factor, promotes growth and glycosaminoglycan synthesis of endothelial cells through its action on smooth muscle cells in an artificial blood vessel model.

To study the interactions between smooth muscle cells and endothelial cells in vitro, we developed an artificial blood vessel model, which consisted of collagen gel containing human aortic smooth muscle cells and human umbilical vein endothelial cells grown on the gel. The blood vessel model was utilized to investigate the role of midkine, a heparin-binding growth factor, in the intercellular interactions that are important in angiogenesis. In the blood vessel model, midkine induced stratification of the endothelial cells and increased their proliferation and glycosaminoglycan synthesis. However, midkine had no effect on the smooth muscle cells or endothelial cells when they were cultured separately. Increased proliferation of the endothelial cells was also attained by coculturing them with smooth muscle cells in the presence of midkine or culturing endothelial cells with the conditioned medium of the smooth muscle cells, which had been treated with midkine. These experiments indicate that the target of midkine was smooth muscle cells, which secreted factor(s) acting on the endothelial cells. We identified interleukin-8 as one such factor; the synthesis of interleukin-8 by the smooth muscle cells was increased by exposure to midkine, and anti-interleukin-8 inhibited the midkine action. Furthermore, interleukin-8 caused stratification of the endothelial cells in the blood vessel model. These results provided evidence that midkine is one of the factors involved in epithelial-mesenchymal interactions.

Aorta↗