PubMed · 11462406
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K Kurosawa. 2001. [Aorta].. https://pubmed.ncbi.nlm.nih.gov/11462406/
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OBJECTIVES: We evaluate the clinical results 1 year after an anatomic reconstruction of the aortic root in which we used a specifically designed aortic root prosthesis that incorporates the sinuses of Valsalva. MATERIAL AND METHODS: The new aortic Dacron prosthesis has a proximal portion in the Dacron conduit that expands on implantation, creating pseudosinuses. During a 12-month period, 28 patients (mean age 59 +/- 14 years) underwent a Bentall operation (12 cases), a remodeling procedure (7 cases), and a reimplantation procedure (9 cases) with the use of a new aortic root conduit. All patients had aortic root aneurysm with an anatomically normal (for the valve-sparing procedure) or diseased aortic valve (for the Bentall operation). Five patients had aortic dissection and 5 had Marfan disease. The mean follow-up was 6 +/- 3 months. All patients underwent postoperative transesophageal and transthoracic echocardiographic studies. RESULTS: All patients survived and were in good clinical condition at the latest follow-up. Postoperative echocardiography showed a marked reduction in ventricular volumes in all patient groups (P <.0005). In the Bentall group the new prosthesis appeared to reduce the tension on the coronary ostial sutures. In patients undergoing both types of valve-sparing procedures a similar normal anatomy of the aortic root was reconstructed. In the reimplantation group the anulus was smaller than in the remodeling group (P =.01). Patients undergoing the reimplantation procedure had less bleeding and a lower incidence of residual valve insufficiency. CONCLUSIONS: The new aortic root prosthesis allowed the reconstruction of the aortic root anatomy in all types of surgical techniques with low postoperative morbidity.
Loss of the modulatory role of the endothelium may be a critical initial factor in the development of diabetic vascular diseases. Exposure of human aortic endothelial cells (HAECs) to high glucose (30 or 44 mmol/l) for 7-10 days significantly increased the release of superoxide anion in response to the calcium ionophore A23187. Nitrate, a breakdown product of peroxynitrite (ONOO(-)), was substantially increased in parallel with a decline in cyclic guanosine monophosphate (GMP). Using immunochemical techniques and high-performance liquid chromatography, an increase in tyrosine nitration of prostacyclin (PGI(2)) synthase (PGIS) associated with a decrease in its activity was found in cells exposed to high glucose. Both the increase in tyrosine nitration and the decrease in PGIS activity were lessened by decreasing either nitric oxide or superoxide anion, suggesting that ONOO(-) was responsible. Furthermore, SQ29548, a thromboxane/prostaglandin (PG) H(2) (TP) receptor antagonist, significantly reduced the increased endothelial cell apoptosis and the expression of soluble intercellular adhesion molecule-1 that occurred in cells exposed to high glucose, without affecting the decrease in PGIS activity. Thus, exposure of HAECs to high glucose increases formation of ONOO(-), which causes tyrosine nitration and inhibition of PGIS. The shunting of arachidonic acid to the PGI(2) precursor PGH(2) or other eicosanoids likely results in TP receptor stimulation. These observations can explain several abnormalities in diabetes, including 1) increased free radicals, 2) decreased bioactivity of NO, 3) PGI(2) deficiency, and 4) increased vasoconstriction, endothelial apoptosis, and inflammation via TP receptor stimulation.
A large number of constituents, such as growth factors, cytokines, and vasoregulatory molecules, contribute a network of cellular interactions to atherosclerotic lesions, and current evidence suggests that granulocyte-macrophage colony-stimulating factor (GM-CSF) is one of these constituents. We conducted this study to determine whether GM-CSF has an effect on the fate and function of macrophages. We examined the effect of GM-CSF on macrophages in vitro with a highly inducible HL60 subclone (HL60/DU-1) that we recently established. HL60 cells have been reported to preserve functional GM-CSF receptors, but a GM-CSF allele was rearranged and partially deleted. HL60/DU-1 cells were devoid of GM-CSF immunoreactivity and of autocrine stimulation of GM-CSF. HL60/DU-1 cells fated to die soon after terminal differentiation of macrophages by 1, 25-dihydroxy vitamin D(3) treatment. We found cell death to be mediated mainly by necrosis, not apoptosis, as confirmed by DNA fragmentation in agarose gel electrophoresis, morphological observation under a fluorescence microscope, and assay of lactate dehydrogenase release. Exogeneously administered GM-CSF rescued cells from necrotic death and caused them to survive and generate superoxide anions. We also conducted immunohistochemical analysis on an atherosclerotic human artery. Macrophages, endothelial cells, and smooth muscle cells were found to be GM-CSF positive in an atherosclerotic lesion. In summary, GM-CSF, which is produced by macrophages, endothelial cells, and smooth muscle cells, is thought to act in an autocrine and a paracrine fashion as a necrosis-inhibiting factor against arterial macrophages. This unique function may play an important role in ensuring survival and promoting function in atherosclerotic lesions.