Histomorphological observation in arterial remodeling following New Zealand rabbit auto-extremity artery transplantation

Objective： To investigate the histomorphological change in auto-extremity artery following transplantation. Methods： 50 New Zealand rabbits were randomly divided into 5 groups（postoperative 1 d, 3 d, 7 d, 14 d, 56 d, n = 10）. Femoral artery was harvested and end-to-side anastomosed with carotid in order to build the auto-extremity arterial graft animal model. On the postoperative 1^st, 35^nd, 7^th, 14th and 56^th days, grafts for morphometric analysis under the Image analysis system were obtained; and electron microscope was scanned to observe endothelial cells. In addition, Immunostaining of sections were performed with the mouse monoclonal antibody of the a -smooth muscle isoform of actin and proliferating cell nuclear antigen antibody. Results： Overall patency rate for all conduits was 86%.The intimal hyperplasia was first observed in the 7^th day group, and continued to increase in the 56^th day group（183.21 ± 111.74） μ m, P 〈 0.01. Additionally, the luminal narrowed（32.43 ± 18.28）% in the 56^th day group. Smooth muscle cells were the mainly hyperplastic components. The most active proliferation of cells was detected in the 14^th day group, where the extracellular matrix gradually deposited in the intima. Conclusion： Moderate intimal hyperplasia occurred in arterial conduits and vascular structure experienced constrictive remodeling after auto-transplantation.

Mechanism of arterial remodeling in chronic allograft vasculopathy

Chronic allograft vasculopathy(CAV)remains a major obstacle for long-term survival of grafts even though therapeutic strategies have improved considerably in recent years.CAV is characterized by concentric and diffuse neointimal formation,medial apoptosis,infiltration of lymphocyte or inflammatory cells,and deposition of extracellular matrix both in arteries and veins.Recent studies have shown that stem cells derived from the recipient contribute to neointimal formation under the regulation of chemokines and cytokines.Arterial remodeling in allografts eventually causes ischemic graft failure.The pathogenesis is multi-factorial with both immunologic and non-immunological factors being involved.The immunological factors have been discussed extensively in other articles.This review focuses mainly on the arterial remodeling that occurs in 3 layers of vessel walls including intimal injury,accumulation of smooth muscle-like cells in the neointimal,medial smooth muscle cell apoptosis,adventitial fibrosis,and deposition of extracellular matrix.

Relationship between coronary arterial remodeling and clinical presen tation

To examine the relationship between coronary arterial remodeling and clinical pr esentation Methods A total of 34 patients with acute (10 with recent myocardial infarction and 24 w i th unstable angina) and 26 with stable (8 with old myocardial infarction and 18 with stable angina) coronary syndrome underwent intravascular ultrasound (IVUS) before intervention Target lesions were classified as soft or hard plaques Q uantitative measurements of cross sectional area (CSA) of external elastic memb rane (EEM), lumen and plaque were performed at the lesion site and at the proxim al and distal reference sites Remodeling index (RI) was expressed by the ratio of EEM CSA at the lesion site to the mean EEM CSA of both proximal and distal r eference sites Positive remodeling was defined as RI>1 05 and negative remode ling as RI<0 95 Results Soft plaque was observed more frequently in acute than in stable coronary syndro me (59% vs 31%), whereas hard plaque was more common in stable coronary syndrome (69% vs 41%) ( P =0 03) The EEM CSA (15 11±2 89 mm 2 vs 13 25±3 10 mm 2, P =0 019) and plaque CSA (10 83± 2 62 mm 2 vs 9 30±2 84 mm 2, P =0 035) were significantly greater at target lesions in patients with acute r ather than stable coronary syndrome, while lumen CSA and percent area stenosis w ere similar in both groups RI was significantly higher (1 08±0 16 vs 0 95 ±0 14, P =0 002) and positive remodeling was more frequent in acute corona ry syndrome (53% vs 23%, P =0 019), whereas negative remodeling was more com mon in stable coronary syndrome (58% vs 24%, P =0 007) Conclusions The study indicates that clinical characteristics of patients with coronary arte ry disease depend largely upon underlying types of coronary arterial remodeling

Carotid remodeling of hypertensive subjects and polymorphism of the angiotensin-converting enzyme gene

Background This study was designed to investigate the relationships between changes in the structure and function of carotid arteries and angiotensin converting enzyme (ACE) gene polymorphism in Chinese hypertensive subjects. Methods Multiplex polymerase chain reaction amplification was used to evaluate the ACE gene insertion/deletion (I/D) polymorphism. High-resolution B-mode ultrasound examinations were performed to detect parameters of carotid artery remodeling. Results Intima-media thickness (IMT) was significantly different among the DD, ID and II genotypes of ACE (DD>ID>II, P <0.05). Carotid internal diameter,distensibility and stiffness were similar among the DD,ID and II genotypes of ACE ( P >0.05) in hypertensive subjects. The frequency of the DD gene and D allele of ACE were higher in patients with thickening carotid than in patients with normal carotid (70.4% vs 24.1%,and 79.5% vs 40.5%,respectively, P <0.001). In multiple stepwise regression analysis,independent risk factors for increased carotid IMT in hypertensive subjects were ACE genotypes ( P <0.001),age ( P <0.001) and carotid internal diameter ( P =0.032). Moreover,triglycerides and total cholesterol were higher in patients with the DD genotype than in those with the II genotype ( P <0.05). Conclusions The I/D polymorphism of the ACE gene was related to IMT,but not to internal diameter,distensibility and stiffness of the carotid in Chinese hypertensive subjects. ACE gene polymorphism was a main risk factor for increased carotid IMT. These results may imply that there is a link between lipid metabolism and ACE genotype polymorphism in Chinese hypertensive subjects.

Adrenomedullin and endocrine control of immune cells during pregnancy

The immunology of pregnancy is complex and incompletely understood. Aberrant immune activity in the decidua and in the placenta is believed to play a role in diseases of pregnancy, such as infertility, miscarriage, fetal growth restriction and preeclampsia. Here, we briefly review the endocrine control of uterine natural killer cell populations and their functions by the peptide hormone adrenomedullin. Studies in genetic animal models have revealed the critical importance of adrenomedullin dosage at the maternal-fetal interface, with cells from both the maternal and fetal compartments contributing to essential aspects underlying appropriate uterine receptivity, implantation and vascular remodeling of spiral arteries. These basic insights into the crosstalk between the endocrine and immune systems within the maternal- fetal interface may ultimately translate to a better understanding of the functions and consequences of dysregulated adrenomedullin levels in clinically complicated pregnancies.