Biomedical Research ; Heart Rate ; Humans ; Pneumoconiosis ; physiopathology

Objective To study the mechanism of restenosis following percutaneous transluminal coronary angioplasty(PTCA),and to replicate a dynamic model of cell proliferation and remoulding of vascular wall at different time points in rabbits after intimal injury.Methods The model of restenosis in common carotid artery was established by balloon injury in 70 rabbits.The indexes such as lumen area,thickness and area of intima and media,and cross sectional area bounded by the external elastic lamina(EELA) were respectively measured by computer image analysis technology at the 1st,3rd,5th, 7th,14th,28th and 35th day after the injury.Results Endothelial cells were denudated at the 1st day after injury.The proliferation of vascular smooth muscle cell(VSMC) was detected on the surface of lumen at 3 days after injury.At the 7th day after injury,the neointima was formed and continuously thicken.The thickness and area of the neointima as well as extracellular matrix were gradually increased after 14 days,and were maximal after 35 days.The thickness and area of media were also gradually increased during 3～14 days and decreased after 28 days.Compared with non-injured vessel,the medial area was obviously increased at the 14th day.The lumen area was decreased at the 5th～7th day after injury and was obviously less than that of non~injured vessel after 14 days.The EELA was gradually increased at the 1st～7th day after injury,and reached its maximum at the 14th day.The EELA was declined gradually after 28 days.Conclusion The progress of restenosis(RS) can be simulated through the model of restenosis in common carotid artery of rabbit established by balloon injury.The intimal proliferation and vascular remodeling are the leading pathogenesis of restenosis.

Objective To study the application of individualized dressing change on tumor patients with PICC. Methods We made different methods of dressing change in accordance with the status of the patients and the seasons, and observed the color and the integrity of the local skin around the puncture points. Results With the exception of 2 cases requested extubation because of tetter on skin around the puncture point, the local skin infection or systemic infection didn't occur in the other 97 cases by individualized dressing change. Conclusions It can reduce the rate of local infection, extends time of catheter retaining, and improves quality of life of tumnor patients with PICC by individualized dressing change

To examine the protective effect of insulin on reoxygenation-induced injury and explore the underlying mechanisms, the model of anoxia/reoxygenation (A/R) injury was established by inducing anoxia for 2 h and reoxygenation for 4 h in cultured cardiomyocytes of neonatal rats. The rats were randomized to four groups receiving vehicle, insulin, LY294002, insulin plus LY294002at the onset of reoxygenation after 2 h of anoxia. At the end of reoxygenation of 4 h, activity of lactate dehydrogenase (LDH) and content of malondialdehyde (MDA) were spectrophotometrically determined, apoptosis of cardiomyocytes were detected by using TUNEL and DNA Ladder, and Western blotting was employed to examine the expression of phosphorylated Akt in all groups. Our results showed that compared with vehicle-treated group, activities of LDH, contents of MDA, apoptosis index (AI) were significantly decreased, and expression of phosphorylated Akt was in creased significantly in insulin-treated group. However, changes in LDH, MDA, AI and phospho rylated Akt resulting from insulin were attenuated or abolished by LY294002 (PI3K inhibitor).These data strongly suggest that early administration of insulin at reoxygenation protects cardiomyocytes from reoxygenation-induced apoptosis through PI3K/Akt signaling pathway.