By using streptozotocin-induced diabetic rats as a studied model, our previous experimental results have indicated that daily oral feeding of garlic extract (100 mg/kg BW) could increase the cardiovascular functions in streptozotocin (STZ) rats; the abnormality of lipid profile was prevented; and garlic extract could increase fibrinolitic activities with the decrease of platelet aggregation. Moreover, the plasma insulin level was increased concomitantly with the decrease of plasma glucose level. However, due to the high incidence of atherosclerosis in diabetes, the present study has been continued for further investigation of the effect of garlic extract on the coronary vascular ultrastructural changes. In addition, to identify the possible mechanism(s) of garlic's therapeutic effects, the cyclooxygenase inhibitor, aspirin, has been included in this present study. By using transmission electron microscopic studies, 16 weeks of daily oral feeding of garlic extract (100 mg/kg BW) caused as an antiatherosclerotic agent at the coronary arteriolar (15-30 microns) wall in STZ-rats. Interestingly, the thickening of coronary capillary (5-10 microns) basement membrane also was significantly attenuated within the group of STZ-rats treated with garlic extract. However, the possible direct action of garlic through the cyclooxygenase pathway has not been confirmed by the results of aspirin: The daily oral feeding of aspirin (10 mg/kg BW) in 16-week STZ-rats has not showed reduced arteriolar vascular wall abnormalities. The irregular patterns of fiber matrix, arranging the basement membrane at the arteriolar walls, were still recognized in the same manner as in STZ-rats. Interestingly, the thickening of the capillary basement membrane occurred in 16-week STZ-rats seems to be attenuated by the aspirin received. At present, garlic extract may open the new era in the medicinal use of garlic to prevent diabetic cardiovascular complications.

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PubMedDate not supplied

Comparison of the effects of mechanical stimulation on venous and arterial smooth muscle cells in vitro.

The proliferation of intimal smooth muscle cells (SMCs) in large muscular arteries and veins often occurs after surgical interventions such as angioplasty and bypass grafting, and may lead to restenosis and graft failure. Clinical observations suggest that increased pulsatile deformation of veins grated into an arterial position may play a role in intimal hyperplasia. Since intimal hyperplasia occurs at the vein/arterial interface of the graft, SMC hyperplasia could be due to the proliferation of either aortic or venous SMCs. Therefore, we compared the effects of in vitro mechanical deformation on the proliferation of aortic SMCs with venous SMCs. Using the Flexercell apparatus (Flexercell Corp., McKeesport, Pa., USA), aortic SMCs, stretched at 3 and 60 cpm did not lead to a significant increase in growth as compared to the nonstretched controls. In contrast, stretch of venous SMCs at 3 and 60 cpm led to a significant increase in growth as compared to the nonstretched controls. These results suggest that the SMC proliferation, as occurs in vein interposition grafts in vivo, may be partially due to a stimulatory response by venous SMCs to increased mechanical stimulation.

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