Objective: To explore the effect of long-term enhanced external counterpulsation (EECP) on morphological damage of endomembrane and endothelium-dependent vasodilatation of the carotid arteries of hypercholesterolemic pigs.
Methods: Eighteen male infant pigs were randomly divided into three groups according to the contents of their diet: the normal control group (n=6), the high-cholesterol feeding control group (n=6) and EECP group (n=6). Porcine model of hypercholesterolemia was reproduced by feeding animals with high-cholesterol diet. After completion of EECP treatment for 36 hours in EECP group, carotid arterial rings were harvested from all animals. Both scanning and transmission electron microscopy was employed to observe the changes in morphology of their endomembrane. At the same time, their vasodilatation response to variant dose of acetylcholine (Ach) was detected.
Results: The surface of endothelium in the normal control group was smooth, and endothelial cells were in regular streamline array, and they were almost in same size, attaching closely to matrix without smooth muscle cell proliferation and lipid infiltration in intima. In contrast, the endothelial cells of hypercholesterolemic pigs were in irregular array, with marked desquamation, resulting in loose linkage. Smooth muscle cells were found to invade into intimal layer and proliferated, and foam cells could also be found in intimal layer. In hypercholesterolemic pigs treated with EECP, slight intimal damage was found. In addition, with Ach dose of 10(-8) mol/L to 10(-5)mol/L, endothelium-dependent vasodilatation ratio in hypercholesterolemic pigs with or without EECP treatment, was significantly lower than that of the normal control group (all P<0.05). However, endothelium-dependent vasodilatation ratio in pigs with EECP treatment was obviously higher compared with hypercholesterolemic pigs without EECP treatment with the dosage of Ach concentration ranged from 10(-7) mol/L to 10(-5) mol/L (all P<0.05).
Conclusion: Long-term EECP ameliorates both the morphological damage and the impaired endothelium-dependent vasodilatation function resulting from hypercholesterolemia, contributing to prevention of atherosclerosis.