Objective Evidences have proved that Enhanced external counterpulsation (EECP) improves endothelial dysfunction and repairs intimal damage by increasing vascular endothelial shear stress. Based on the assumption that unbalanced apoptosis of vascular endothelial cells (VECs) may have played a pivotal role in the pathogenesis of atherosclerotic lesions, we hypothesised that long-term EECP protects VECs from apoptosis in hypercholesteronlemic pigs.
Methods 18 male domestic pigs were randomly assigned to 3 groups: one normal control group with a normal diet (Normal, n=6) and two hypercholesterolemic groups (HC, n=12) fed with atherosclerosis-inducing cholesterol-rich chow diet, one of which received EECP (HC, HC+EECP, n=6, respectively). Pigs in the HC+EECP group were treated with EECP for 2 h every other day for 36 h. In the end of the study, the animals were sacrificed, and the thoracic and abdominal aortas harvested. The thoracic aortas were sampled for both scanning and transmission electronic microscopy (SEM and TEM)whereas the abdominal aortas were stained in Sudan-III of fatty streak for macroscopic evaluation. Vascular endothelial cells (VECs) were isolated from the thoracic aorta by collagenase. TUNEL was used to detect the apoptotic index of VECs. The abdominal aortas were collected for histopathological studies.
Results Fatty streaks or plaques were hardly found in the normal group but clearly observable in the HC group. Atherosclerotic lesions were much less severe in the EECP group than in the HC group. SEM analysis revealed that aortic VECs were irregularly arrayed, markedly desquamated, and shrank into smaller size, which indicated apoptotic events resulting in remarkable damage of endothelium in HC group. In contrast, the VECs in HC+EECP group were arrayed in a relatively streamline fashion, less desquamated and shrank, and manifested comparatively mild endothelial damage. TEM examination of aortas in HC group showed desquamated VECs loosely attached to the matrix along with foam cells, which indicated intimal damage. Apoptotic VECs at early, middle, late stage and even apoptotic bodies were visible on intimal surface. But these changes were relatively mild in EECP-treated animals. The apoptotic index in the HC+EECP group was significantly lower than that of the HC group, but still higher than that of the Normal group ((177±12)%, (237±23)%, (127±36)%, respectively, p<0.05).
Conclusions EECP alleviates hypercholesterolaemia-induced atherosclerotic damage to the vascular intima and endothelium, and protects VECs from apoptosis, thereby delaying the progression of early atherosclerotic lesions. The therapeutic benefit of EECP in terms of endothelial protection may be attributed to the inhibition of VEC apoptosis.
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