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Basic science: Experiment research
e0215 Enhanced external counterpulsation protects vascular endothelial cells from apoptosis in hypercholesterolemic pigs
  1. Yan Xiong
  1. Division of Emergency Medicine, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China


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 three 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 enhanced external counterpulsation (HC, HC+EECP, n=6, respectively). Pigs in the HC+EECP group were treated with EECP for 2 h every other day for a total of 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 whereas the abdominal aortas were stained in Sudan-III of fatty streak for macroscopic evaluation. Meanwhile, vascular endothelial cells (VECs) were isolated from the thoracic aorta by the use of collagenase. TUNEL method was used to detect the apoptotic index of VECs. At the same time, the abdominal aortas were collected for histopathological studies.

Results Fatty streaks or plaques, positively stained by Sudan dye, were hardly found in the normal group but clearly observable in the HC group. And among the cholesterol-diet animals, atherosclerotic lesions were much less severe in the EECP group than in the HC group. Scanning electronic microscopic 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. Transmission electronic microscopic 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. Nonetheless, these changes were relatively mild in EECP-treated animals. Meanwhile, 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 vascular endothelial cells 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.

  • Atherosclerosis
  • endothelial cell
  • apoptosis
  • enhanced external counterpulsation

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