Effects of Enhanced External Counterpulsation on Plasma ET, MDA, and SOD Levels in Patients with Acute Cerebral Infarction
Authors
Zhu Wenbing, Niu Jingzhong, Xu Jianmin, Wang Jiansheng
Zhongshan Hospital, Affiliated to Shanghai Medical University
Source: usecp.com (Compiled, reviewed, and organized by Dr Gong)
Abstract
Objective: To investigate the therapeutic mechanism of Enhanced External Counterpulsation (ECP) in cerebral infarction by measuring changes in plasma endothelin (ET), malondialdehyde (MDA), and superoxide dismutase (SOD) levels before and after treatment.
Methods: Twenty patients with acute cerebral infarction were treated with ECP and compared to a control group of 22 patients receiving conventional pharmaceutical therapy.
Results: Following treatment, the ECP group showed a significant decrease in ET and MDA levels and a significant increase in SOD activity (P<0.05), with improvements exceeding those of the control group.
Conclusion: ECP effectively intervenes in the pathological process of acute cerebral infarction, reducing oxidative stress damage and protecting vascular endothelial function.
Materials and Methods
1. Study Subjects
ECP Group: 20 patients (14 males, 6 females); age range 47–77 years, mean age 65.40±8.43 years.
Control Group: 22 patients (13 males, 9 females); age range 48–79 years, mean age 67.77±7.66 years.
Inclusion Criteria: All cases were confirmed as cerebral infarction of the internal carotid artery system via head CT or MRI.
2. Treatment Protocols
Both groups received baseline oral therapy including Vitamin B1 and Piracetam.
ECP Group: Utilized a US-ECP counterpulsator with a cuff pressure of 0.45 kg/cm2. Treatment was administered 1 hour daily for a 12-day course. Additionally, 500 mL of low-molecular-weight dextran was administered intravenously daily.
Control Group: Received only the daily intravenous infusion of 500 mL low-molecular-weight dextran for 12 days.
3. Measurement Indices and Methods
Plasma ET: Measured via radioimmunoassay.
Serum MDA: Measured via Yagi's fluorescence method (test kits from Nanjing Jiancheng Bioengineering Institute).
Serum SOD: Measured via xanthine oxidase method using a Japanese-made Model 751 UV spectrophotometer (test kits from Nanjing Jiancheng).
Results
Before treatment, both groups exhibited plasma ET and MDA levels above normal values, while SOD activity was below normal. Post-treatment, both groups showed improvement, but the ECP group demonstrated superior efficacy in enhancing antioxidant capacity and reducing vasoconstrictive substances.
Table 1. Comparison of ET, SOD, and MDA Levels Before and After Treatment (xˉ±s)
| Group | n | Phase | ET (pg/ml) | SOD (Nu/ml) | MDA (nmol/ml) |
|---|---|---|---|---|---|
| ECP | 20 | Pre-treatment | 87.89±28.89 | 79.15±20.43 | 5.19±1.50 |
| Post-treatment | 79.69±38.44∗ | 90.19±24.57∗ | 4.05±1.57∗ | ||
| Control | 23 | Pre-treatment | 88.66±43.19 | 81.48±38.42 | 5.37±1.53 |
| Post-treatment | 82.24±44.91 | 90.04±27.89 | 4.17±1.71∗ |
Note: ∗ denotes P<0.05 compared to the same group before treatment.
Correlation Analysis: Statistical analysis showed that plasma ET content was positively correlated with MDA content and negatively correlated with SOD activity.
Discussion and Conclusion
1. Impact on Oxidative Stress Damage
MDA is the end product of lipid peroxidation, reflecting the degree of tissue attack by free radicals. Conversely, SOD is a primary antioxidant enzyme responsible for scavenging free radicals. This study found that ECP treatment significantly reduced MDA levels while increasing SOD activity, suggesting that ECP enhances the body’s ability to clear free radicals and mitigates reperfusion injury or oxidative stress caused by persistent ischemia.
2. Vascular Endothelial Function and Vasospasm
Endothelin (ET) is a potent vasoconstrictive peptide; elevated levels following cerebral infarction can exacerbate vasospasm and neural damage. The ECP group showed a more pronounced decrease in ET, indicating that counterpulsation improves blood supply to the ischemic zone through hemodynamic changes, thereby reducing endothelial damage and the subsequent release of ET.
3. Association Between ET and Free Radicals
The positive correlation between ET and MDA suggests that elevated endothelin may exacerbate pathological progression by promoting free radical generation. The multi-targeted intervention of ECP—reducing endothelin levels while simultaneously increasing SOD activity—is a core mechanism for its efficacy in acute cerebral infarction.
Conclusion
Enhanced External Counterpulsation (ECP) exerts significant biochemical effects in the treatment of acute cerebral infarction by effectively regulating ET, MDA, and SOD levels. The therapy is safe, lacks significant side effects, and holds substantial clinical value for broader application.