Validity of D-penicillamine in experimental cerebral vasospasm therapy

IF 0.4 Q4 CLINICAL NEUROLOGY Interdisciplinary Neurosurgery: Advanced Techniques and Case Management Pub Date : 2023-11-28 DOI:10.1016/j.inat.2023.101917

Ersin Haciyakupoglu , Evren Yüvrük , Sebahattin Haciyakupoglu , Milos Arsenovic , Erol Akgül , Dervis Mansuri Yilmaz , Sait Polat

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Abstract

Background

Cerebral vasospasm is a reversible vessel constriction following subarachnoid hemorrhage. Immunoreactive and inflammatory mechanisms induce long-term vasoconstriction and vessel dilatation inhibition. We hypothesized that D-penicillamine depresses this process given that it reduces the concentration of free oxygen (O₂) radicals. We evaluated the effects of D-penicillamine on cerebral vasospasm in rabbits induced with subarachnoid hemorrhage, achieved by autologous blood injection in the basal cistern.

Materials and methods

Four experimental groups were studied: Group 1: basilar angiography, Group 2: basilar angiography + D-penicillamine, Group 3: subarachnoid hemorrhage (SAH), and Group 4: SAH + D-penicillamine. Vessel diameter and cerebral vasospasm were evaluated angiographically in each group. Vascular degeneration was studied by electron microscopy of the basilar artery. Free O₂ radicals were investigated based on measurements of the levels of vascular superoxide dismutase and malondialdehyde. Myasthenia gravis–like side effects of D-penicillamine application were analyzed by electromyography and electron microscopy of the orbicularis oculi muscle.

Results

We detected a 9.03% decrease in basilar artery constriction in Group 4 compared with Group 3. In addition, levels of free O₂ radicals were reduced in Groups 2 and 4. Application of D-penicillamine resulted in the prevention of basilar artery wall degeneration, without myasthenia gravis–like side effects.

Conclusion

Our study indicated that D-penicillamine application induced vasodilatation and had anti-inflammatory effects.

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d -青霉胺在实验性脑血管痉挛治疗中的有效性

背景:脑血管痉挛是蛛网膜下腔出血后可逆的血管收缩。免疫反应和炎症机制诱导长期血管收缩和血管扩张抑制。我们假设d -青霉胺抑制这一过程，因为它降低了游离氧(O2)自由基的浓度。本研究通过自体基底池注血，观察d -青霉胺对兔蛛网膜下腔出血所致脑血管痉挛的影响。材料与方法实验分为四组:第一组:基底动脉造影，第二组:基底动脉造影+ d -青霉胺，第三组:蛛网膜下腔出血，第四组:SAH + d -青霉胺。各组血管造影检查血管直径和脑血管痉挛情况。电镜观察基底动脉血管变性。通过测量血管超氧化物歧化酶和丙二醛的水平来研究游离氧自由基。采用眼轮匝肌肌电图和电镜分析d -青霉胺应用后的重症肌样副作用。结果与3组相比，4组基底动脉收缩减少9.03%。此外，第2组和第4组的自由基水平均有所降低。应用d -青霉胺可预防基底动脉壁变性，无重症肌无力样副作用。结论应用d -青霉胺可使大鼠血管舒张，具有抗炎作用。

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