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Turkish Neurosurgery 2018

The Effects of Proanthocyanidin on Vasospasm After Experimental Subarachnoidal Hemorrhage in Rats.

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پیوند در کلیپ بورد ذخیره می شود
Cem Yilmaz
Tufan Cansever
Atilla Kircelli
Ozlem Isiksacan Ozen
Fatih Aydemir
Aykan Akar
Hakan Caner

کلید واژه ها

خلاصه

OBJECTIVE

Delayed ischemic neurological deficit (DIND) and cerebral vasospasm (CV) remain the most common and debilitating neurological complications following aneurysmal subarachnoidal hemorrhage (SAH). Many reports demonstrate the importance of proanthocyanidins (PR) on the vascular system, including endothelium-dependent relaxation of blood vessels. These effects of PR on the cerebral vascular system were examined in this study. < p < MATERIAL and METHODS: Fifty-two adult Sprague-Dawley male rats were used for the experimental double hemorrhage model. They were divided to control, sham, pre- and post-interventional treatment groups. 100 mg/kg PR was administered for the treatment for respect to groups. Basilar artery diameter (BAD) and arterial wall thickness were measured and the apoptosis ratio of the endothelial cells was calculated. Arterial walls were examined electron microscopically (EM).

RESULTS

There were significant differences between the groups except control and pre-SAH (p=0.37) and post-SAH and pre- SAH groups (p=0.15) with respect to BAD. According to arterial wall thickness, apoptosis ratio, and grading, there were significant differences between the groups except control and pre-SAH (p=0.85, p=0.49 and p=0.18 respectively) and SAH and post-SAH (p=0.08, p=0.21 and p=0.24 respectively) groups. EM findings revealed that pro-apoptotic and pro-necrotic degenerated endothelial cells with seldom vacuolization in post-SAH treatment group which were more serious in SAH group.

CONCLUSIONS

Pre-SAH administration of PR induces better vasodilatation and protection of basilar artery (BA) from vasospasm (VS), which could yield neuroprotective and vasodilatator effects. In addition, PR appears to be involved in relieving oxidative damage, with an antioxidant-antiapoptotic-antinecrotic effect that may contribute to vascular dilation.

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