Vural Murat, Cosan T Erhan, Ozbek Zuhtu, Cosan Didem, Sahin Fezan, Burukoglu Dilek
Department of Neurosurgery, Medical Faculty, Eskisehir Osmangazi University, Dede Mah. Alp Konutlari, Alp-4, D-Blok, Daire-2, Eskisehir, Turkey.
Acta Neurochir (Wien). 2009 Sep;151(9):1135-41. doi: 10.1007/s00701-009-0391-5. Epub 2009 May 13.
Vasospasm is a significant reason for poor clinical outcome in subarachnoid haemorrhage (SAH). One of the possible causes of vasospasm is attributed to the inhibition of Na(+)/K(+)-ATPase and increased intracellular calcium. Although digoxin, a cardiac glycoside (CG), inhibits the Na(+)/K(+)-ATPase, diverse and contradictory biological actions of CGs have also been reported. This study aimed to investigate the effect of digoxin on an experimental vasospasm after subarachnoid haemorrhage (SAH) in rats.
The rats used in the study were divided into normal, saline, SAH, and drug groups. A double-haemorrhage method was applied for the SAH groups. Normal saline or blood samples were injected into the cisterna magna. No surgical procedures were performed on the normal group. For the drug groups, daily digoxin was administered intraperitoneally after saline or blood injections. On days 3 and 7 after injections, the brains and basilar artery sections of all the groups were prepared for light-microscopic examination. The wall thickness and luminal area of the basilar artery were calculated by using medical imaging software.
Increased wall thickness and reduced vessel luminal area were conspicuously significant in the SAH groups which did not receive digoxin. In SAH groups after digoxin administration, the vessel wall thickness decreased, and no significant change was found in vessel wall thickness when compared with the normal and saline groups. The vessel luminal area was not reduced in SAH after digoxin administration.
These results suggest that digoxin administration in experimental SAH may have a beneficial effect on the protection against vasospasm. If further investigations support our results, the present study may offer a new insight into the treatment of SAH.
血管痉挛是蛛网膜下腔出血（SAH）临床预后不良的重要原因。血管痉挛的可能原因之一是钠钾ATP酶受抑制及细胞内钙增加。虽然地高辛这种强心苷（CG）可抑制钠钾ATP酶，但也有报道称CG具有多种相互矛盾的生物学作用。本研究旨在探讨地高辛对大鼠蛛网膜下腔出血（SAH）后实验性血管痉挛的影响。
研究中使用的大鼠分为正常组、生理盐水组、SAH组和药物组。SAH组采用双次出血法。将生理盐水或血液样本注入大鼠脑池。正常组未进行手术操作。对于药物组，在注射生理盐水或血液后每天腹腔注射地高辛。在注射后第3天和第7天，对所有组的大脑和基底动脉切片进行光镜检查。使用医学成像软件计算基底动脉的壁厚和管腔面积。
未接受地高辛的SAH组中，壁厚增加和管腔面积减小显著。给予地高辛后的SAH组中，血管壁厚降低，与正常组和生理盐水组相比，血管壁厚无显著变化。给予地高辛后，SAH组的血管管腔面积未减小。
这些结果表明，在实验性SAH中给予地高辛可能对预防血管痉挛有有益作用。如果进一步的研究支持我们的结果，本研究可能为SAH的治疗提供新的见解。
