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Updated: Jul 17, 2025
A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage
Published on: July 28, 2018
Nimodipine Reduces Microvasospasms After Experimental Subarachnoid Hemorrhage
Julian Schwarting1,2,3,4, Biyan Nathanael Harapan1,3,4, Xiangjiang Lin1,4
1Institute for Stroke and Dementia Research (ISD) (J.S., B.N.H., X.L., N.P., N.A.T.).
Background:
The only established pharmacological treatment option improving outcomes for patients suffering from subarachnoid hemorrhage (SAH) is the L-type-calcium channel inhibitor nimodipine. However, the exact mechanisms of action of nimodipine conferring neuroprotection after SAH have yet to be determined. More recently, spasms of the cerebral microcirculation were suggested to play an important role in reduced cerebral perfusion after SAH and, ultimately, outcome. It is unclear whether nimodipine may influence microvasospasms and, thus, microcirculatory dysfunction. The aim of the current study was, therefore, to assess the effect of nimodipine on microvasospasms after experimental SAH.
Methods:
Male C57Bl/6 N mice (n=3-5/group) were subjected to SAH using the middle cerebral artery perforation model. Six hours after SAH induction, a cranial window was prepared, and the diameter of cortical microvessels was assessed in vivo by 2-photon-microscopy before, during, and after nimodipine application.
Results:
Nimodipine significantly reduced the number of posthemorrhagic microvasospasms. The diameters of nonspastic vessels were not affected.
Conclusions:
Our results show that nimodipine reduces the formation of microvasospasms, thus, shedding new light on the mode of action of a drug routinely used for the treatment of SAH for >3 decades. Furthermore, L-type Ca2+ channels may be involved in the pathophysiology of microvasospasm formation.
