• Daniela Canova, Silvestro Roatta, Giuseppe Micieli, and Daniele Bosone.
• Neurovascular Laboratory, C. Mondino National Institute of Neurology, IRCCS, Pavia, Italy. daniela.canova@unito.it
• Funct Neurol. 2012 Jul 1; 27 (3): 169-76.

AbstractThe cerebrovascular effects of nimodipine are still poorly understood even in the healthy condition; in particular, its effects on tissue oxygenation have never been investigated. The aim of the present study was to investigate changes in cerebral oxygenation and blood volume upon oral administration of nimodipine (90 mg) in the healthy condition. In eight subjects, changes in cerebral tissue oxygenation and blood volume were determined simultaneously with changes in blood velocity of the middle cerebral artery (VMCA) by using, respectively, near infrared spectroscopy (NIRS) and transcranial Doppler ultrasonography (TCD). The subjects also underwent noninvasive assessment of arterial blood pressure (ABP) and end-tidal CO2. TCD and NIRS CO2 reactivity indices were al-so extracted. Nimodipine significantly reduced ABP (11±13%) and increased heart rate, as well as NIRS oxygenation(6.0±4.8%) and blood volume indices (9.4±10.1%), while V(MCA) was not significantly decreased (2.0±3.5%). Nimodipine slightly but significantly reduced the V(MCA) response to changes in pCO2 whereas the CO2 reactivity of NIRS parameters was improved. The observed changes in cerebral tissue oxygenation and blood volume indicate nimodipine-induced cerebrovascular dilation and increased perfusion, while the effect on V(MCA)possibly results from dilation of the insonated artery. The present results cast doubt on the putative nimodipine-induced impairment of CO2 reactivity.

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