Hemodynamic evolution of acute focal ischemia

• Applicant: Dr. Ulrike Hoffmann
• Subject Area: Cognitive, Systems and Behavioural Neurobiology
• Term: from 2008 to 2011
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 78866432

Within the healthy brain, neurons, glia and blood vessels form a “neurovascular unit” that adapt cerebral blood flow (CBF) to functional and metabolic demands. During focal cerebral ischemia an “inverse (i. e., vasoconstrictive) neurovascular coupling” [15] has been observed: anoxic depolarization (AD) and subsequent recurrent periinfarct spreading depolarizations (PID´s) are accompanied by vasoconstriction. Thereby, PID’s may cause step-wise reductions in blood flow and expansion of the compromised territory [37]. However, the sequence of causality is not fully clear [42]. In the present study I will use the mouse model of distal middle cerebral artery occlusion (dMCAO). I will monitor CBF, oxygen availability, [K+]e , [Ca2+]e, volume of the extracellular space (ECV), and DC potential in order (i) to characterize the time course, degree, and spatial distribution of episodic hypoperfusions accompanying AD and PID´s, (ii) to determine whether and how episodic hypoperfusions are linked to changes in ECV, cerebral blood volume (CBV) and oxygenation, (iii) to study the spatio - temporal relationship between episodic hypoperfusion and ischemic depolarizations and (iv) to show the extent to which number, degree, and duration of PID’s as well as spatial dimensions of the hypoperfusion imaged by laser speckle flowmetry (LSF) correspond to tissue outcome at 12h-7d after dMCAO.

• DFG Programme: Research Fellowships
• International Connection: USA
• Host: Professor Michael Moskowitz