Metabolic fingerprints discriminating severity of acute ischemia using in vivo high‐field ¹H magnetic resonance spectroscopy

Abstract

Despite the improving imaging techniques, it remains challenging to produce magnetic resonance (MR) imaging fingerprints depicting severity of acute ischemia. The aim of this study was to evaluate the potential of the overall high‐field 1H MR Spectroscopy (1H‐MRS) neurochemical profile as a metabolic signature for acute ischemia severity in rodent brains. We modeled global ischemia with one‐stage 4‐vessel‐occlusion (4VO) in rats. Vascular structures were assessed immediately by magnetic resonance angiography. The neurochemical responses in the bilateral cortex were measured 1 h after stroke onset by 1H‐MRS. Then we used Partial‐Least‐Squares discriminant analysis on the overall neurochemical profiles to seek metabolic signatures for ischemic severity subgroups. This approach was further tested on neurochemical profiles of mouse striatum 1 h after permanent middle cerebral artery occlusion, where vascular blood flow was monitored by laser Doppler. Magnetic resonance angiography identified successful 4VO from controls and incomplete global ischemia (e.g., 3VO). 1H‐MR spectra of rat cortex after 4VO showed a specific metabolic pattern, distinct from that of respective controls and rats with 3VO. Partial‐Least‐Squares discriminant analysis on the overall neurochemical profiles revealed metabolic signatures of acute ischemia that may be extended to mice after permanent middle cerebral artery occlusion. Fingerprinting severity of acute ischemia using neurochemical information may improve MR diagnosis in stroke patients.

Amide proton transfer-weighted magnetic resonance imaging for the diagnosis of symptomatic chronic intracranial artery stenosis: a feasibility study

“…Low pH in cells may cause tissue damage by activating destructive enzymes such as proteases and lipases (12). Previous APTw and MRS studies (46)(47)(48) have confirmed an increase in lactic acid, a decrease in MTR asym , and neuron damage in the acute infarction area. With the increase in the ischemic injury time, the acidification gradually eased and the pH increased.…”