Abstract

Increased water T 2 values indicates the presence of vasogenic edema. Decreased apparent diffusion coefficient (ADC) maps reveal ischemic areas displaying cytotoxic edema. ADC and T 2 abnormalities spread through the middle cerebral artery (MCA) territory up to 24 h after middle cerebral artery occlusion (MCAO). Also, it was found that ADC and T 2 contours closely match at 3.5 and 24 h. Since butanediol reduces vasogenic edema and improves energy status in various models of ischemia, we used these two techniques to investigate putative improvements in cytotoxic and vasogenic edema after permanent MCAO performed on rats. Rats were given no treatment ( n = 8), or a treatment with 25 mmol/kg intraperitoneal (i.p.) butanediol ( n = 5), 30 min before and 2.5 h after MCAO. Quantitative ADC and T 2 maps of brain water were obtained, from which the volumes presenting abnormalities were calculated at various time points up to 24 h. Effects of butanediol on the ADC and T 2 values in these areas were determined. Butanediol reduced neither the ADC volume nor the initial ADC decline. However, it reduced T 2 volumes by 32% at 3.5 h and 15% at 24 h ( p < 0.05), and reduced T 2 increase in the striatum at 3.5 h post-MCAO. Therefore, our results show for the first time that a pharmacological agent such as butanediol can delay the development of vasogenic edema but does not limit the development of vasogenic edema but does not limit the development of cytotoxic edema. ADC imaging detects areas of severe metabolic disturbance but not moderately ischemic peripheral areas where butanediol is presumed to be more efficacious.

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