Figure 6
Figure 6. Influence of RNase on brain edema in a stroke model in rats. Middle cerebral artery occlusion was induced in rats using the endovascular suture occlusion technique. Prior to occlusion, animals were pretreated with either saline (control), RNAse, or DNase, respectively. (A) Hemispheric brain water content was measured using a wet-dry method, and the increase of brain water content of the ischemic hemisphere in relation to lesion volume was calculated (edema-lesion ratio); values represent the mean (± SEM; n = 10 in each animal group). (B) Ischemic lesion/infarct volume was determined by MRI (expressed as percentage of the volume of the hemisphere); values represent the mean (± SEM; n = 10 in each animal group). (C) To follow vescular leakage, Evans Blue extravasation following transient middle cerebral artery occlusion for 90 minutes was analyzed in the infarcted area (□) and in the corresponding contralateral hemisphere (■). Values represent the mean (± SEM; n = 5) in each panel. *P < .05.

Influence of RNase on brain edema in a stroke model in rats. Middle cerebral artery occlusion was induced in rats using the endovascular suture occlusion technique. Prior to occlusion, animals were pretreated with either saline (control), RNAse, or DNase, respectively. (A) Hemispheric brain water content was measured using a wet-dry method, and the increase of brain water content of the ischemic hemisphere in relation to lesion volume was calculated (edema-lesion ratio); values represent the mean (± SEM; n = 10 in each animal group). (B) Ischemic lesion/infarct volume was determined by MRI (expressed as percentage of the volume of the hemisphere); values represent the mean (± SEM; n = 10 in each animal group). (C) To follow vescular leakage, Evans Blue extravasation following transient middle cerebral artery occlusion for 90 minutes was analyzed in the infarcted area (□) and in the corresponding contralateral hemisphere (■). Values represent the mean (± SEM; n = 5) in each panel. *P < .05.

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