| Background The mortality and disability incidence of acute cerebral infarction was high and accounted for 75 percent of ischemic vascular diseases, which has severely threatened personal health and life quality for its. Early diagnosis and treatment was important to prognosis. And It was necessary to assess whether the ischemic penumbra (IP) was present. The purpose in our study is to determine the value of MR diffusion weighted imaging (DWI) and diffusion tensor imaging (DTI) on IP of rat middle cerebral artery occlusion (MCAO) model.Materials and Methods Ninety mature male Wistar rats were randomly divided into three groups, pseudo-operative group (n=5), permanent ischemia group and neuroprotective additive group respectively. MCAO model was made by modified Zea-Longa method. In neuroprotective additive group, scutellarin was injected with 3ml/kg by caudal vein 1.5h after model successfulness.MR imaging was performed with GE 1.5T Twin Speed Infinity with Excite I magnetic resonance system. Three inch surface coil was used. The sequences included axial DWI, DTI and T2WI. The examination time was 0.5h, 1h, 2h, 3h, 4h, 5h, 6h, 9h, 12h, 15h, 18h, 21h, 24h and 48h in permanent ischemia group, but 2h, 3h, 4h, 5h, 6h, 24h and 48h in neuroprotective additive group.Four region of interest (ROI) were measured. Point 1, 2 and 3 were located within the high signal intensity region on DWI. Point 1 was infarct core, Point 3 was infarct margin, and Point 2 was the midpoint between Point 1 and 3. Point 4 demonstrated normal signal intensity just adjacent to high signal intensity on DWI.Parameters measured included apparent diffusion coefficient (ADC), average diffusion coefficient (DCavg), fractional anisotropy (FA), relative anisotropy (RA) and volume ratio (VR). The relative ratios between infarct lesions and collateral normal brain were calculated. Statistical analysis was performed by SPSS 11.0 software package. Differences were considered statistically significant at P less than 0.05. The rats were decapitated after MRI examination, and HE pathologic stain were performed. Results(1) The evolution of rADCThe evolution of rADC was similar in permanent ischemia group and neuroprotective additive group. The rADC of Point 1 was lower than 1 at all time, remarkably reduced at 3h, slightly elevated at 9h and then declined. The rADC of Point 2 and 3 was lowest at 3h. There was no peak of rADC of Point 4.In permanent ischemia group, there were significant differences of rADC between Point 1 and 2 within 3h, Point 1 and 3 within 12h, Point 2 and 3 from 4h to 12h (P<0.05). There were significant differences between Point 4 and 1 at all time, among Point 4 with Point 1, 2 and 3 after 15h (PO.05).In neuropretective additive group, there were significant differences of rADC between Point 1 and 2, Point 1 and 3, Point 1 and 3, Point 1 and 4, Point 2 and 4, Point 3 and 4 within 6h and at 24h (PO.05).None were significantly different between permanent ischemia group and neuroprotective group within 2h, at 24h and 48h (P>0.05). The rADC of neuroprotective additive group significantly differed from those of permanent ischemia group during 3h6h (PO.05).(2) The evolution of rDCavgThe evolution of rDCavg was similar to rADC in permanent ischemia group. In neuroprotective additive group, rDCavg of Point 1, 2 and 3 was lower than 1 at alltime and was lowest in Point 1. It slightly elevated at 4h and then declined at 24h. The rDCavg of Point 4 decreased unremarkably.In permanent ischemia group, there were significant differences of rDCavg between Point 1 and 2 within 3h, Point 1 and 3 within 12h, Point 2 and 3 from 4h to 15h(P<0.05).In neuropretective additive group, there were significant differences of rDCavg between Point 1 and 4, Point 2 and 4 at all time, Point 2 and 3 from 2h to 5h, Point 1 and 3 from 2h to 48h (P<0.05).None were significantly different between permanent ischemia group and neuroprotective group within 2h and at 48h (P>0.05). The rDCavg of neuroprotective additive group significantly differed from those of permanent ischemia group during 3h24h (PO.05).(3) The evolution of rFAIn permanent ischemia group, FA was higher than normal after lh, and lower than normal after 9h in Point 1, 2 and 3. FA of Point 3 was sudden higher than normal at 12h. FA of Point 4 had no obvious change. In neuroprotective additive group, rFA of Point 1 was higher than 1 at 3h and 5h, but lower than 1 at 4h and 48h. FA of Point 2 and 3 increased after lh, decreased after 4h, and was similar to that of Point 1 at 48h. FA of Point 4 had no obvious change.In permanent ischemia group, none of rFA were significantly different before 4h (P>0.01). There were significant differences of rFA between Point 2 and 3, Point 3 and 4 from 4h to 24h, between Point 1 with Point 2, 3 and 4 after 9h (PO.01).In neuropretective additive group, all of rFA were significantly different except those between Point 2 and 3 before 2h, Point 1 and 2 after 24h (PO.01).Between permanent ischemia group and neuroprotective group, there significant difference between Point 2 and 3 at all time, Point 1 and 2 during 3h6h and at 48h, Point 1 and 3 at 24h (PO.05).Conculsion(1) With the development of infarct lesions, the range of IP decreased progressively from core to periphery. The necrosis region was mainly located in the infarct core. After 4h, the necrosis region extended to Point 2, and IP was located between Point 2 and 3. After 12h, the necrosis region extended to Point 3, and IP disappeared.(2) In neuroprotective additive group, IP was present between Point 2 and 3 within 6h, and could be prolonged to 24h.(3) Within 4h, FA was higher than normal, suggesting the presence of cytotixic edema. With the occurrence of vasogenic edema, FA declined, corresponding with the change of ADC and DCavg.(4) In hyperacute stage of ischemia, ADC and DCavg showed transient pseudo-normalization. In permanent ischemia group, the time was 9h, but in neuroprotective group the time was earlier, suggesting cytotoxic edema attenuated.(5) The sensitivity of anisotropy was lower than that of isotropy because of small ROI and arrangement of nerve tract.Key Words: Brain Ischemia;Magnetic Resonance Imaging;Ischemic Penumbra;Neuroprotective Additive;Experimental Study;Animal... |