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Delayed Muscle Injuries in Arterial Insufficiency: Contrast-enhanced MR Imaging and 31P Spectroscopy in Rats1

Roberto M. Asperio, DVM, PhD, Elena Nicolato, PhD, Pasquina Marzola, PhD, Paolo Farace, PhD, Ernesto Lunati, PhD, Andrea Sbarbati, MD, PhD and Francesco Osculati, MD

1 From the Department of Morphological-Biomedical Sciences, Institute of Anatomy and Histology, University of Verona, Medical Faculty, Strada Le Grazie 8, 37134 Verona, Italy. Received July 25, 2000; revision requested September 7; final revision received January 22, 2001; accepted February 12. F.O. supported by Ministero dell’Università e della Ricerca Scientifica e Tecnologica grant 9805406803. Address correspondence to A.B. (e-mail: sbarbati@borgoroma.univr.it).



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Figure 1. Coronal T2-weighted multisection spin-echo MR images (2,000/60) acquired in the fifth rat in our series during the repair period in the ischemic area (arrow). A, 1 day, B, 7 days, and C, 14 days, and D, 3 months. The lesion was still detectable 3 months after ischemia induction.

 


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Figure 2. Coronal pre- and postcontrast (*) T1-weighted spin-echo MR images (100/10) acquired 24 hours (A, A*), 7 days (B, B*), 14 days (C, C*), and 3 months (D, D*) after muscle ischemia induction. T1-weighted images were acquired on the same sections as the T2-weighted images in Figure 1 before and approximately 2 minutes after contrast material administration. Gadopentetate dimeglumine strongly enhances the signal intensity of the affected area (arrows).

 


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Figure 3. Coronal dynamic contrast-enhanced T1-weighted spin-echo MR images (100/10) of the ischemic leg and the normal leg 3 months after ischemia induction. The first image was obtained before contrast material injection; the last image, after contrast material injection. The other images were obtained pixel by pixel with the formula: {Delta}SI = SI(t) - SIpre. Signal intensity enhancement started to become relevant approximately 30 seconds after injection and reached a plateau after 60 seconds. Arrows = affected area.

 


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Figure 4. Graph shows time dependence of (SIpost - SIpre) in the ischemic leg and the normal leg at different times after ischemia induction (mean ± SEM). Data were obtained in the ischemic leg 1 day ({blacklozenge}), 7 days ({blacksquare}), and 14 days ({blacktriangleup}) after ischemia induction and in the contralateral nonischemic leg ({bullet}). {ddagger} = 1 day was significantly different from the control (unpaired t test; P < .05). * = 1, 7, and 14 days were significantly different from the control (unpaired t test, P < .05). The curves obtained in the affected areas showed rapid enhancement; this was followed by a plateau after approximately 60 seconds.

 


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Figure 5. Graph shows time dependence of (SIpost - SIpre) in the ischemic leg ({blacklozenge}) and the normal leg ({blacksquare}) 3 months after ischemia induction (mean ± SEM). The time range was 0-128 seconds. {ddagger} = Three months was significantly different from the control (paired t test; P < .05). * = Three months was significantly different from the control (paired t test; P < .01). The enhancement was still substantially higher in the affected area, as compared with that in the contralateral leg.

 


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Figure 6. Graph shows time dependence of (SIpost - SIpre) in the ischemic leg ({blacklozenge}) and the normal leg ({blacksquare}) 3 months after ischemia induction (mean ± SEM). The time range was 2.8-71.8 minutes. * = Three months was significantly different from the control (unpaired t test; P < .05). # = Three months was significantly different from the control (unpaired t test; P < .01). The affected area showed enhancement substantially higher than that in the contralateral leg.

 


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Figure 7a. (a) Graph shows time dependence of the ratio (PCr)/(PCr + Pi) in ischemic legs ({circ}) and in normal legs ({square}) 3 months after ischemia induction. Values are expressed as mean ± SEM for five rats. In each curve, the first point was acquired at rest. The second and third points were acquired at electrical stimulation of the muscle to induce an isometric contraction. The remaining four points were acquired during recovery. The marked (*) ratio (PCr)/(PCr + Pi) at 3 months was significantly different from the control (unpaired t test; P < .01). (b) Graph shows the mean values of the ratio (PCr)/(PCr + Pi) for six rats at 4 days ({lozenge}, dotted line), 21 days ({square}, dashed line) and 50 days ({triangledown}, solid line) after ischemia induction. At the marked time (*), the values at 50 and 21 days were significantly different (paired t test; P < .05).

 


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Figure 7b. (a) Graph shows time dependence of the ratio (PCr)/(PCr + Pi) in ischemic legs ({circ}) and in normal legs ({square}) 3 months after ischemia induction. Values are expressed as mean ± SEM for five rats. In each curve, the first point was acquired at rest. The second and third points were acquired at electrical stimulation of the muscle to induce an isometric contraction. The remaining four points were acquired during recovery. The marked (*) ratio (PCr)/(PCr + Pi) at 3 months was significantly different from the control (unpaired t test; P < .01). (b) Graph shows the mean values of the ratio (PCr)/(PCr + Pi) for six rats at 4 days ({lozenge}, dotted line), 21 days ({square}, dashed line) and 50 days ({triangledown}, solid line) after ischemia induction. At the marked time (*), the values at 50 and 21 days were significantly different (paired t test; P < .05).

 


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Figure 8. Photomicrograph shows the ultrastructure of the gastrocnemius muscle after femoral arterial removal. Myofibers display irregular expansions of the sarcolemma (large asterisks). Basal laminar thickening is observed in the endomysial capillaries (small asterisk). Collagen fibers (F) are abundant in the interstitial space. (Lead citrate and uranyl acetate stain; original magnification, x12,500.)

 





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