Volume 65, Issue 4 (3 2007)
Tehran Univ Med J 2007, 65(4): 11-18 |
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Shabanzadeh A R, Ghafarpour M, Shuaib A, Bodaghabadi M. The effect of ultrasound on thromboembolic model of brain stroke in rat. Tehran Univ Med J 2007; 65 (4) :11-18
URL: http://tumj.tums.ac.ir/article-1-796-en.html
URL: http://tumj.tums.ac.ir/article-1-796-en.html
Abstract: (6360 Views)
Background: Ultrasound (US) has been used in neuroprotection after cerebral ischemia however, its use is controversial. Application of US in combination with fibrinolytic agents may improve fibrinolytic effects. In this study the effects of US, alone or in combination with tissue plasminogen activator (tPA), on brain ischemic injury were examined and we studied whether US is protective in the brain injured by ischemia under normothermic conditions.
Methods: We performed two studies. In the first study, rectal and brain temperatures were compared. In the second study, we studied whether US alone or in combination with tPA is neuroprotective in thromboembolic stroke. To induce focal cerebral ischemia, a clot was formed in a catheter. Once the clot had formed, the catheter was advanced 17 mm in the internal carotid artery until its tip was 1-2 mm away from the origin of the middle cerebral artery (MCA). The preformed clot in the catheter was then injected, and the catheter was removed. The wound was then closed and the infarction volume, edema and neurological deficits were measured after MCA occlusion.
Results: The temperature in the brain was approximately 0.50 ºC lower than the rectal temperature. In the control, US+low tPA, low tPA, US+high tPA and, high tPA groups, the infarct volume (%) was 34.56±4.16, 17.09±6.72, 21.25±7.8, 13.5±10.72 and 20.61±6.17 (mean ±SD) at 48 h after MCA occlusion, respectively. The results indicate that US alone reduces the infarct volume by 30% compared to that of the control group (P<0.05). US improved neurological deficits and reduced brain edema significantly (p<0.05).
Conclusions: This study indicate that US appears to have a protective effect, alone and in combination with tPA, in an embolic model of stroke.
Methods: We performed two studies. In the first study, rectal and brain temperatures were compared. In the second study, we studied whether US alone or in combination with tPA is neuroprotective in thromboembolic stroke. To induce focal cerebral ischemia, a clot was formed in a catheter. Once the clot had formed, the catheter was advanced 17 mm in the internal carotid artery until its tip was 1-2 mm away from the origin of the middle cerebral artery (MCA). The preformed clot in the catheter was then injected, and the catheter was removed. The wound was then closed and the infarction volume, edema and neurological deficits were measured after MCA occlusion.
Results: The temperature in the brain was approximately 0.50 ºC lower than the rectal temperature. In the control, US+low tPA, low tPA, US+high tPA and, high tPA groups, the infarct volume (%) was 34.56±4.16, 17.09±6.72, 21.25±7.8, 13.5±10.72 and 20.61±6.17 (mean ±SD) at 48 h after MCA occlusion, respectively. The results indicate that US alone reduces the infarct volume by 30% compared to that of the control group (P<0.05). US improved neurological deficits and reduced brain edema significantly (p<0.05).
Conclusions: This study indicate that US appears to have a protective effect, alone and in combination with tPA, in an embolic model of stroke.
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