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. 2013 Jan;44(1):255-9.
doi: 10.1161/STROKEAHA.112.663476. Epub 2012 Nov 1.

VSports app下载 - Early insulin glycemic control combined with tPA thrombolysis reduces acute brain tissue damages in a focal embolic stroke model of diabetic rats

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Early insulin glycemic control combined with tPA thrombolysis reduces acute brain tissue damages in a focal embolic stroke model of diabetic rats

Xiang Fan et al. Stroke. 2013 Jan.

Abstract

Background and purpose: Therapeutic effects of early insulin glycemic control for poststroke hyperglycemia in combination with tissue-type plasminogen activator (tPA) thrombolytic therapy have not yet been studied but are of great clinical interest VSports手机版. In this study, we tested the effects of insulin plus tPA combination in a model of focal embolic stroke in Type I diabetic rats. .

Methods: Streptozotocin was used to produce Type I diabetes in male Wistar rats for 6 weeks and then embolic focal strokes were induced. All rats were treated with insulin or saline at 1 hour followed by tPA or saline at 1. 5 hour after stroke. Mortality, infarction, hemispheric swelling, hemorrhagic transformation, and perfusion defects were examined at 24 hours after stroke. Total plasma plasminogen activator inhibitor-1 antigen and activity levels were measured before stroke and 1. 5, 3, and 6 hours after stroke by ELISA. V体育安卓版.

Results: Early insulin glycemic control alone or tPA thrombolysis alone had no significant effects on ischemic infarction. However, early insulin glycemic control combined with tPA significantly reduced brain infarction and swelling, ameliorated tPA-associated hemorrhagic transformation, and improved plasma perfusion at 24 hours after stroke. We also found that the combination significantly decreased plasma plasminogen activator inhibitor-1 antigen level at 6 hours and plasminogen activator inhibitor-1 activity at 1 V体育ios版. 5 and 6 hours after stroke. .

Conclusions: Early insulin glycemic control may be beneficial in combination with tPA thrombolysis for ischemic stroke with diabetes mellitus or poststroke hyperglycemia. VSports最新版本.

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Figures

Figure 1
Figure 1
Acute brain tissue outcomes of insulin combined with tPA thrombolytics in diabetic stroke rats. A. Blood glucose levels were monitored over the times up to 24 hours after stroke. B. At 24 hours after stroke, ischemic infarct volumes were quantified on TTC-stained brain slices. C. Hemispheric swelling were quantified on the same TTC-stained brain slices. D. Intracerebral hemorrhage volumes were quantified with hemoglobin assay at 24 hours after stroke. Data were expressed as mean ± sd, * P<0.05, n=9 or 10 per group.
Figure 1
Figure 1
Acute brain tissue outcomes of insulin combined with tPA thrombolytics in diabetic stroke rats. A. Blood glucose levels were monitored over the times up to 24 hours after stroke. B. At 24 hours after stroke, ischemic infarct volumes were quantified on TTC-stained brain slices. C. Hemispheric swelling were quantified on the same TTC-stained brain slices. D. Intracerebral hemorrhage volumes were quantified with hemoglobin assay at 24 hours after stroke. Data were expressed as mean ± sd, * P<0.05, n=9 or 10 per group.
Figure 2
Figure 2
Cerebral perfusion of tPA thrombolytics with/without early insulin glycemic control in diabetic stroke rats. A. Laser Doppler flowmetry monitored regional cerebral blood flow for up to 1 hour after treatments. B. Representative microvessels perfused with FITC–dextran of coronal rat brain sections treated with tPA or insulin plus tPA combination at 24 hours after stroke. C. Relative microvasculature area perfused with FITC-dextran. Data were expressed as mean ± sd. * P<0.05, n=5 per group.
Figure 3
Figure 3
Effects of early insulin glycemic control combined with tPA in plasma PAI-1 antigen and activity levels. Platelet free plasma samples were collected at pre-stroke, 1.5, 3, and 6 hours after stroke. A. Changes of plasma PAI-1 antigen levels over the times up to 6 hours after stroke. B. Changes of plasma PAI-1 activity levels over the times up to 6 hours after stroke. Data were expressed as mean ± sd of relative fold changes of pre-stroke baseline. *P<0.05 vs pre-stroke baseline within the same treatment group; #<0.05 between groups at the same examining time point; n= 7 per group.

References

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