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Omental transposition decreases ischemic brain damage examined in a new ischemia model
C Vatansev1, M E Ustün, C O Oğün
1Department of General Surgery, Meram Faculty of Medicine, Selçuk University, Konya, Turkey. cvatansev@hotmail.com
Purpose:
The aim of this study was to determine whether omental transposition at the time of focal cerebral ischemia can decrease ischemic brain damage produced in dogs, in a new ischemia model, which had been described by us.
Methods:
In group 1 (n = 5), the left internal carotid artery and arterial circle of the brain (posterior communicating artery in humans) were occluded permanently. In group 2 (n = 5), additionally to this ischemia model, omental transposition was performed simultaneously. In the postoperative early period (first 24 h), single photon emission computed tomography (SPECT) and in the late period (72-96 h) SPECT and magnetic resonance imaging (MRI) of the brain were performed. Mann-Whitney U, paired t and Wilcoxon signed rank tests were used for statistical analyses, and p < 0.05 was considered significant.
Results:
The dogs had a neurological score (NS) of 3.6 +/- 0.5 and 3.4 +/-0.5 in groups 1 and 2, respectively, in the early period (p > 0.05). In the late period, the dogs had an NS of 4.4 +/- 0.5 and 5.6 +/- 0.5 in groups 1 and 2, respectively (p < 0.05). The NS of each group differed significantly between the early and late period (p < 0.05). Early SPECT imaging showed 50 +/- 7.0% and 52 +/- 8.4% hypoperfusion corresponding to the left middle cerebral artery territory in groups 1 and 2, respectively (p > 0.05). In the late period, the degree of hypoperfusion decreased to 34 +/- 5.5% and 12 +/- 4.8% in groups 1 and 2, respectively (p < 0.05). The degree of hypoperfusion in both groups changed significantly between the early and late period (p < 0.05). In T(1)- and T(2)-weighted MRI images, the volume of the lesion in group 1 was significantly greater than in group 2 (p < 0.001).
Conclusion:
In our new ischemia model, simultaneous omental transposition is helpful in reversing the neurologic deficit and cerebral ischemic damage.