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Background: Platelet activation causes morphologic changes of platelets, including both the spherical shape and pseudopodia formation increasing platelet distribution width (PDW), ascribed to platelet anisocytosis. Furthermore, coagulation is activated in vaso-occlusive situations, increasing PDW. Early diagnosis of progressive activation of coagulation or any factor declining PDW levels, can prevent these thromboembolic diseases successfully. The probable beneficial effect of the molecule "U-74389" was studied hematologically using blood mean platelet distribution width PDW) levels. Methods: 40 rats of mean weight 231.875g were used in the study. PDW levels were measured at 60 min of reoxygenation (groups A and C) and at 120 min of reoxygenation (groups B and D) with administration of the drug U-74389G in groups C and D. Results: U-74389G administration kept significantly increased the PDW levels by 1.79%±0.76% (p=0.0314). Reoxygenation time non significantly declined the PDW levels by 0.745%±0.81% (p=0.3280). However, U-74389G administration and reoxygenation time together kept significantly increased the PDW levels by 0.96%±0.46% (p=0.0396). Conclusion: U-74389G administration whether it interacted or not with reoxygenation time borderline declines from significant to non significant the PDW levels, within short-time study period of 2 hours. This finding has huge clinical interest in coagulopathy prevention or reversion.

This experimental study examined the effect of the antioxidant drug U-74389G, on a rat model and particularly in a renal ischemia-reperfusion protocol. The effects of that molecule were studied biochemically using blood mean urea levels. Forty rats of mean weight 231.875 g were used in the study. Urea levels were measured at 60 min of reperfusion (groups A and C) and at 120 min of reperfusion (groups B and D). The drug U-74389G was administered only in groups C and D. U-74389G administration significantly decreased the predicted urea levels by 11.35%±2.73% (P=0.0001). Reperfusion time non-significantly increased the predicted urea levels by 2.26%±3.29% (P=0.4103). However, U-74389G administration and reperfusion time together significantly decreased the predicted urea levels by 6.31%±1.70% (P=0.0005). U-74389G administration whether it interacted or not with reperfusion time had significant decreasing effect on the urea serum levels, reflecting a respective renal function augmentation.

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Objective: The aim of this experimental study was to examine the effect of the antioxidant drug “U-74389G” on a rat model using an ischemia reperfusion protocol. The effect of U-74389G was studied biochemically by measuring mean blood creatinine levels. Materials and Methods: Forty rats were used in the study. Creatinine levels were measured at 60 min of reperfusion (groups A and C) or at 120 min of reperfusion (groups B and D), where groups A and B were controls and groups C and D received U-74389G administration. Results: U-74389G administration significantly decreased the predicted creatinine levels by 21.02 ± 5.06% (p = 0.0001). Reperfusion time non-significantly increased the predicted creatinine levels by 4.20 ± 6.12% (p = 0.4103). However, U-74389G administration and reperfusion time together produced a significant combined effect in decreasing the predicted creatinine levels by 11.69 ± 3.16% (p = 0.0005). Conclusion: Independent of reperfusion time, U-74389G administration significantly decreased the creatinine levels in an ischemic rat model. This study demonstrates that short-term U-74389G administration improves renal function by increasing creatinine excretion.