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Introduction This study compared the excretory effects, the erythropoietin (Epo) and antioxidant drug U-74389G exert on serum creatinine levels through kidneys. 2 preliminary studies were used for this purpose including respectively one drug used in a renal ischemia­reperfusion (IR) protocol of an animal model. The preliminary studies are part of the present work. The subjects were pretreated in preliminary studies but the results of the same subjects were simply compared in the current work. Materials and methods The serum creatinine levels were evaluated at the 60th reperfusion min (for groups A, C and E) and at the 120th reperfusion min (for groups B, D and F) after IR in the 60 rats. Groups A and B received no drugs, rats from groups C and D were administered with Epo, whereas rats from groups E and F were administered with U-74389G. Results The first preliminary study recommended a non-significant excretory effect of Epo (p-value = 0.4430 > 0.05) than placebo for serum creatinine levels. The second preliminary study proved a very significant excretory effect of U-74389G (p-value = 0.0005 < 0.05) than placebo for serum creatinine levels. These 2 studies were co-evaluated since they came from the same experimental setting. The outcome of the co-evaluation was that U-74389G has at least 5-fold significant excretory action (p-value = 0.0000 < 0.05) than Epo for serum creatinine levels. Conclusions The U-74389G presents surprising effective excretory potencies for serum creatinine levels maybe of great importance in hemodialysis patients.

Introducción Este estudio comparó los efectos excretores que la eritropoyetina (Epo) y el fármaco antioxidante U-74389G ejercen sobre los niveles de creatinina sérica a través de los riñones. Se utilizaron 2 estudios preliminares incluyendo, respectivamente, un fármaco utilizado en una rata protocolo de reperfusión de isquemia renal. Los estudios preliminares son parte del presente trabajo. Los sujetos fueron pretratados en estudios preliminares, pero los resultados de los mismos sujetos fueron comparados simplemente en el trabajo actual. Materiales y métodos Se evaluaron los niveles de creatinina sérica en la 60.ª reperfusión en minutos (para los grupos A, C y E) y en la 120.ª reperfusión en minutos (para los grupos B, D y F) después de isquemia renal en las 60 ratas. Los grupos A y B no recibieron fármacos, a las ratas de los grupos C y D se les administró Epo, mientras que las ratas de los grupos E y F se les administró U-74389G. Resultados El primer estudio preliminar recomendó un efecto excretor no significativo de la Epo (valor p = 0,4430 > 0,05) comparado con el placebo para los niveles de creatinina sérica. El segundo estudio preliminar demostró un efecto excretor muy significativo del U-74389G (valor p = 0,0005 < 0,05) comparado con el placebo para los niveles de creatinina sérica. Estos 2 estudios fueron coevaluados, ya que procedían del mismo entorno experimental. El resultado fue que el U-74389G tiene una acción excretora significativa de al menos 5 veces (p = 0,0000 < 0,05) la Epo para los niveles de creatinina sérica. Conclusiones El U-74389G presenta sorprendentes potencias excretoras efectivas para los niveles de creatinina sérica, tal vez de gran importancia en pacientes en hemodiálisis.

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AIM: This study compared the hematopoietic capacities of erythropoietin (Epo) and antioxidant drug U-74389G, based on 2 preliminary studies. The provided results on hematocrit levels augmentation were co-evaluated in a hypoxia reoxygenation protocol of an animal model. MATERIALS AND METHODS: Hematocrit levels were evaluated at the 60th reoxygenation min (for groups A, C and E) and at the 120th reoxygenation min (for groups B, D and F) in 60 rats. Groups A and B received no drugs, rats from groups C and D were administered with Epo; whereas rats from groups E and F were administered with U-74389G. RESULTS: The first preliminary study of Epo non-significantly increased the hematocrit levels by 0.24%+1.38% (p-value=0.8586). The second preliminary study of U-74389G significantly raised the hematocrit levels by 3.16%+1.33% (p-value=0.0196). These 2 studies were co-evaluated since they came from the same experimental setting. The outcome of the co-evaluation was that U-74389G has approximately 12.66-fold higher hematopoietic potency than Epo (p-value=0.0000). CONCLUSION: The anti-oxidant capacities of U-74389G provide satisfactory acute hematopoietic properties; presenting approximately 12.66-fold hematocrit level rise than epo (p-value=0.0000).

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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.

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Aims: This experimental study evaluated the effect of the antioxidant drug U-74389G on hematocrit levels using a rat model of hypoxia and reoxygenation following an established protocol. Methods: Forty rats with a mean weight of 231.875 g were employed in the study. Hematocrit levels were determined at 60 min (groups A and C) and at 120 min (groups B and D) after starting reoxygenation. Groups A and B received no drugs, whereas U-74389G was administered to rats for groups C and D. Results: U-74389G administration significantly increased hematocrit levels by 4.73%±2.25% (p=0.0435). Reoxygenation time increased hematocrit levels non significantly by 3.96%±2.29% (p=0.1025). U-74389G administration combined with reoxygenation time significantly increased hematocrit levels by 3.16%±1.33% (p=0.0196). Conclusions: U-74389G administration, whether it interacted or not with reoxygenation time, significantly increased hematocrit levels in the short term in a rat model of hypoxia and reoxygenation.

Objetivos: Este estudo experimental avaliou o efeito da droga antioxidante U-74389G nos níveis de hematócrito, utilizando um modelo murino de hipóxia e reoxigenação, de acordo com um protocolo estabelecido. Métodos: Quarenta ratos com um peso médio de 231,875 g foram utilizados no estudo. Os níveis de hematócrito foram determinados aos 60 min (grupos A e C) e aos 120 minutos (grupos B e D) após o início da reoxigenação. Os grupos A e B não receberam nenhuma droga, enquanto que a U-74389G foi administrada aos ratos dos Grupos C e D. Resultados: A administração de U-74389G aumentou significativamente os níveis de hematócrito em 4,73%±2,25% (p=0,0435). O tempo de reoxigenação aumentou não significativamente os níveis de hematócrito em 3,96%±2,29% (p=0,1025). Aadministração de U-74389G combinada com o tempo de reoxigenação aumentou significativamente os níveis de hematócrito em 3,16%±1,33 (p=0,0196). Conclusões: A administração de U-74389G, quer interagindo ou não com o tempo de reoxigenação, aumentou significativamente, no curto prazo, os níveis de hematócrito em um modelo murino de hipóxia e reoxigenação.

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AIM: The aim of this experimental study was to examine the effect of the antioxidant drug "U-74389G", on rat model and particularly in a hypoxia-reoxygenation protocol. The beneficial effect or non-effectiveness of that molecule were studied hematologically using blood mean platelet count. Results were that U-74389G administration interacted or not with reoxygenation time decreased the platelet count by 6.12% ± 3.58% (p = 0.0857) and 12.83% ± 5.79% (p = 0.0303) respectively. CONCLUSIONS: U-74389G administration interacted or not with reoxygenation time decreases the platelet count within short-term time of 2 hours by different significance levels.

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UNLABELLED: The AIM of this experimental study was to evaluate the effect of the antioxidant drug "U-74389G" in a rat model of hypoxia reoxygenation (HR) using the previously established protocol. Effects of treatment were evaluated by mean red blood cell distribution width (RDW) levels. MATERIALS AND METHODS: 40 rats of a mean weight of 231.875 g were employed in the study. RDW levels were determined at 60 min (groups A and C) and at 120 min (groups B and D) after starting the reoxygenation. Groups A and B received no drugs, whereas rats from groups C and D were administered with U-74389G. RESULTS: demonstrated that U-74389G administration significantly decreased the RDW levels by 4.96% + 2.27% (p = 0.0175). Reoxygenation time non-significantly decreased the RDW levels by 0.27% + 2.41% (p = 0.8889). Together, U-74389G administration and reoxygenation time non-significantly decreased the RDW levels by 2.54% + 1.39% (p = 0.0679). CONCLUSIONS: U-74389G administration particulary in concert without reperfusion declines the RDW levels even within the short - time context of 1.5 hours reperfusion.

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Objective: to examine the effect of erythropoietin testing on rat model and particularly the ischemia reperfusion protocol. Methods: experimental study of 40 rats weighing 247.7 g as average. The beneficial effect or non-effectiveness of the erythroproietin molecule on the blood creatine phosphokinase levels was biochemically studied. It was measured 60 min (groups A and C) and 120 min (groups B and D) after reperfusion with no administration of erythropoietin in groups C and D. Results: Erythropoietin administration significantly increased the creatine phosphokinase levels to 3586.05 IU/L (1873.115 IU/L-5298.985 IU/L;p= 0.0001). This finding was in accordance with the result of paired t-test (p= 0.0001). Reperfusion time significantly increased the CPK levels to 557.35 IU/L (-1513.284 IU/L-2627.984 IU/L; p= 0.5890), also in accordance with paired t-test (p= 0.4661). The interaction of erythropoietin administration and reperfusion time significantly increased the creatine phosphokinase levels to 1988.282 IU/L (918.2646 IU/L-3058.299 IU/L; p= 0.0006). Conclusions: Erythropoietin administration, reperfusion time and their interaction generally increase short-term effects on blood creatine phosphokinase after ischemia reperfusion injury.

Objetivo: examinar el efecto del test de eritropoyetina en un modelo de rata, particularmente el protocolo de isquemia reperfusión. Métodos: estudio experimental en el que se usaron 40 ratas con un peso medio de 247,7 g. Se estudió bioquímicamente el beneficio o el no efecto de la molécula de eritropoyetina en la creatín fosfokinasa sanguínea. Esta se midió en dos momentos: 60 min después de la reperfusión (grupos A y C) y 120 min después de esta (grupos B y D). No se administraron eritropoyetina en los grupos A y B, contrario a los grupos C y D. Resultados: la administración de eritropoyetina aumentó significativamente la creatín fosfokinasa sanguínea a 3586,05 UI/L (1873,115 IU/L-5298,985 UI/L; p= 0,0001), de acuerdo también con el test pareado t-test (p= 0,0001). El tiempo de reperfusión incrementó significativamente la creatín fosfokinasa sanguínea a 557,35 UI/L (-1513,284 UI/L-2627,984 UI/L; p= 0,5890), de acuerdo con el test aplicado t-test (p= 0,4661). La interacción de la administración de eritropoyetina y el tiempo de reperfusión elevó significativamente los niveles de creatín fosfokinasa sanguínea a 1988,282 UI/L (918,2646 IU/L-3058,299 IU/L; p= 0,0006). Conclusión: la administración de eritropoyetina, el tiempo de reperfusión y su interacción, generalmente incrementa los efectos a corto plazo en la creatín fosfokinase sanguínea después del daño por isquemia reperfusión.

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OBJECTIVE: The aim of this experimental study was to assess the effect of erythropoietin on a rat model, particularly under a renal ischemia reperfusion protocol. The beneficial or lack of effects of that molecule on the excreted renal product of serum uric acid were studied biochemically. MATERIAL AND METHODS: Forty rats were used with a mean weight of 247.7 gr. Serum uric acid levels were measured measured at 60 min after reperfusion (Groups A and C) and at 120 min after reperfusion (groups B and D). RESULTS: 1) Erythropoietin administration non-significantly decreased the serum uric acid levels non-significantly by 0.02 mg/dL [-0.2415423 mg/dL-0.2015423 mg/dL] (p=0.8560), in accordance with the paired t-test (p=0.8438). Reperfusion time non-significantly increased the serum uric acid levels non-significantly by 0.17 mg/dL [-0.0444933 mg/dL-0.3844933 mg/dL] (p=0.1169), in accordance with the paired t-test (p=0.1648). 3) The interaction of erythropoietin administration and reperfusion time non-significantly increased the serum uric acid levels non-significantly by 0.1 mg/dL [-0.0295564 mg/dL-0.2295564 mg/dL] (p=0.1264). CONCLUSION: Erythropoietin administration, reperfusion time and their interaction have no significant short-term alterations on serum uric acid levels. Conclusions cannot be extracted by non-significant p-values within 2 hours. Obviously, longer study times may permit safer results.

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It is controversial whether the administration of thyroid hormone to patients with nonthyroidal illness has any beneficial effect. Two groups of patients undergoing abdominal hysterectomy under the same general anesthesia were studied. Group A consisted of 15 women taking chronically l-thyroxine therapy (1.8 mug/kg daily), and group B (control) consisted of 16 apparently healthy euthyroid women taking placebo. Thyroid hormones, cortisol, and interleukin (IL)-6 were measured 1 day before and 1, 2, 3, and 6 days after surgery. Total triiodothyronine (TT(3)) decreased to a significantly greater degree (P <.05) and for a longer period of time in group B than in group A. The significant increase of reverse T(3) (rT(3)) noted early in group B failed to reach the baseline levels until the end of the study, whereas in group A, rT(3) returned to the preoperative values by day 2. Both groups had similar free thyroxine (FT(4)) at baseline. FT(4) increased significantly at day 1 and remained significantly elevated throughout the postoperative period in group B only. Serum TT(4), thyroid-stimulating hormone (TSH), and cortisol did not change significantly in either group. In all patients, IL-6 increased significantly to a peak value at day 1, showing a slow decrease thereafter. A stronger negative correlation was found between T(3) and IL-6 in group B than in group A (r = -.66, P <.0001 v r = -.38, P <.001, respectively) and a strong positive correlation was observed between rT(3) and IL-6 in group B only (r =.57, P <.001). The long-term treatment with T(4) seems to attenuate the decrease of serum T(3), which occurs during the development of nonthyroidal illness postoperatively. The elevation of IL-6 accounted for a greater proportion of the variations of the T(3) and rT(3) in the control group B than in the T(4)-treated group A.

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