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The Assessment of Reperfusion Inflammatory Injury in Ischemic Preconditioned Diabetic Rats

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Abstract Objective: The assessment of systemic reperfusion injury and the contractile force of the peripheral muscles post-acute ischemia of the hind limbs in healthy versus diabetic ischemic preconditioned rats. Method: The study included 16 Wistar rats divided into two groups: the control group and the diabetic ischemic preconditioned group. Acute ischemia was induced, followed by reperfusion. The assessment of reperfusion injury used biochemical, histopathological and functional determinations (peak tetanic tension-PTT, specific tension-ST). Results: Ischemia-reperfusion injury was more severe in control group regarding creatine-kinase (CK) (CK1=470.13 IU/L versus CK2=230.88 IU/L, p=0.0001) and myoglobin (390.25 ng/mL versus 47.99 ng/mL, p=0.025). Cytolysis enzymes were significantly increased in diabetic preconditioned rats (Alanine aminotransferase ALAT1=46 IU/L, ALAT2=167.8 IU/L, p=0.02; Aspartate aminotransferase ASAT1=106 IU/L, ASAT2=237.5 IU/L, p=0.016). Functional assessment (PTT and ST) highlighted roughly equal values. A paradoxical response occurred in diabetic rats (the contractile force increased during the period of the stimulation). Histopathological findings showed that rhabdomyolysis was more severe in the control group, while inflammatory systemic response due to reperfusion injury was less expressed in diabetic ischemic preconditioned rats. Conclusions: Ischemic preconditioning reduces the severity of reperfusion injury and allows the preservation of contractile muscle function in diabetic rats.
Title: The Assessment of Reperfusion Inflammatory Injury in Ischemic Preconditioned Diabetic Rats
Description:
Abstract Objective: The assessment of systemic reperfusion injury and the contractile force of the peripheral muscles post-acute ischemia of the hind limbs in healthy versus diabetic ischemic preconditioned rats.
Method: The study included 16 Wistar rats divided into two groups: the control group and the diabetic ischemic preconditioned group.
Acute ischemia was induced, followed by reperfusion.
The assessment of reperfusion injury used biochemical, histopathological and functional determinations (peak tetanic tension-PTT, specific tension-ST).
Results: Ischemia-reperfusion injury was more severe in control group regarding creatine-kinase (CK) (CK1=470.
13 IU/L versus CK2=230.
88 IU/L, p=0.
0001) and myoglobin (390.
25 ng/mL versus 47.
99 ng/mL, p=0.
025).
Cytolysis enzymes were significantly increased in diabetic preconditioned rats (Alanine aminotransferase ALAT1=46 IU/L, ALAT2=167.
8 IU/L, p=0.
02; Aspartate aminotransferase ASAT1=106 IU/L, ASAT2=237.
5 IU/L, p=0.
016).
Functional assessment (PTT and ST) highlighted roughly equal values.
A paradoxical response occurred in diabetic rats (the contractile force increased during the period of the stimulation).
Histopathological findings showed that rhabdomyolysis was more severe in the control group, while inflammatory systemic response due to reperfusion injury was less expressed in diabetic ischemic preconditioned rats.
Conclusions: Ischemic preconditioning reduces the severity of reperfusion injury and allows the preservation of contractile muscle function in diabetic rats.

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