Severe muscle damage after a short period of ischemia and reperfusion in an animal model.

BACKGROUND: Skeletal muscle ischemia-reperfusion injuries result in a loss of contractile function, leading to limb disability or amputation. Ischemia causes hypoxia and cellular energy failure, which is aggravated by reperfusion due to the inflammatory response and oxidative stress. The consequences of the injury vary according to the duration of the period of ischemia and reperfusion. Therefore, the present work aims to evaluate ischemia-reperfusion injuries induced in the skeletal muscles of Wistar rats submitted to 3 different application periods based on morphological and biochemical parameters. METHODS: For this, a tourniquet was applied to the root of the animals' hind limbs, occluding arterial and venous blood flow, and it was followed by reperfusion-the removal of the tourniquet. The groups were: control (without tourniquet); I30'/R60' (30 minutes of ischemia and 1 hour of reperfusion); I120'/R120' (2 hours and 2 hours); and I180'/R180' (3 hours and 3 hours). RESULTS: All ischemia-reperfusion groups showed characteristics of muscle injury. Microscopic analyses of the extensor digitorum longus, soleus, tibialis anterior, and gastrocnemius muscles showed a significant increase in the number of injured muscle fibers in the ischemia-reperfusion groups compared to the control group. There were also significant differences between the ischemia-reperfusion groups in all muscles, showing a progressive increase in the degree of injury. The quantification of the number of injured muscle fibers between the muscles revealed that at I30'/R60', the soleus muscles had a higher number of injuries in relation to the other muscles, with statistical significance. In the I120'/R120' group, the gastrocnemius muscles presented a significantly greater number of injured fibers. There were no significant differences in the I180'/R180' group. The serum levels of creatine kinase in the I180'/R180' group were significantly higher than in the control and I30'/R60' groups. CONCLUSIONS: Therefore, it was evident that the 3 ischemia-reperfusion models used were capable of causing cell damage, with these findings being more pronounced in the I180'/R180' group.

Association between neuronal degeneration and supraphysiological doses of two types of anabolic steroids in rat brain.

The anabolic androgenic steroids (AAS) are natural compounds that are precursors or derivatives of testosterone and, as a consequence of indiscriminate use, cause irreversible neuronal effects. For this study, 70 brain samples were used from male Wistar rats, separated into 14 groups, divided into: control, sedentary, and exercise groups; in the concentrations: 5 mg, 10 mg, and 15 mg. Two different AAS were used: Testosterone Cypionate (TC) and Nandrolone Decanoate (ND). The encephali followed all the conventional histological procedures, for further analysis of the estimates of neuron bodies of the Locus coeruleus; also being carried out the techniques of the Tunnel Assay and Von Kossa staining. The results obtained show significant values different from the control group: Testosterone Cypionate (TCS): 5 mg (25,00 ± 4,47); 10 mg (23,67 ± 4,45) and 15 mg (21,93 ± 5,65), as well as for Nandrolone Decanoate (ND) in the doses: 5 mg (23,40 ± 3,81); 10 mg (22,80 ± 3,80) and 15 mg (22,80 ± 4,54) being the values of the control group (CGS) 34,27 ± 6,06. For the groups that exercised, the values were: TCT 5 mg 20,87 ± 3,23; TCT 10 mg 21,93 ± 4,91 and TCT 15 mg 21,47 ± 4,36 while, the Nandrolone Decanoate (ND) groups, in the different doses were: NDT 5 mg 21,53 ± 4,34; NDT 10 mg 23,53 ± 1,68 and NDT 15 mg 23,40 ± 2,20, also expressing significant values different from the control group. When comparing the sedentary control group with the animals that exercised, a statistically significant difference was observed being: CGS 34,27 ± 6,06; TCT 5 mg; 20,87 ± 3,23; NDT 5 mg 21,53 ± 4,34; TCT 10 mg 21,93 ± 4,91; NDT 10 mg 23,53 ± 1,68; TCT 15 mg 21,47 ± 4,36 and NDT 15 mg 23,40 ± 2,20. The results of this study, point out that both steroids drastically reduce neuronal density in the Locus coeruleus area inferring that, the possible cause of neuronal death is necrosis, caused by intracellular calcium imbalance.