Cerebral Ischemia/Reperfusion Injury in the Hyperthyroid Rat

Background: Hyperthyroidism as a risk factor for stroke is not conclusive. There are no definite data on the relationship between ischemic cerebrovascular injury and hyperthyroidism. This study was designed to define whether the outcomes of post‑ischemic stroke injury are influenced by chronic hyperthyroidism. Methods: Two groups of hyperthyroid (HT) and control euthyroid rats of equal numbers (n=22) were included in the study. Hyperthyroidism was induced for 4 weeks by adding L‑thyroxine (300 μg/kg) to drinking water. The middle cerebral artery occlusion technique was used to induce focal cerebral ischemia. Neurological disability (neurological deficit score [NDS]) was evaluated after 24 hours, and the rats were sacrificed to obtain their brain. Triphenyl Tetrazolium Chloride (TTC) staining and Evans Blue (EB) extravasation were used to quantify cerebral infarct volume and cerebrovascular integrity disruption. Data analysis was done using SPSS, version 21. Results: Thyroid hormones levels, T3 (314±7 vs. 198±3 ng/dL; P=0.001) and T4 (9.8±0.3 vs. 3.08±0.07 μg/dL; P=0.001), were significantly higher in the HT group than in the controls. Furthermore, most clinical signs seen in hyperthyroid patients were also present in the HT group. Comparison of the data on cerebral ischemia between the HT and control groups showed significant increases in the NDS (2.76±0.16 vs. 2.23±0.09; P=0.03), cerebral infarct volume (479±12 vs. 266±17 mm3; P=0.001), and EB extravasation (50.08±2.4 vs. 32.6±1.2 μg/g; P=0.001) in the former group. Conclusion: The intensified cerebral infarct size and cerebrovascular integrity disruption suggested that chronic hyperthyroidism aggravated post‑stroke injury in the rats. More investigation is required to analyze the pathological mechanisms underlying the association between cerebrovascular disease and hyperthyroidism.