| ORIGINAL ARTICLE |
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| Year : 2018 | Volume
: 4
| Issue : 1 | Page : 1-6 |
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An investigation of postmortem urotensin II receptor levels in brain and kidney tissues in a rat model of cardiac ischemia
Mustafa Talip Sener1, Erol Akpinar2, Elif Cadirci2, Zekai Halici2, Irfan Cinar2, Ahmet Nezih Kok1
1 Department of Forensic Medicine, Faculty of Medicine, Ataturk University, Erzurum 25240, Turkey
2 Department of Pharmacology, Faculty of Medicine, Ataturk University, Erzurum 25240, Turkey
Correspondence Address:
Erol Akpinar
Department of Pharmacology, Faculty of Medicine, Ataturk University, Erzurum 25240
Turkey
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jfsm.jfsm_75_17
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This study aimed to investigate changes in postmortem urotensin II receptor (UTR) levels in brain and kidney tissues in a rat model of cardiac ischemia. The rats were divided into two groups: a control group and a cardiac ischemia-induced group. Cardiac ischemia was created by an intraperitoneal injection of a single lethal dose of isoproterenol (ISO; 850 mg/kg). Plasma UT, blood urea nitrogen, and creatinine levels were determined 0 h postmortem. Brain and kidney UTR mRNA expression levels were determined 0, 1, 3, 6, 12, 24, 48, and 72 h postmortem. The histopathological appearance of brain and kidney tissues was also evaluated. Plasma UT and plasma creatinine levels were increased in the cardiac ischemia-induced group as compared with those in the control group (P < 0.001). Ischemia resulted in histopathological changes in brain and cerebellum tissue. The morphological evaluation revealed Purkinje cell degeneration (P = 0.037) and dark neurons (P = 0.004). The UTR expression level decreased after 1 h postmortem in the brain and after 3 h postmortem in the kidneys in the cardiac ischemia-induced group as compared with that in the control group (P < 0.001). The observed changes in UTR expression levels may be valuable in clinical practice in the field of forensic medicine. These changes may be used as a marker in postmortem evaluations of sudden death caused by ischemia-induced cardiac shock. |
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