NDLI: Propofol reduces nitric oxide-induced apoptosis in testicular ischemia-reperfusion injury by downregulating the expression of inducible nitric oxide synthase.

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Propofol reduces nitric oxide-induced apoptosis in testicular ischemia-reperfusion injury by downregulating the expression of inducible nitric oxide synthase.

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Year: 2008 Volume: 52 Issue: 2

Year: 2008 Volume: 52 Issue: 1

Propofol reduces nitric oxide-induced apoptosis in testicular ischemia-reperfusion injury by downregulating the expression of inducible nitric oxide synthase.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Yagmurdur, H. Ayyildiz, A. Karaguzel, E. Akgul, T. Ustun, H. Germiyanoglu, C.
Description	Country affiliation: Turkey Author Affiliation: Yagmurdur H ( Clinic of Anesthesiology and Reanimation, The Ministry of Health Ankara Research and Training Hospital, Ankara, Turkey. hyagmurdur@yahoo.com)
Abstract	BACKGROUND: The aim of the present study was to investigate the underlying mechanisms in the preventive effects of intravenous anesthetics on testicular ischemia-reperfusion injury. METHODS: Forty male Wistar Albino rats were randomly assigned to four groups of 10 rats each. Anesthesia was induced and maintained with thiopental in groups 1 and 2 and with propofol in groups 3 and 4. Groups 2 and 4 received left testicular ischemia (torsion) for 1 h and reperfusion (detorsion) for 24 h. Groups 1 and 3 (control groups) had no testicular torsion and detorsion. At 24 h of reperfusion, animals were killed and ipsilateral testes were removed for determination of tissue nitric oxide (NO) levels and immunohistochemical evaluation of endothelial nitric oxide synthase (eNOS), inducible NOS (iNOS), and apoptosis protease-activating factor 1 (APAF-1). RESULTS: Between groups 1 and 3, there were no differences in tissue NO levels and eNOS, iNOS, and APAF-1 expressions. iNOS and APAF-1 expressions were markedly increased in group 2, but these parameters were at the mild to moderate level in group 4 at 24 h of reperfusion. Also, elevated expression of iNOS was accompanied by a high NO production in group 2 compared with group 4. Although eNOS expressions were increased in both the groups (groups 2 and 4), there were no significant differences between these groups. CONCLUSIONS: Propofol as an anesthetic agent may attenuate germ cell-specific apoptosis and decrease NO biosynthases through downregulation of iNOS expression in an animal model of testicular torsion and detorsion.
File Format	HTM / HTML
ISSN	00015172
Issue Number	3
Volume Number	52
e-ISSN	00015172
Journal	Acta Anaesthesiologica Scandinavica
Language	English
Publisher	Wiley
Publisher Date	2008-03-01
Publisher Place	Great Britain (UK)
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Anesthesiology Anesthetics, Intravenous Pharmacology Apoptosis Drug Effects Propofol Reperfusion Injury Prevention & Control Testis Blood Supply Animals Apoptotic Protease-activating Factor 1 Analysis Biological Markers Immunohistochemistry Male Nitric Oxide Metabolism Nitric Oxide Synthase Type Ii Nitric Oxide Synthase Type Iii Random Allocation Rats Rats, Wistar Pathology Physiopathology Spermatic Cord Torsion Chemistry Journal Article
Content Type	Text
Resource Type	Article
Subject	Anesthesiology and Pain Medicine

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