Η βουμετανίδη (bumetanide) φαίνεται να μπλοκάρει την ενεργό επαναρρόφηση χλωριούχου νατρίου με αποτέλεσμα την απέκκριση χλωριούχου νατρίου και ύδατος και, ως εκ τούτου την πρόκληση διούρησης. Η δράση της βουμετανίδης ασκείται κυρίως επί του ανιόντος σκέλους της αγκύλης του Henle, φαίνεται όμως ότι το φάρμακο δρα επίσης και επί των εγγύς ουροφόρων σωληναρίων. Πηγή: Γαληνός Οδηγός Φαρμάκων

. 2020 Jun 30;194599820937670.

 doi: 10.1177/0194599820937670. Online ahead of print.

Effect of Bumetanide on Facial Nerve Regeneration in Rat Model

Ecem Sevim Longur 1, Özgür Yiğit 2, Çiğdem Kalaycık Ertugay 2, Ela Araz Server 2, Turgut Adatepe 3, Dilek Akakın 4, Oya Orun 5, Ayça Karagöz Köroğlu 4

Affiliations 

Affiliations

• 1Department of Otorhinolaryngology-Head and Neck Surgery, Ercis State Hospital, Van, Turkey.
• 2Department of Otorhinolaryngology-Head and Neck Surgery, University of Health Sciences, Istanbul Training and Research Hospital, Istanbul, Turkey.
• 3Department of Neurology, University of Health Sciences, Istanbul Training and Research Hospital, Istanbul, Turkey.
• 4Department of Histology and Embryology, School of Medicine, Marmara University, Istanbul, Turkey.
• 5Department of Biophysics, School of Medicine, Marmara University, Istanbul, Turkey.

• PMID: 32600218
 
• DOI: 10.1177/0194599820937670

Abstract

Objective: We investigated the effects of bumetanide alone and in combination with dexamethasone on facial nerve regeneration in rats with facial paralysis.

Study design: A prospective controlled animal study.

Setting: An animal laboratory.

Subjects and methods: Facial paralysis was induced in 32 Wistar rats that we then divided into 4 groups: group 1, control; group 2, bumetanide; group 3, dexamethasone; group 4, bumetanide and dexamethasone. Electroneurography was performed 1, 2, and 4 weeks later, and nerve regeneration was evaluated by electron and light microscopy and Western blotting in week 4.

Results: Regarding the comparison between preoperative values and week 4, the latency difference in group 1 (1.25 milliseconds) was significantly higher than those of groups 2 to 4 (0.56, 0.34, and 0.10 milliseconds, respectively; P = .001). The latency increment in groups 2 and 3 was higher than that of group 4 (P = .002 and P = .046) in week 4, whereas groups 2 and 3 did not differ significantly (P = .291). Amplitude difference was not statistically significant from week 4 among all groups (all P > .05). The number of myelinated axons was significantly higher in all treatment groups than in the control group (P = .001). Axon number and intensity were significantly higher in group 4 as compared with groups 2 and 3 (P = .009, P = .005).

Conclusion: After primary neurorrhaphy, dexamethasone and bumetanide alone promoted nerve recovery based on electrophysiologic and histologic measures. Combination therapy was, however, superior.

Keywords: aquaporin; bumetanide; facial paralysis; regeneration.

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