Nicorandil, an Adenosine Triphosphate Sensitive Potassium Channel Opener, Induced by Intravenous Propofol Anesthesia, Motor Co-Ordination Properties in Rodent Models

Jayaprakash Somasundaram; Manoj G Tyagi; Subramaniam Kannan

Volume : VII, Issue : XI, November - 2018

Nicorandil, an Adenosine Triphosphate Sensitive Potassium Channel Opener, Induced by Intravenous Propofol Anesthesia, Motor Co-Ordination Properties in Rodent Models

Jayaprakash Somasundaram, Manoj G Tyagi, Subramaniam Kannan

Abstract :

OBJECTIVE:

The objective of this study was the effects of an adenosine triphosphate sensitive Potassium channel opener nicorandil may suppress or induced anesthetic action induction of propofol, on motor performance in mice.

MATERIAL AND METHODS:

48 Swiss Albino mice were included in the study in 8 groups of 6 animals in each (n=6). Treatment groups are solvent control, Methohexital alone, Propofol alone, Pretreated nicorandil with Propofol, nicorandil with PLC inhibitor Endothelin–1 , pretreated Endothelin–1 with Propofol, Pretreated with nicorandil, Endothelin–1 with Propofol , Pretreated with potassium channel blocker glibenclamide with Propofol.

RESULTS:

The effect of Adenosine triphosphate sensitive Potassium channel opener nicorandil with propofol on muscle function the present study demonstrates that significantly Enhanced muscle function, as evidenced by increased grip strength, as well as Decreased fatigue. Potassium channel opener nicorandil Partialy inhibition the muscle strength the grip strength compared with propofol alone. P<0.01** (Forelimb, 86.6± 6.2, Hindlimb 74.8± 4.0) Grip strength of the mice Propofol alone treated was significantly inhibitied. Grip strength test showed increase of (a) forelimb and (b) hindlimb grip strength in the mice treated with the nicorandil with propofol. A decline in muscle strength has been reported potassium channel blocker with propofol.

CONCLUSIONS:

The effects of propofol on the endothelin–1–induced activation of muscle function. K_ATP channels regulate the memane potential, which controls calcium entry through voltage–dependent calcium channels, and thereby contractility through changes in intracellular calcium. Present study have suggested that opening K_ATP channels in vascular smooth muscle causes vasodilatations