IA Ahmed

Bio: IA Ahmed is an academic researcher. The author has contributed to research in topics: Calcium in biology & General anaesthetic. The author has an hindex of 1, co-authored 1 publications receiving 4 citations.

A comparative study of anaesthetic agents on high voltage activated calcium channel currents in identified molluscan neurons

Abstract: O_LIUsing the two electrode voltage clamp configuration, a high voltage activated whole-cell Ca2+ channel current (IBa) was recorded from a cluster of neurosecretory Light Yellow Cells (LYC) in the right parietal ganglion of the pond snail Lymnaea stagnalis. C_LIO_LIRecordings of IBa from LYCs show a reversible concentration-dependent depression of current amplitude in the presence of the volatile anaesthetics halothane, isoflurane and sevoflurane, or the non-volatile anaesthetic pentobarbitone at clinical concentrations. C_LIO_LIIn the presence of the anaesthetics investigated, IBa measured at the end of the depolarizing test pulse showed proportionally greater depression than that at measured peak amplitude, as well as significant decrease in the rate of activation or increase in inactivation or both. C_LIO_LIWithin the range of concentrations used, the concentration-response plots for all the anaesthetics investigated correlate strongly to straight line functions, with linear regression R2 values > 0.99 in all instances. C_LIO_LIFor volatile anaesthetics, the dose-response regression slopes for IBa increase in magnitude, in order of gradient: sevoflurane, isoflurane and halothane, a sequence which reflects their order of clinical potency in terms of MAC value. C_LI

Ketamine attenuates the Na^＋-dependent Ca^2＋ overload in rabbit ventricular myocytes in vitro by inhibiting late Na^＋ and L-type Ca^2＋ currents

Abstract: Aim:Intracellular Ca2+ ([Ca2+]i) overload occurs in myocardial ischemia. An increase in the late sodium current (INaL) causes intracellular Na+ overload and subsequently [Ca2+]i overload via the reverse-mode sodium-calcium exchanger (NCX). Thus, inhibition of INaL is a potential therapeutic target for cardiac diseases associated with [Ca2+]i overload. The aim of this study was to investigate the effects of ketamine on Na+-dependent Ca2+ overload in ventricular myocytes in vitro.Methods:Ventricular myocytes were enzymatically isolated from hearts of rabbits. INaL, NCX current (INCX) and L-type Ca2+ current (ICaL) were recorded using whole-cell patch-clamp technique. Myocyte shortening and [Ca2+]i transients were measured simultaneously using a video-based edge detection and dual excitation fluorescence photomultiplier system.Results:Ketamine (20, 40, 80 μmol/L) inhibited INaL in a concentration-dependent manner. In the presence of sea anemone toxin II (ATX, 30 nmol/L), INaL was augmented by more than 3-fold, while ketamine concentration-dependently suppressed the ATX-augmented INaL. Ketamine (40 μmol/L) also significantly suppressed hypoxia or H2O2-induced enhancement of INaL. Furthermore, ketamine concentration-dependently attenuated ATX-induced enhancement of reverse-mode INCX. In addition, ketamine (40 μmol/L) inhibited ICaL by 33.4%. In the presence of ATX (3 nmol/L), the rate and amplitude of cell shortening and relaxation, the diastolic [Ca2+]i, and the rate and amplitude of [Ca2+]i rise and decay were significantly increased, which were reverted to control levels by tetrodotoxin (TTX, 2 μmol/L) or by ketamine (40 μmol/L).Conclusion:Ketamine protects isolated rabbit ventricular myocytes against [Ca2+]i overload by inhibiting INaL and ICaL.

NO and H2O2 Modulate Ca2+, Ca2+ Dependent K+ Currents and IntracellularCalcium Concentration of Cultured, Identified Lymnaea Neurons

Abstract: 1Physology Research Centre, Department of Physiology, School of Medicine, Ahwaz Jundishapur University of Medical Sciences, Ahwaz, Iran 2Dipartimento di Biologia, Università Degli Studi di Napoli Federico II, Napoli, Italy 3Institute of Ageing and Chronic Diseases, The APEX building, University of Liverpool, UK *Corresponding Author: William Winlow, Dipartimento di Biologia, Università Degli Studi di Napoli Federico II, Napoli, Italy and Institute of Ageing and Chronic Diseases, The APEX building, University of Liverpool, UK.