We studied the functional performance of quasitrapezoidal current biphasic stimulating pulse to selectively activate specific nerve fibers in the isolated rat sciatic nerve exposed to anesthetic bupivacaine. The stimulus should predominantly stimulate myelinated Aβ-fibres, minimize the stimulation of the myelinated Aα-fibers and Aδ-fibres, and bypass the stimulation of the non-myelinated C-fibres. Compound action (CAPs) were measured with two pairs of recording hook electrodes at the two sites along the nerve segment located at the distances of 9.6 and 19.2 mm from the stimulating cathode. Isolated nerves were placed in the moist chamber and were stimulated at frequency of 1 Hz with supramaximal quasitrapezoidal biphasic current pulses ic = 2.5 to 3.35 mA in duration of 50 µs. Subsequently, nerves were exposed to bupivacaine dissolved in physiological solution at two different concentrations (3.8; n = 3 and 7.7 µM; n = 3) for 60 min at room temperature (22 °C). The evoked CAPs were digitalized at the sampling rate 100 kHz and stored on the computer. CAP parameters such as peak amplitude, peak to peak amplitude, time to peak were monitored/ analyzed for 60 min in 10 minutes intervals. Time response curves, as determined by % inhibitions of CAPs amplitude by bupivacaine were compared to control CAPs amplitude and time required to reduce CAPs for 25, 50 and 75 % then determined. The maximal blockade of CAPs amplitude was observed 60 min after exposure to 3.8 and 7.7 µM bupivacaine. Both concentrations of bupivacaine also prolonged ‘time to peak’ parameter in the CAP1 and CAP2.
B.03 Paper at an international scientific conference
COBISS.SI-ID: 4005242We discuss the effects of cold-rolling and post-processing of platinum ribbons for implantable electrodes. The mechanical and electrical properties of the electrodes were evaluated by the nanoindenter, light microscope and resistance measurement apparatus.
B.03 Paper at an international scientific conference
COBISS.SI-ID: 14488347Some internal and external stimuli elicit stress responses on the cellular level and at the level of the organism. When the stimulus is brief and its intensity mild to moderate, it triggers adaptation changes that improve the cell's or organism's survival. This adaptation is achieved through a variety of cellular mechanisms such as induction of repair mechanisms, improved removal of damaged macromolecules, upregulation of endogenous antioxidant defences, and prevention of apoptosis triggering by moderate stressors. The key intracellular signalling pathways involved in stress adaptation are the mTORCl and SIRTl. Manipulating these stress adaptation signalling pathways with a variety of agents, improves the cellular adaptation to stress, prolongs cell survival, and improves the transplantation outcome in animal models and in clinical trials. The challenge for the future is to fine-tune the numerous experimental techniques to suit the needs of transplantation and regenerative medicine.
F.21 Development of new health/diagnostic methods/procedures
COBISS.SI-ID: 31960793