RESUMEN
The time course and spatial extent of movement-related suppression of the detection of weak electrical stimuli (intensity, 90% detected at rest) was determined in 118 experiments carried out in 47 human subjects. Subjects were trained to perform a rapid abduction of the right index finger (D2) in response to a visual cue. Stimulus timing was calculated relative to the onset of movement and the onset of electromyographic (EMG) activity. Electrical stimulation was delivered to 10 different sites on the body, including sites on the limb performing the movement (D2, D5, hand, forearm and arm) as well as several distant sites (contralateral arm, ipsilateral leg). Detection of stimuli applied to the moving digit diminished significantly and in a time-dependent manner, with the first significant decrease occurring 120 ms before movement onset and 70 ms before the onset of EMG activity. Movement-related and time-dependent effects were obtained at all stimulation sites on the homolateral arm as well as the adjacent trunk. A pronounced spatiotemporal gradient was observed: the magnitude of the movement-related decrease in detectability was greatest and earliest at sites closest to the moving finger and progressively weaker and later at more proximal sites. When stimuli were applied to the distant sites, only a small (approximately 10%), non-time-dependent decrease was observed during movement trials. A simple model of perceptual performance adequately described the results, providing insight into the distribution of movement-related inhibitory controls within the CNS.
Asunto(s)
Dedos/fisiología , Movimiento/fisiología , Desempeño Psicomotor/fisiología , Detección de Señal Psicológica/fisiología , Tacto/fisiología , Adolescente , Adulto , Estimulación Eléctrica , Electromiografía , Femenino , Antebrazo/fisiología , Lateralidad Funcional , Mano/fisiología , Humanos , Masculino , Especificidad de Órganos , Hombro/fisiología , Muslo/fisiología , Tórax/fisiología , Factores de TiempoAsunto(s)
Acetilcolina/farmacología , Antiarrítmicos/farmacología , Corazón/efectos de los fármacos , Piperidinas/farmacología , Piridinas/farmacología , Tetrodotoxina/farmacología , Potenciales de Acción/efectos de los fármacos , Animales , Calcio/metabolismo , Agregación Celular , Células Cultivadas , Embrión de Pollo , Corazón/embriología , Corazón/fisiología , Modelos Biológicos , Contracción Miocárdica/efectos de los fármacos , Miocardio/citología , Técnicas de Placa-Clamp , Sulfanilamidas/farmacologíaRESUMEN
To investigate the actions of lidocaine and diltiazem on the ischemic alterations associated with the onset of acute ischemic arrhythmias, the left anterior descending coronary artery was occluded for 6-min periods separated by 30 min of reperfusion, under control conditions and after injection of lidocaine (2.4-3.8 micrograms/mL of plasma) or diltiazem (390-510 ng/mL) in open-chest anesthetized pigs. Sixty-one unipolar electrograms were continuously recorded in the ischemic zone. Isochronal maps and isopotential maps were determined by computer analysis. The magnitude of beat-to-beat alternation of unipolar waveforms was described by the difference between the time integrals subtended by electrograms of consecutive beats. Activation times were prolonged by ischemia and the ST segment became elevated. Delay and ST elevation developed at a faster rate in the presence of lidocaine than under control conditions, but were reduced by diltiazem. ST-T alternation was not significantly different between control and lidocaine occlusions, but the incidence of negative T waves and that of ventricular tachycardia degenerating to fibrillation were higher in lidocaine occlusions than in control occlusions. In contrast, unipolar waveform alternation and negative T waves were virtually abolished by diltiazem, even at fast pacing rates (180-210 beats/min) at which diltiazem did not reduce ST elevation. Ventricular arrhythmias also were abolished by diltiazem. Thus, lidocaine and diltiazem produce opposite effects on the ischemic alterations most closely associated with the initiating mechanism of tachycardia. This could be related to differences between these drugs with regard to their actions on transmembrane currents during repolarization.