RESUMEN
Experimental studies have identified an anomalous grain size dependence associated with the critical tensile pressure that a metal may sustain before catastrophic failure by cavitation processes. Here we derive the first quantitative theory (and its associated closed-form solution) capable of explaining this phenomena. The theory agrees well with experimental measurements and atomistic calculations over a very wide range of conditions. Utilizing this theory, we are able to map out three distinct regimes in which the critical tensile pressure for cavitation failure (i) increases with decreasing grain size in accordance with conventional wisdom, (ii) nonintuitively decreases with decreasing grain size, and (iii) is independent of grain size. The theory also predicts microscopic signatures of the cavitation process which agree with available data.
RESUMEN
The effect of sulfated cholecystokinin octapeptide (CCK-8S) on the generation of slow wave depolarisation in the rat caudate-putamen (CPu) was studied using in vivo voltammetry. Pressure-ejection of 50 microM CCK-8S into the CPu induced voltammetric signals recorded at widely spaced Nafion-coated carbon fiber microelectrodes. Based on the in vitro selectivity properties of the electrodes, the signals were predominantly due to increases in extracellular concentrations of dopamine (DA). The similar propagation rates of the signals induced by CCK-8S and 100 mM KCl suggests that the CCK-8S-induced signals represent a slow wave depolarization (SWD). Since the CPu was refractory to a second CCK-8S stimulus, the effects of CCK antagonists on DA signals associated with 100 mM KCl-induced SWD were evaluated. Proglumide (4-64 mg/kg) and lorglumide (20-640 micrograms/kg), administered intravenously, decreased KCl-induced DA signals in the CPu in a dose-dependent manner. The antagonistic effect of lorglumide on the KCl-induced signals was partly reversed 130 min after drug administration. The generation of a SWD by CCK-8S and the inhibitory effects of CCK-8S antagonists on KCl-induced signals suggest that the susceptibility of the CPu to KCl-induced SWD may be enhanced by CCK-8S.