The companion paper by Nakatani and Scholz <2004> shows that a hydrothermal frictional healing mechanism results from local solution transfer. Here we evaluate this mechanism with the model of Brechet and Estrin <1994>, which assumes that the healing occurs by stress-driven asperity creep. The absence of a clear temperature dependence of the healing parameter b in the narrow tested range of 100--200¿C is consistent with the model's prediction. The analysis also indicates that the mechanism involves a high stress assist parameter Ωσ = 200 kJ/mol, which is consistent with the contact stress being the indentation hardness, σ ~ 10 GPa, and the activation volume Ω being the molar volume, both of which are reasonable. For this to be consistent with the observed temperature enhanced kinetics of healing also requires that the activation energy exceed 200 kJ/mol. This is much higher than the 20--70 kJ/mol known for low contact stress pressure solution. The analysis of several previously published studies of hydrothermal healing of hard silicates yielded the same results. Hence, if the underlying process is stress driven, it must have a different mechanism at high stress than at low stress. Alternatively, a solution transfer mechanism driven by something other than stress could be the underlying mechanism, but this is inconsistent with other aspects of our experimental results. On the other hand, the same analysis of phenomena that are independently inferred to proceed under relatively low contact stress yielded the parameter values consistent with low-stress pressure solution.