Note: This is not an area where I know the litterature well
Where are many counteracting processes to consider for this question. For instance, the rate of evolution will be affected by the rate of mutation, the distribution of positive and deleterious mutations, strength of selection, whether the fitness effects are small or large, if fitness effects depend on interactions between multiple mutations or single mutations with large effect, asexual vs. sexual populations, and processes such as genetic drift.
A recent review that is useful for your question is Lanfear et al (2014). They focus on how substitution rate is affected by effective population size, and go through both theoretical and empirical evidence. They conclude that in most cases, most mutations are deleterious, and that drift and selection are the most important effects in determining rates of evolution. They also state the effect of effective population size (Ne) is likely to depend if mutations are dominated by deleterious or advantagious mutations, and they expect the rate of evolution to be negatively correlated with Ne when deletious mutations dominate evolution and a positive correlation to Ne when advantagious mutations dominate.
A paper by Rozen et al (2008) indicates that while large populations are more effective in fixing mutations with large positive effects, small populations can be more effective in complex "rugged" adaptive landscapes.
While such determinism speeds adaptation on the smooth adaptive landscape represented by the simple environment, it can limit the ability of large populations from effectively exploring the underlying topography of rugged adaptive landscapes characterized by complex environments.
However, this does not deal directly with the rate of evolution, but mostly about attaining the highest possible fitness in a particular fitness landscape. Another interesting paper is Desai et al. (2007), but I haven't looked through this yet. However, they find (for asexual bacteria) that the speed of adaptation scales less than linearly with population size, and similar results have also been found in studies from Lenski's group. Their interpretation is that evolution is driven by multiple concurrent mutations of small effect and not one-by-one fixation of single mutations (which would favour large populations more).
For your case of evolution of resistance, I think one crucial thing is if you expect resistance to be driven by a few single mutations or combinations of many mutations that interact (related to whether resistance is "easy" or "hard" to evolve). From what I understand, the first case should favour a single large population (since they will fix mutations for resistance more quickly), while the second case might favour many smaller populations (since you might get more effective exploration of combinations of mutations)
These are just a few starting points in a very large field, and I hope that you find them useful.