Micro-Macro: Selective Integration of Microfeatures Inside Low-Cost Macromolds for PDMS Microfluidics Fabrication.

Microfluidics has become a very promising technology in recent years, due to its great potential to revolutionize life-science solutions. Generic microfabrication processes have been progressively made available to academic laboratories thanks to cost-effective soft-lithography techniques and enabled important progress in applications like lab-on-chip platforms using rapid- prototyping. However, micron-sized features are required in most designs, especially in biomimetic cell culture platforms, imposing elevated costs of production associated with lithography and limiting the use of such devices. In most cases, however, only a small portion of the structures require high-resolution and cost may be decreased. In this work, we present a replica-molding method separating the fabrication steps of low (macro) and high (micro) resolutions and then merging the two scales in a single chip. The method consists of fabricating the largest possible area in inexpensive macromolds using simple techniques such as plastics micromilling, laser microfabrication, or even by shrinking printed polystyrene sheets. The microfeatures were made on a separated mold or onto existing macromolds using photolithography or 2-photon lithography. By limiting the expensive area to the essential, the time and cost of fabrication can be reduced. Polydimethylsiloxane (PDMS) microfluidic chips were successfully fabricated from the constructed molds and tested to validate our micro-macro method.

Role of alpha adrenoceptors and nitric oxide on cardiovascular responses in acute and chronic hypertension.

The contribution of α-adrenoceptors and nitric oxide (NO) on the alterations of sympathetically mediated cardiovascular responses after acute (AcH) and chronic (ChH) hypertension was evaluated in pithed aortic coarcted hypertensive rats. Pressor and tachycardia response produced by electrical stimulation of preganglionic sympathetic fibers or exogenous noradrenaline (NA) were recorded in the absence and presence of prazosin (α(1)-antagonist), rauwolscine (α(2)-antagonist), or N (G)-nitro-L-arginine methyl ester (L-NAME; an inhibitor of NO synthase). Compared with age-matched sham-operated rats (Nt), the pressor response produced by electrical stimulation or NA was smaller in AcH rats and larger in ChH rats. Prazosin caused a decrease of pressor response elicited by electrical stimulation or NA in all groups. However, this effect was higher in ChH. Rauwolscine produced a similar increase of sympathetically mediated pressor response in Nt and AcH rats. Nevertheless, this antagonist did not affect the sympathetically mediated pressor response in ChH rats. In addition, rauwolscine did not affect the NA-induced pressor response in all groups. The pressor response elicited by L-NAME was larger in all groups compared without L-NAME and in presence of L-arginine. Moreover, L-NAME in the presence of NA increased sympathetically mediated pressor response is in all groups, compared without it or in the presence of L-arginine. Compared with Nt, basally produced NO in aortic rings was increased in AcH but decreased in ChH. Collectively, our data suggest that decreased cardiovascular reactivity in AcH is due to an increase in basally produced NO. In ChH, enhanced cardiovascular response appears to be associated with a decrease in produced NO and an increase in released NA from sympathetic nerves.