Paper-based microfluidic devices by asymmetric calendaring.

We report a simple, efficient, one-step, affordable method to produce open-channel paper-based microfluidic channels. One surface of a sheet of paper is selectively calendared, with concomitant hydrophobization, to create the microfluidic channel. Our method involves asymmetric mechanical modification of a paper surface using a rolling ball (ball-point pen) under a controlled amount of applied stress (σz) to ascertain that only one side is modified. A lubricating solvent (hexane) aids in the selective deformation. The lubricant also serves as a carrier for a perfluoroalkyl trichlorosilane allowing the channel to be made hydrophobic as it is formed. For brevity and clarity, we abbreviated this method as TACH (Targeted Asymmetric Calendaring and Hydrophobization). We demonstrate that TACH can be used to reliably produce channels of variable widths (size of the ball) and depths (number of passes), without affecting the nonworking surface of the paper. Using tomography, we demonstrate that these channels can vary from 10s to 100s of microns in diameter. The created hydrophobic barrier extends around the channel through wicking to ensure no leakages. We demonstrate, through modeling and fabrication, that flow properties of the resulting channels are analogous to conventional devices and are tunable based on associated dimensionless numbers.

Impact of surgery on nitric oxide in rats: evidence for activation of inducible nitric oxide synthase.

We investigated the effect of euvolemic surgical preparation, on chemical indices of activity of the nitric oxide (NO) system, in anesthetized, acutely prepared rats. The urinary excretion of NO2+NO3 (UNOXV) and cGMP (UcGMPV) increased progressively during the experiment. Pretreatment with aminoguanidine or dexamethasone, inhibitors of inducible NO synthase (iNOS), prevented the increase in UNOXV and UcGMPV but had no impact on mean arterial pressure (BP), renal vascular resistance (RVR) or GFR. Since these variables did not change in the conscious rat, the increased UNOXV results from some aspect of the acute surgical preparation. When acutely prepared rats received L-NAME, a non-specific NOS inhibitor, BP and RVR increased but paradoxical increases in UNOXV and UcGMPV were also seen. Nonselective NOS inhibition (+L-NAME) was fatal in 50% of acutely prepared rats, causing cardiac contracture. The same dose of L-NAME produced no deaths in either conscious chronically catheterized rats or in acutely prepared rats, previously subjected to sterile surgery and acute L-NAME in the conscious state. These data indicate that acute, nonsterile surgery induces expression of iNOS, but that the additional NO generated has no obvious cardiovascular/renal actions. Acute UNOXV and UcGMPV do not predict total NO production, or "hemodynamically active" NO. Generalized NO inhibition in rats acutely stressed by surgery/anesthesia can be fatal.

Human atrial natriuretic peptide infusion and ovarian venous progesterone secretion in Yucatan micropigs.

Chronic indwelling catheters were implanted in the ovarian and external jugular veins of Yucatan micropigs during the luteal phase. Infusion of hypertonic saline (0.4 mol NaCl l-1) increased the concentration of porcine immunoreactive atrial natriuretic peptide in ovarian venous blood plasma by 0.61-1.81 fmol ml-1 more than that of the saline control group. Conversely, endogenously released porcine immunoreactive atrial natriuretic peptide was associated with low ovarian venous progesterone concentrations. Infusion of human atrial natriuretic peptide induced a dose-dependent increase in the progesterone concentration in ovarian venous blood. The results reported here suggest a duality in the ovarian response to atrial natriuretic peptide: a decrease in progesterone secretion in response to low concentrations and stimulated progesterone secretion in response to high concentrations of this peptide.