The design of polymers and oligomers that mimic the complex structures and remarkable biological properties of proteins is an important endeavor with both fundamental and practical implications. Recently, a number of nonnatural peptides with designed sequences have been elaborated to provide biologically active structures; in particular, facially amphiphilic peptides built from ␤-amino acids have been shown to mimic both the structures as well as the biological function of natural antimicrobial peptides such as magainins and cecropins. However, these natural peptides as well as their ␤-peptide analogues are expensive to prepare and difficult to produce on a large scale, limiting their potential use to certain pharmaceutical applications. We therefore have designed a series of facially amphiphilic arylamide polymers that capture the physical and biological properties of this class of antimicrobial peptides, but are easy to prepare from inexpensive monomers. The design process was aided by molecular calculations with density functional theory-computed torsional potentials. This new class of amphiphilic polymers may be applied in situations where inexpensive antimicrobial agents are required.

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Objective: ' To determine whether alkalinization with sodium bicarbonate (NaHCO,) in near-lethal hyperkalemia either lowers potassium (K) rapidly or shortens duration of cardiac conduction disturbances. Methods: A controlled canine laboratory investigation of 3 treatments for severe hyperkalemia. Conditioned dogs (n = 8; 17-30 kg) received, in random order, 2 mmolkg of each of 3 treatments (matched in sodium and water) in separate experiments 2 1 week apart: 1.05% NaHCO, over 60 minutes (infusion therapy); 8.4% NaHCO, over 5 minutes, then 14 mL/kg sterile water over 55 minutes (bolus therapy); 8.4% NaCl over 5 minutes, then 14 mwkg sterile water over 55 minutes (saline therapy). Prior to administering one of the above therapies, the animals were anesthetized with 0.5-2.5% isoflurane and ventilated to maintain a normal Pcoz. After 30 minutes of equilibration, 2 mmol/kg/hr (loading dose) of a 2-mmoVmL KC1 solution was given until idioventricular or relative junctional bradycardic dysrhythmias were sustained for 15 minutes. Then KC1 was decreased to 1 mmol/kg/hr (maintenance dose) for 2 hours and 45 minutes. Treatment was begun after 45 minutes of maintenance KCI infusion. Results: The pretreatment K level (all studies) was 9.06 2 0.82 mmoVL (mean 2 SD). Although the mean K level decreased more after saline therapy than after bolus therapy at every time, differences were neither statistically significant nor clinically important during the first 30 minutes. The means of the differences in decreases (saline minus bolus) were small, 0.26 (95% CI, -0.48 to 1.00) at 15 minutes, 0.16 (95% CI, -0.67 to 0.98) at 30 minutes. Dysrhythmia duration was shorter with bolus therapy than for saline therapy in only 1 of 5 dogs ( p = 0.38). Conclusions: Hypertonic saline bolus lowered plasma K as effectively as NaHC03 bolus in this animal model within the first 30 minutes. Clinically meaningful decreases due to alkalinization alone within 30 minutes are unlikely.