There are nearly 700,000 annual US emergency department (ED) visits for acute heart failure (AHF). While blood pressure is elevated on most of these visits, acute therapy remains focused on preload and not afterload reduction. Data from recent prospective studies suggest AHF patients with concomitant acute hypertension benefit from intravenous (IV) vasodilators. To better understand the use of vasodilators for such patients, we conducted a systematic review of 1) currently available intravenous vasodilators for ED patients with AHF, or 2) intravenous vasodilators which are not yet available, but have completed Phase III clinical trials in AHF, and may be available for ED use in the future. We employed multi-term search queries to retrieve research involving nitroglycerin, nitroprusside, enalaprilat, hydralazine, relaxin and nesiritide. A total of 2001 unique citations were identified from three databases: PubMed, EMBASE, and CINAHL. Of these, 1966 were excluded based on established review criteria, leaving 35 published papers for inclusion. Our primary finding was that IV nitrovasodilators, when used in the treatment of AHF in ED and ED-like settings, do improve short-term symptoms and appear safe to administer. There is no data suggesting they impact mortality. Other commonly used vasodilators such as hydralazine and enalaprilat have very little published data about their safety and efficacy. Of note, few studies enrolled patients early in their course of treatment. Thus, to assess the specific impact of vasodilator therapy on both short- and long-term outcomes, future research efforts should focus on patient recruitment in the ED setting.

The effects of abamectin (AVMB1) on intracellular potassium ion activity (aKi) and resting membrane potential (Em) of the skeletal muscle cells of final instar larvae of Phormia terraenovae (Diptera) were investigated using K+‐selective micro‐electrodes. Bathing the preparation in 10− M AVMB1(+ 1 ml litre−1 dimethylsulfoxide) for 60 min caused a significant (31%) decrease in aKi, whilst Em depolarized on average by 19 mV (nearly 50% of the original control value). The difference EK‐Em increased by 9 mV, although EK (potassium equilibrium potential) remained more negative than Em. These results could be due to a cationic effect of AVMB1 possibly involving an increase in K+ and Na+ conductances of the muscle plasma membrane.