Infants seen in the ED for bronchiolitis have a prolonged disease course, with substantial burden to the family. Symptom duration may be influenced by a propensity toward atopy. Clinicians may use this information for counseling families.

Background-Adenosine (Ado) and dipyridamole are alternatives to exercise stress for myocardial perfusion imaging.Though generally safe, side effects frequently occur that cause patient discomfort and sometimes lead to premature termination of the study or require aminophylline administration. Recently, a new class of A 2A Ado receptor agonists was synthesized. ATL193 and ATL146e are 2-propynylcyclohexyl-5Ј-N-ethylcarboxamido derivatives of Ado. The study goals were to evaluate the potency and selectivity of these new compounds on recombinant canine Ado receptors and to evaluate their hemodynamic properties in dogs to assess their usefulness as vasodilators for myocardial perfusion imaging. Methods and Results-In assays of recombinant canine Ado receptors, ATL-193 and ATL-146e were highly selective for the A 2A over the A 1 and A 3 receptors and were more potent than MRE-0470 and CGS-21680. In 16 anesthetized dogs, the agonists were administered by infusion (ATL-193; nϭ7 normal) or bolus injection (ATL-146e; nϭ9 critical left anterior descending coronary artery stenosis), and hemodynamic responses were compared with those of Ado. Both agonists produced dose-dependent coronary flow (CF) elevation without provoking the hypotension observed with Ado.After an ATL-146e bolus, the CF increase was sustained for several minutes, providing ample time for injection and myocardial uptake of 99m Tc-sestamibi, and CF returned to baseline within 20 minutes. The CF increase was completely blocked by the selective A 2A antagonist ZM241385 (3 g · kg Ϫ1 · min Ϫ1 ). Conclusions-ATL-193 and ATL-146e are highly potent and selective Ado A 2A receptor agonists with excellent potential for use as vasodilators for myocardial perfusion imaging. An important advantage of ATL-146e is the ability to administer it by bolus injection.

GA. Cardioprotection by adenosine A2A agonists in a canine model of myocardial stunning produced by multiple episodes of transient ischemia. Am J Physiol Heart Circ Physiol 292: H3164 -H3171, 2007. First published February 16, 2007; doi:10.1152/ajpheart.00743.2005.-We sought to determine whether administration of a very low, nonvasodilating dose of a highly selective adenosine A2A receptor agonist or ATL-146e) would be cardioprotective in a canine model of myocardial stunning produced by multiple episodes of transient ischemia. Twenty-four anesthetized open-chest dogs underwent either 4 (n ϭ 12) or 10 cycles (n ϭ 12) of 5-min left anterior descending coronary artery (LAD) occlusions interspersed by 5 or 10 min of reperfusion. Left ventricular thickening was measured from baseline through 180 min after the last occlusion-reperfusion cycle. Regional flow was measured with microspheres. In 12 of 24 dogs, A2A receptor agonist was infused intravenously beginning 2 min prior to the first occlusion and continuing throughout reperfusion at a dose below that which produces vasodilatation (0.01 g ⅐ kg Ϫ1 ⅐ min Ϫ1 ). Myocardial flow was similar between control and A2A receptor agonist-treated animals, confirming the absence of A2 receptor agonist-induced vasodilatation. During occlusion, there was severe dyskinesis with marked LAD zone thinning in all animals. After 180 min of reperfusion following the last cycle, significantly greater recovery of LAD zone thickening was observed in A2A receptor agonist-treated vs. control animals in both the 4-cycle (91 Ϯ 7 vs. 56 Ϯ 12%, respectively; P Ͻ 0.05) and the 10-cycle (65 Ϯ 9 vs. 8 Ϯ 16%, respectively; P Ͻ 0.05) occlusion groups. The striking amount of functional recovery observed with administration of low, nonvasodilating doses of adenosine A2A agonist ATL-193 or ATL-146e supports their further evaluation for the attenuation of postischemic stunning in the clinical setting. left ventricular dysfunction; demand ischemia; reperfusion injury MYOCARDIAL STUNNING IS A FORM of reversible reperfusion injury characterized by prolonged depression of left ventricular (LV) contractile function in viable myocardium despite restoration of normal or near-normal resting blood flow (7,28). Clinical studies have demonstrated that many patients with coronary artery disease experience repetitive episodes of myocardial ischemia in the same vascular territory while going about their daily activities (14). Echocardiographic and radionuclide studies have demonstrated that severe postischemic contractile dysfunction, or myocardial stunning, occurs following periods of exercise or pharmacological stress-induced ischemia (15,30,34). Importantly, animal studies have shown that frequent episodes of myocardial ischemia that occur in close temporal proximity have a cumulative effect on the deterioration of myocardial contractility, and some (29, 33, 52) have proposed that repetitive myocardial stunning following demand ischemia is the mechanism for myocardial hibernation. In addition, this phenomenon has ...

Viral bronchiolitis is the most common cause of hospitalization among infants. Despite its prevalence, no consistently effective therapy has been found to date, providing the driving force behind much of the ongoing research into this illness. In this review, we present a summary of the most recent published trials of interventions for bronchiolitis. Included are studies evaluating bronchodilators, corticosteroids, positive pressure ventilation, as well as 3 newer therapies for bronchiolitis: heliox, mucolytics, and leukotriene receptor antagonists.