ABSTRACT
Dengue virus (DENV) is an arthropod-borne virus (family Flaviviridae) causing dengue fever or dengue hemorrhagic fever. Here, we report the first fatal DENV infection imported into Germany. A female traveler was hospitalized with fever and abdominal pain after returning from Ecuador. Due to a suspected acute acalculous cholecystitis, cholecystectomy was performed. After cholecystectomy, severe spontaneous bleeding from the abdominal wound occurred and the patient died. Postmortem analysis of transudate and tissue demonstrated a DENV secondary infection of the patient and a gallbladder wall thickening (GBWT) due to an extensive edema.
Subject(s)
Severe Dengue/mortality , Travel , Adult , Fatal Outcome , Female , Germany , HumansABSTRACT
Recently direct myocardial effects of antikaliuretic diuretics with respect to contractility parameters and prevention of digitalis-induced arrhythmias were published. In order to test the value of these reports we measured the effect of potassium-canrenoate and triamterene on cardiac output and on digitalis-induced arrhythmias in patients during diagnostic and the therapeutic flow directed right heart catheterization (Swan-Ganz) in our intensive care unit. In addition the influence of these drugs on (Na+ + K+)-ATPase and on (3H)g-strophanthin binding to human cardiac cell membranes was investigated to gain information on the mechanism of their action. Triamterene (100-200 mg p.o.) was without any effect on cardiac output, the same was found true for potassium-canrenoate given in a single dose (200-1000 mg intravenously). However, when applied in two doses (200 mg i.v. and 60 min later 400 mg i.v.), potassium-canrenoate increased cardiac output by 11 percent (p less than 0.05). Only in 2 out of 14 patients potassium-canrenoate (200-400 mg i.v.) suppressed digitalis-induced ventricular ectopic beats. Canrenone, the active metabolite of potassium-canrenoate displaces [(3H)]g-strophanthin from its binding sites in human cardiac cell membranes and inhibits (Na+ + K+)-ATPase activity. These in vitro effects were measured at the same concentrations as found in vivo after "therapeutical" doses. The effects of triamterene in this respect were found only in extremely high concentrations. Our results imply that canrenone has cardiac glycoside-like effects in human cardiac cell membranes.
Subject(s)
Diuretics/pharmacology , Heart/drug effects , Adenosine Triphosphatases/antagonists & inhibitors , Adult , Aged , Arrhythmias, Cardiac/physiopathology , Canrenoic Acid/pharmacology , Cardiac Output/drug effects , Cell Membrane/drug effects , Cell Membrane/enzymology , Coronary Disease/physiopathology , Digoxin/blood , Dose-Response Relationship, Drug , Drug Interactions , Female , Humans , In Vitro Techniques , Male , Middle Aged , Myocardium/enzymology , Myocardium/metabolism , Ouabain/metabolism , Potassium/metabolism , Receptors, Drug , Sodium , Triamterene/pharmacologyABSTRACT
Stereospecific binding sites for (-) [3H]-alprenolol, a beta-adrenergic antagonist, have been identified in guinea-pig myocardial broken cell preparations. The concentration of the sites was 0.3 pmoles per mg of protein and the dissociation constant (at 37 degrees C) 10(-8) M. A close correlation between the ability of various beta-adrenergic antagonists to compete with tracer alprenolol binding and to block the response of isoprenaline-stimulated myocardial adenylate cyclase has been found. Low affinity sites for the labelled beta-adrenergic antagonist in contrast to stereospecific sites are heat stable and do not discriminate between the (-) and the (+) forms of the beta-adrenergic antagonists. Adenylate cyclase in guinea-pig myocardial tissue is poorly stimulated by isoprenaline or 5'-guanylylimidodiphosphate. This is attributed to a high basal activity which could be lowered by a preincubation at 37 degrees C.
