Posttraumatic stress disorder (PTSD) is an extremely debilitating disease with a broad array of associated symptoms, making the disorder difficult to diagnose and treat. In humans, patients seem to benefit from group therapy or other means of promoting social behavior. To test these effects on our rodent model of PTSD, adult, male rats were housed in either single or pair conditions prior to and during an acute stressor to induce PTSD-like behaviors in these rats. Subsequently, rats were assessed for PTSD-like symptoms to determine the effect of social housing on stress-induced phenotypes. Posttrauma phenotypes, including enhanced fear conditioning and anxiety-related behavior, persisted regardless of the animal's housing condition. It is possible that any housing driven improvements to stress-induced phenotypes would require longer periods of pair housing than were used in these experiments. Although PTSD patients show improved health outcomes following social interaction or group therapy, the fear and anxiety phenotypes seen following an acute stressor in an animal model of the disease endured despite an animal's housing condition.
Summary: The effects of intravenous encainide on digoxin-induced atrial ectopic tachycardia (AET) were investigated in the rat using 3-channel simultaneous limblead electrocardiography. Pentobarbital-anesthetized (35 mg/kg, intraperitoneal) adult male rats were given digoxin subcutaneously, 30 mg/kg. After onset of AET, rats received either saline (0.5 ml/kg) or encainide; 0.25,0.5, 1 .O, or 2.0 mg/kg intravenously in repeated doses at 15-min intervals. At all doses, encainide converted digoxininduced AET to ventricular arrhythmias, prolonged recovery time, and increased mortality in comparison to salinetreated animals. An additional gmup of anesthetized rats was not given digoxin. These animals received encainide (2.0 mg/kg, intravenously) in repeated doses at 15-min intervals and developed dose-related increases in the P-R interval only. Blood samples were obtained by cardiac puncture from 12 additional anesthetized, digoxin-treated rats 5 min after the fourth intravenous dose of saline (0.5 ml/kg, n=6) orencainide (l.Omg/kg, n=6). Serum was prepared and analyzed by affinity column-mediated immunoassay. Digoxin levels were the same in both groups. These results suggest that encainide may exacerbate digoxin-induced arrhythmias (pmarrhythmic effect) in this species. In view of our findings of digoxin-encainide interactions in the rat, we recommend caution if these drugs are coadministered in humans.
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