9 research outputs found
EFFECTS OF AMIODARONE ON REFRACTORY VENTRICULAR-FIBRILLATION IN ACUTE MYOCARDIAL-INFARCTION - EXPERIMENTAL-STUDY
Objectives. The aim of this study was to evaluate the efficacy of a
single dose of intravenous amiodarone in facilitating defibrillation of
ventricular fibrillation refractory to lidocaine and epinephrine plus
direct current countershocks in experimental acute myocardial
infarction.
Background. Amiodarone has been hailed as the most effective single
antiarrhythmic drug for the treatment of ventricular arrhythmias.
However, intravenous amiodarone has only sporadically been used in the
defibrillation of ventricular fibrillation in acute myocardial
infarction.
Methods. Acute myocardial infarction was induced in 60 dogs by ligation
of the proximal left anterior descending coronary artery for 2 h.
Animals that developed spontaneous ventricular fibrillation were treated
with lidocaine and epinephrine plus five direct-current countershocks.
Dogs with ventricular fibrillation refractory to this regimen were
randomized to further treatment with additional intravenous
administration of epinephrine and bolus lidocaine plus
less-than-or-equal-to 15 direct-current countershocks (group 1) or
administration of amiodarone, 10 mg/kg body weight intravenously,
followed by defibrillation with direct-current countershock (group II).
Results. Sixteen (27%) of the 60 dogs in which the protocol was
attempted developed spontaneous ventricular fibrillation 21 min after
ligation and were included in the study. Lidocaine and epinephrine plus
five direct-current countershocks succeeded in converting ventricular
fibrillation in one dog (6%). The other 15 dogs were randomized to
group I (8 dogs) or group II (7 dogs). Defibrillation was achieved in
one of the eight dogs in group I and in six of the seven dogs in group
II (p < 0.005).
Conclusions. In an experimental model of acute ischemia, intravenous
amiodarone (10 mg/kg) influences positively the response to
defibrillation of ventricular fibrillation refractory to lidocaine and
epinephrine plus direct current countershocks
A licensing step links AID to transcription elongation for mutagenesis in B cells
Activation-induced deaminase (AID) is important for inducing desirable mutations at the B cell receptor genes for effective antibody responses. Here the authors show that three key arginine residues of AID link AID-chromatin association with transcription elongation to license AID for specific mutagenesis in B cells