Influence of cholinergic blockade on the development ...
|Title||Influence of cholinergic blockade on the development of epinephrine-induced ventricular arrhythmias in halothane- and isoflurane-anesthetized dogs|
|Author(s)||Kip A. Lemke, W. J. Tranquilli, J. C. Thurmon, G. J. Benson, W. A. Olson|
|Abstract||The arrhythmogenic effects of anaesthetic drugs were assessed using the arrhythmogenic dose of epinephrine (ADE) model. The purpose of this study was to determine the influence of cholinergic blockade (CB) produced by glycopyrrolate (G) on ADE in 1.5 minimum alveolar concentration (MAC) halothane (H)- and isoflurane (I)-anaesthetized dogs. Eight dogs (weighing between 12.5 and 21.5 kg) were randomly assigned to 4 treatment groups (H, HG, I and IG), each treatment replicated 3 times. Anaesthesia was induced and maintained with H (1.31%, end-tidal [ET]) or I (1.95%, ET) in oxygen. Ventilation was controlled (carbon dioxide [PCO2] 35 to 40 mmHg, ET). G was administered 10 minutes before ADE determination at a dose of 22 micro g/kg (11 micro g/kg, i.v., and 11 micro g/kg, i.m.). The ADE was determined by IV infusion of epinephrine at sequentially increasing rates of 1.0, 2.5 and 5.0 micro g/kg/min; and defined as the total dose of epinephrine producing at least 4 ectopic ventricular contractions (EVCs) within 15 seconds during a 3-minute infusion and up to 1 minute after the end of the infusion. Total dose was calculated as the product of infusion rate and time to arrhythmia. Values are reported as means +or- standard error. The ADE ( micro g/kg) for H, HG, I and IG were 1.53 +or- 0.08, 3.37 +or- 0.46, 1.61 +or- 0.21 and >15.00, respectively. Heart rates (HRs) (beats/min) and systolic pressures (mmHg) at the time of arrhythmia formation for H, HG, I and IG were (60.3 +or- 4.0 and 142 +or- 7.6), (214.0 +or- 13.1 and 239.2 +or- 7.1), (62.9 +or- 4.5 and 151.9 +or- 6.3) and (226.3 +or- 6.1 and 323.5 +or- 3.4), respectively. The H and I ADE were not different. The GH ADE was significantly less than the IG ADE. The H and I ADE were significantly less than the HG and IG ADE. It is concluded that epinephrine infusion in halothane- and isoflurane-anaesthetized dogs: (1) two distinct mechanisms are responsible for the development of arrhythmias, (2) CB produced by G significantly increases ADE but is associated with higher rate pressure products (RPP) and myocardial work, and (3) ADE methodology could be improved by determining ADE with and without CB..|
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