摘要:

The arrhythmogenic effects of anesthetic drugs are 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)‐anesthetized dogs. Eight dogs (weighing between 12.5 and 21.5 kg) were randomly assigned to four treatment groups (H, HG, I, and IG) and each treatment was replicated three times. Anesthesia 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 μg/kg (11 μg/kg, intravenous [IV]and 11 μg/kg, intramuscular [IM]). The ADE was determined by IV infusion of epinephrine at sequentially increasing rates of 1.0, 2.5, and 5.0 μg/kg/min; and defined as the total dose of epinephrine producing at least four 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. Data were analyzed using a randomized complete block analysis of variance. When significant (P15.00, 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 ±4.0 and 142.0 ± 7.6), (213.0 ± 13.1 and 239.2 ± 7.1), (62.9 ± 4.5 and 151.9 ± 6.3), and (226.3 ± 6.1 and 323.5 ± 3.4), respectively. The H and I ADE were not different. The HG ADE was significantly less than the IG ADE. The H and I ADE were significantly less than the HG and IG ADE. We conclude the following from the results of this study of epinephrine infusion in halothane‐ and isoflurane‐anesthetized 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 determi

ISSN:0161-3499    

DOI:10.1111/j.1532-950X.1994.tb00446.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

A randomized, blinded, crossover study was designed to evaluate the respiratory, cardiovascular, and behavioral effects of butorphanol given postoperatively to oxymorphone‐premedicated and surgically stimulated dogs. Nine healthy adult dogs were premedicated intramuscularly with atropine (0.04 mg/kg), acepromazine (0.10 mg/kg), and oxymorphone (0.2 mg/kg). Anesthesia was induced with thiamylal (12 mg/kg) and maintained with halothane in oxygen. According to the protocol of a concurrent study, all dogs had percutaneous endoscopic gastrostomy (PEG) feeding tubes placed during the first anesthetic episode and removed during the second anesthetic episode. All dogs received postoperatively either butorphanol tartrate (0.2 mg/kg) or an isovol‐umetric dose of saline placebo, both given intravenously. Respiratory rate (RR), tidal volume (TV), minute ventilation (MV), end‐tidal CO2concentration (ETCO2). heart rate (HR), and indirect diastolic (DP), systolic (SP) and mean arterial (MAP) blood pressures were measured at times 0, 2, 5, 10, 20, 40, 80, and 120 minutes after injection. The time from injection of the test drug until extubation was recorded. RR, MV, HR, and DP were significantly (P<.05) increased, while ETco2was significantly decreased, for a minimum of 30 minutes in butorphanol‐treated dogs compared with saline controls. TV, SP, and MAP were transiently (≤15 minutes) increased in butorphanol‐treated dogs compared with saline controls. There was no significant difference between the times to extubation in the butorphanol‐treated dogs versus the saline

ISSN:0161-3499    

DOI:10.1111/j.1532-950X.1994.tb00447.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

ISSN:0161-3499    

DOI:10.1111/j.1532-950X.1994.tb00448.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

ISSN:0161-3499    

DOI:10.1111/j.1532-950X.1994.tb00449.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY