The effects of atropine and methotrimeprazine on the epinephrine-induced arrhythmias in halothane-anesthetized dogs

The effects of atropine and methotrimeprazine on epinephrine-induced ventricular arrhythmias were evaluated in halothane-anesthetized dogs. Ten mixed-breed dogs were assigned to 3 treatments (saline, atropine, and methotrimeprazine) in a randomized complete block design. Anesthesia was induced and maintained with halothane (1.5 minimum alveolar concentration) in oxygen. Controlled ventilation was used throughout to maintain eucapnia. Saline, atropine (0.05 mg/kg, IV) or methotrimeprazine (0.5 mg/kg, IV) were administered and, 5 minutes later the arrhythmogenic dose of epinephrine (ADE) was measured by IV infusion of progressively increasing infusion rates of epinephrine, until the ventricular arrhythmia criterion was met (at least 4 ectopic ventricular contractions (EVCs) during a 15-second period). Data were analyzed using a student's t-test for ADE values and multivariate profile analysis for heart rate (HR), arterial blood pressure (ABP), and rate pressure product (RPP). The ADE increased in atropine- and methotrimeprazine-treated groups, whereas 1 and 4 animals from these groups did not develop any ventricular arrhythmia, respectively. Epinephrine induced multiform premature ventricular contractions (PVCs) in the atropine group, whereas ventricular escape beats were observed in the control and methotrimeprazine groups. Heart rate and RPP decreased, and ABP increased at the time of ADE observation in the control group. Epinephrine infusion in the atropine group caused marked increases in HR, ABP, and RPP, which were associated with pulsus alternans in 2 animals. It was concluded that 1) the presence of cholinergic blockade influences the type of ventricular arrhythmia induced by epinephrine; 2) increased ADE values recorded following atropine administration must be cautiously interpreted, since in this situation the PVCs were associated with signs of increased myocardial work and ventricular failure; and 3) the use of a broader arrhythmia criterion (EVCs instead of PVCs) may not allow a direct comparison between ADE values, since it includes ventricular arrhythmias mediated by different mechanisms.

Sedative and cardiorespiratory effects of acepromazine or atropine given before dexmedetomidine in dogs

To test the hypothesis that acepromazine could potentiate the sedative actions and attenuate the pressor response induced by dexmedetomidine, the effects of acepromazine or atropine were compared in six healthy adult dogs treated with this alpha(2)-agonist. In a randomised block design, the dogs received intravenous doses of either physiological saline, 0.05 mg/kg acepromazine or 0.04 mg/kg atropine, 15 minutes before an intravenous dose of 5 mu g/kg dexmedetomidine. The dogs' heart rate was reduced by 50 to 63 per cent from baseline and their mean arterial blood pressure was increased transiently from baseline for 20 minutes after the dexmedetomidine. Atropine prevented the alpha(2)-agonist-induced bradycardia and increased the severity and duration of the hypertension, but acepromazine did not substantially modify the cardiovascular effects of the a2-agonist, except for a slight reduction in the magnitude and duration of its pressor effects. The dexmedetomidine induced moderate to intense sedation in all the treatments, but the dogs' sedation scores did not differ among treatments. The combination of acepromazine with dexmedetomidine had no obvious advantages in comparison with dexmedetomidine alone, but the administration of atropine before dexmedetomidine is contraindicated because of a severe hypertensive response.

Comparative study between atropine and hyoscine-N-butylbromide for reversal of detomidine induced bradycardia in horses

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Evaluation of cardiorespiratory effects of combinations of dexmedetomidine and atropine in cats

The cardiovascular effects of dexmedetomidine alone or in combination with atropine were studied in six cats. Cats underwent four treatments in a randomized crossover design as follows: DEX15, saline + dexmedetomidine 15 mu g/kg; DEX30, saline + dexmedetomidine 30 mu g/kg; ADEX15, atropine + dexmedetomidine 15 mu g/kg; ADEX30, atropine + dexmedetomidine 30 mu g/kg. Pulse rate (PR) and systolic arterial pressure (SAP) decreased in DEX15 and DEX30. Premedication with atropine was effective in preventing bradycardia (PR < 100 beats/min) and resulted in a biphasic effect in blood pressure. Hypertension was followed by a gradual decrease in SAP. Rate pressure product decreased in DEX15 and DEX30 whereas in ADEX15 and ADEX30 it remained within baseline values for at least 60 min. Although premedication with atropine in cats sedated with dexmedetomidine prevents bradycardia, it induces hypertension and increases myocardial oxygen consumption. The magnitude of cardiovascular effects produced by dexmedetomidine in cats does not seem to be dose-related. (C) 2009 ESFM and AAFP. Published by Elsevier Ltd. All rights reserved.

Effects of tiletamine/zolazepam-romifidine-atropine in ocelots (Leopardus pardalis)

Objectives: To evaluate the effects of a combination of tiletamine-zolazepam-romifidine-atropine in ocelots. Design: Prospective experimental trial. Animals: Eight captive adult ocelots (three females and five males). Methods: Calculated doses of tiletamine-zolazepam (3.75 mg kg -1), romifidine (50 μg kg-1) and atropine (0.04 mg kg-1) were administered intramuscularly. After immobilization, animals were weighed and the real doses determined. Heart rate, respiratory frequency, noninvasive systolic, diastolic, and mean arterial pressure, arterial oxygen hemoglobin saturation, and rectal temperature were measured. Data were analyzed by means of ANOVA for repeated measures, followed by the Tukey test to compare values over time. Results: Doses administered were 3.4 ± 0.6 mg kg-1 of tiletamine-zolazepam, 0.04 ± 7.0 mg kg-1 of romifidine, and 0.03 ± 0.007 mg kg-1 of atropine. The mean time to recumbency and duration of immobilization were 7.0 ± 4.5 and 109.2 ± 27.9 minutes, respectively. The median times to standing and walking were 52.3 [0-90] and 2.3 [0-69.3] minutes, respectively. A decrease in heart rate was observed 45 minutes following drug administration. Arterial blood pressure was maintained during the study. Conclusions and clinical relevance: This protocol produced good immobilization in ocelots with minimal changes over time in cardiovascular parameters.

Effects of a dexmedetomidine constant rate infusion and atropine on changes in global perfusion variables induced by hemorrhage followed by volume replacement in isoflurane-anesthetized dogs

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Effects of physical and chemical immobilization on hematologic and biochemical variables in captive brown brocket deer (Mazama gouazoubira)

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

A preliminary trial comparison of several anesthetic techniques in cats

The aim of this study was to investigate the effect of several drug combinations (atropine, xylazine, romifidine, methotrimeprazine, midazolam, or fentanyl) with ketamine for short term anesthesia in cats. Twelve cats were anesthetized 6 times by using a cross-over Latin square protocol: methotrimeprazine was combined with midazolam, ketamine, and fentanyi; midazolam and ketamine; romifidine and ketamine; and xylazine and ketamine. Atropine was combined with romifidine and ketamine, and xylazine and ketamine. Temperature, heart rate, and respiratory rate decreased in all groups. Apnea occurred in 1 cat treated with methotrimeprazine, romifidine, and ketamine, suggesting that ventilatory support may be necessary when this protocol is used. Emesis occurred in some cats treated with alpha(2)-adrenoceptor agonists, and this side effect should be considered when these drugs are used.

Evaluation of Hemodynamic, Metabolic, and Electrolytic Changes After Graft Reperfusion in a Porcine Model of Intestinal Transplantation

Background. We sought to establish an anesthetic protocol to evaluate the hemodynamic, metabolic, and electrolytic changes after graft reperfusion in pigs undergoing orthotopic intestinal transplant (ITX).Methods. Fifteen pigs were distributed into two groups: GI (n = 6), without immunosuppression, and GII (n = 9), immunosuppressed before surgery with tacrolimus (0.3 mg/kg). The animals were premedicated at 1 hour before surgery with IM acepromazine (0.1 mg/kg), morphine (0.4 mg/kg), ketamine (10 mg/kg), and atropine (0.044 mg/kg IM). Anesthesia induction used equal proportions of diazepam and ketamine (0.1-0.15 mL/kg/IV) and for maintenance in IV infusion of xylazine (1 mg/mL), ketamine (2 mg/mL), and guaiacol glyceryl ether 5% (50 mg/mL), diluted in 250 mL of 5% glucose solution. In addition, recipient pigs were treated with isofluorane inhalation. Heart rate (HR), systolic (SAP), mean (MAP), and diastolic (DAP) arterial pressure, pulse oximetry, respiratory frequency (f), capnography, body temperature (T), blood gas analysis (pH, PaCO(2), PaO(2), base excess, BE; HCO(3)(-), SatO(2)), serum potassium (K), calcium (Ca), sodium, hematocrit (Hct), and glucose (Glu) were measured at four times; MO: after incision (basal value); M1: 10 minutes before reperfusion; and M2 and M3: 10 and 20 minutes after graft reperfusion.Results. All groups behaved in a similar pattern. There was significant hypotension after graft reperfusion in GI and GII (M2 = 56.2 +/- 6.4 and M3 = 57.2 +/- 8.3 mm Hg and M2 = 65.7 +/- 10.2 and M3 = 67.8 +/- 16.8 mm Hg, respectively), accompanied by elevated HR. The ETCO(2) was elevated at M2 (42 mm Hg) and M3 (40 mm Hg). Metabolic acidosis was observed after reperfusion, with significant increase in K levels.Conclusion. The anesthetic protocol for donors and recipients was safe to perform the procedure, allowing control of hemodynamic and metabolic changes after reperfusion without differences regarding immunosuppression.

Anestesia intravenosa total utilizando propofol ou propofol/cetamina em cadelas submetidas à ovariossalpingohisterectomia

Objetivou-se avaliar os efeitos cardiorrespiratório e analgésico da infusão contínua com propofol e propofol/cetamina em cadelas pré-medicadas com atropina e xilazina, submetidas a ovariossalpingohisterectomia (OSH). em seis cadelas (GP) a indução anestésica foi realizada com propofol (5mg kg-1 iv), seguido da manutenção anestésica com o mesmo fármaco em infusão contínua intravenosa na taxa inicial de 0,4mg kg-1.min-1. Outras seis cadelas (GPC) receberam a associação de propofol (3,5mg kg-1 iv) e cetamina (1mg kg-1 iv) como indução anestésica. Depois, foi feita manutenção anestésica em infusão contínua intravenosa inicial com 0,28mg kg-1.min-1 e 0,06mg kg-1.min-1 de propofol e cetamina, respectivamente. Os seguintes parâmetros foram mensurados durante a anestesia a cada 10 minutos: freqüências cardíaca (FC) e respiratória (f), pressão arterial sistólica, média e diastólica (PA), concentração final expirada de CO2 (EtCO2), volume minuto (VM), pressão parcial de gás carbônico (PaCO2), pressão parcial de oxigênio (PaO2), saturação de oxigênio na hemoglobina (SatO2), pH, bicarbonato, glicemia e temperatura retal (T). Observou-se redução da pressão arterial média entre 20 e 40 minutos de anestesia no GP. Ocorreu redução da temperatura, hipercapnia e acidose respiratória em ambos os grupos durante a anestesia. A PaO2, o bicarbonato e a glicose aumentaram de forma significativa apenas no GPC durante a anestesia. Houve necessidade de aumentar em 50 e 20% a taxa de infusão de propofol no GP e GPC respectivamente para anestesia cirúrgica satisfatória. Dessa forma, ambos os protocolos mostraram-se seguros e suficientes do ponto de vista de anestesia cirúrgica para realização da OSH em cadelas, desde que a ventilação assistida ou controlada seja instituída quando necessária e a velocidade de infusão do propofol seja 0,6 e 0,34mg kg-1.min-1 nos grupos GP e GPC, respectivamente.

Parametria da associação do midazolam ou diazepam em cães pré-tratados pela atropina e tratados pela dexmedetomidina e quetamina

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Effects of AV3V lesion on pilocarpine-induced pressor response and salivary gland vasodilation

The cholinergic agonist pilocarpine injected intraperitoneally (ip) increases mean arterial pressure (MAP) and superior mesenteric (SM) vascular resistance and reduces submandibular/sublingual gland (SSG) vascular resistance. In the present study, we investigated the effects of electrolytic lesions of the anteroventral third ventricle (AV3V) region on the changes in MAP, SM, and SSG vascular resistances induced by ip pilocarpine. Male Holtzman rats anesthetized with urethane (1.0 g/kg) and chloralose (60 mg/kg) were submitted to sham or electrolytic AV3V lesions and bad pulsed Doppler flow probes implanted around the arteries. Contrary to sham rats, in 1-h and 2-day AV3V-lesioned rats, pilocarpine (4 mu mol/kg) ip decreased MAP (-41 +/- 4 and -26 4 mm Hg, respectively, vs. sham: 19 +/- 4 mm Hg) and SM (-48 +/- 11 and -45 +/- 10%, respectively, vs. sham: 41 +/- 10%) and hindlimb vascular resistances (-65 +/- 32 and -113 +/- 29%, respectively, vs. sham: 19 +/- 29%). In 7-day AV3V-lesioned rats, pilocarpine produced no changes on MAP and SM and hindlimb vascular resistances. Similar to sham rats, pilocarpine reduced SSG vascular resistance 1 h after AV3V lesions (-46 +/- 6%, vs. sham: -40 +/- 6%), but it produced no effect 2 days after AV3V lesions and increased SSG vascular resistance (37 6%) in 7-day AV3V-lesioned rats. The responses to ip pilocarpine were similar in 15-day sham and AV3V-lesioned rats. The cholinergic antagonist atropine methyl bromide (10 nmol) iv slightly increased the pressor response to ip pilocarpine in sham rats and abolished for 40 min the fall in MAP induced by ip pilocarpine in 1-h AV3V-lesioned rats. The results suggest that central mechanisms dependent on the AV3V region are involved in the pressor responses to ip pilocarpine. Although it was impaired 2 and 7 days after AV3V lesions, pilocarpine-induced salivary gland vasodilation was not altered 1 h after AV3V lesions which suggests that this vasodilation is not directly dependent on the AV3V region. (c) 2005 Elsevier B.V. All rights reserved.

Central muscarinic receptors signal pilocarpine-induced salivation

Although cholinergic agonists such as pilocarpine injected peripherally can act directly on salivary glands to induce salivation, it is possible that their action in the brain may contribute to salivation. To investigate if the action in the brain is important to salivation, we injected pilocarpine intraperitoneally after blockade of central cholinergic receptors with atropine methyl bromide (atropine-mb). In male Holtzman rats with stainless steel cannulas implanted into the lateral ventricle and anesthetized with ketamine, atropine-mb (8 and 16 nmol) intracerebroventricularly reduced the salivation induced by pilocarpine (4 mumol/kg) intraperitoneally (133 +/- 42 and 108 +/- 22 mg/7 min, respectively, vs. saline, 463 +/- 26 mg/7 min), but did not modify peripheral cardiovascular responses to intravenous acetylcholine. Similar doses of atropine-mb intraperitoneally also reduced pilocarpine-induced salivation. Therefore, systemically injected pilocarpine also enters the brain and acts on central muscarinic receptors, activating autonomic efferent fibers to induce salivation.