Atracurium besylate, a nondepolarizing neuromuscular blocking agent, was administered to 24 isoflurane-anesthetized domestic chickens. Birds were randomly assigned to 4 groups, and atracurium was administered at dosage of 0.15, 0.25, 0.35 or 0.45 mg/kg of body weight. The time of onset of twitch depression, the amount of maximal twitch depression, and the duration of muscular relaxation were recorded. After return to control twitch height, atracurium was further administered to achieve > 75% twitch depression. When twitch depression reached 75% during noninduced recovery, 0.5 mg of edrophonium/kg was administered to reverse the muscle relaxation. Throughout the experimental period, cardiovascular, arterial blood gas, and acid-base variables were monitored. The effective dosage of atracurium to result in 95% twitch depression in 50% of birds, (ED95/9595) was calculated, using probit analysis, to be 0.25 mg/kg, whereas the ED95/95 the dosage of atracurium to result in 95% twitch depression in 95% of birds, was calculated by probit analysis to be 0.46 mg/kg. The total duration of action at dosage of 0.25 mg/kg was 34.5 +/- 5.8 minutes; at the highest dosage (0.45 mg/kg), total duration increased to 47.8 +/- 10.3 minutes. The return to control twitch height was greatly hastened by administration of edrophonium. Small, but statistically significant changes in heart rate and systolic blood pressure, were associated with administration of atracurium and edrophonium. These changes would not be clinically relevant. In this study, atracurium was found to be safe and reliable for induction of muscle relaxation in isoflurane anesthetized chickens.

Platelet aggregation and adenosine triphosphate (ATP) release were measured by use of the impedance method in blood samples obtained from 25 adult female Beagles before and after sedation with acepromazine (0.13 mg/kg of body weight) and atropine (0.05 mg/kg), and during general anesthesia. General anesthesia was induced by IV administration of thiamylal (average dosage, 2.1 mg/kg, range, 1.2 to 4.2 mg/kg) and was maintained with halothane in oxygen. Samples of jugular venous blood were obtained from each dog, using citrate as anticoagulant. Platelet count was done on each sample. Platelet aggregation and ATP released from the aggregating platelets were measured within 2.5 hours of sample collection, using a whole-blood aggregometer. Adenosine diphosphate (ADP) or collagen was used as aggregating agent. For each aggregating agent, platelet aggregation and ATP release were measured over 6 minutes. After sedation with acepromazine and atropine, significant (P < 0.01) reduction was observed in platelet count (from median values of 341,000 cells/microliter to 283,000 cells/microliter) and in the ability of platelets to aggregate in response to ADP (from 14.0 to 7.0 Ohms). During the same period, maximal release of ATP in response to collagen also was reduced (from 5.56 micromoles to 4.57 micromoles; P < 0.01); however, this difference ceased to be significant when ATP release was normalized for platelet count. During general anesthesia and surgery (200 minutes after sedation), platelet count and aggregation responses to ADP and collagen had returned to presedation values. None of the dogs in this study appeared to have hemostasis problems during surgery. In conclusion, sedation with acepromazine and atropine induces measurable inhibition of ADP-induced platelet aggregation that resolves during subsequent general anesthesia and surgery. Transient inhibition of platelet aggregation is not manifested by a change in gross hemostasis during surgery.

Gastric dilatation was experimentally induced in 6 anesthetized dogs maintained with constant-dose isoflurane in oxygen. An intragastric balloon was used to distend the stomach with a constant 30 mm of Hg for 3.5 hours. The PaCO2, was maintained between 35 and 45 mm of Hg, using intermittent positive-pressure ventilation. Cardiopulmonary measurements prior to stomach distension (baseline) were compared with measurements taken during 0.1, 0.5, 1.0, 1.5, 2.5, and 3.5 hours of stomach distension by analyzing the change from baseline in a randomized-block analysis with each dog as a block. After distending the stomach, cardiac index increased (P < 0.01) from 1.5 to 3.5 hours. Stroke volume did not change, thus the increase in the, cardiac index was attributable to an increase in heart rate. During inflation, increases were observed in systemic arterial, pulmonary arterial, and right atrial pressure. Respiratory frequency was unchanged; however, to maintain PaCO2, constant, it was necessary to progressively increase peak airway pressure. Although PaO2, tended to decrease during gastric dilation, the dogs were never hypoxemic. These results indicate that when our methods are used to maintain a constant anesthetic dose of isoflurane in oxygen, an observed increase in cardiovascular performance is expected. This differs from other studies in anesthetized dogs that have shown reduction in cardiovascular performance following gastric dilatation.

Dissection, injection, and surgical studies in feline cadavers and in anesthetized cats were conducted to determine the feasibility of using the gracilis muscle as the basis for a free musculocutaneous flap. The vascular pedicle of the flap consisted of the femoral artery and vein. Mean length (1.6 +/- 0.2 cm) of the vascular pedicle and mean artery (1.33 +/- 0.19 mm) and vein (2.55 +/- 0.38 mm) diameters were satisfactory for microvascular transfer. Fluorometry revealed overlying cutaneous perfusion in the flaps on the basis of their muscle vascular pedicles. To ensure survival of the flap, the muscular branches of the femoral artery and vein supplying the gracilis muscle had to be carefully preserved during surgical elevation of the flap.

Eight adult horses were used in a study to determine ketamine's ability to reduce halothane requirement. To obtain steady-state plasma concentrations of 0.5, 1.0, 2.0, 4.0, and 8.0 microg/ml, loading doses and constant infusions for ketamine were calculated for each horse on the basis of data from other studies in which the pharmacokinetic properties of ketamine were investigated. Blood samples for determination of plasma ketamine concentrations were collected periodically during each experiment. Plasma ketamine concentrations were determined by capillary gas chromatography/mass spectrometry under electron-impact ionization conditions, using lidocaine as the internal standard. Halothane minimal alveolar concentration (MAC; concentration at which half the horses moved in response to an electrical stimulus) and plasma ketamine concentration were determined after steady-state concentrations of each ketamine infusion had been reached. Plasma ketamine concentrations > 1.0 microg/ml decreased halothane MAC. The degree of MAC reduction was correlated directly with the square root of the plasma ketamine concentration, reaching a maximum of 37% reduction at a plasma ketamine concentration of 10.8 +/- 2.7 microg/ml. Heart rate, mean arterial blood pressure, and the rate of increase of right ventricular pressure did not change with increasing plasma ketamine concentration and halothane MAC reduction. Cardiac output increased significantly during ketamine infusions and halothane MAC reduction. Our findings suggest that plasma ketamine concentrations > 1.0 microm/ml reduce halothane MAC and produce beneficial hemodynamic effects.

Sixty-eight cattle under general anesthesia were splenectomized. The transthoracic approach was used to provide better access to the spleen and to facilitate ligature of the major splenic vessels. The procedure was easier and less time-consuming, compared with other surgical approaches, and is considered to be less stressful to the animals. Postoperative recovery was complete in 67 of 68 cattle. After surgery, 1 animal developed respiratory tract disease that was thought to have been unrelated to the surgery.

This study was designed to test analgesia, duration, and cardiovascular changes induced by meperidine (MEP) and oxymorphone (OXY) following methoxyflurane (MOF) and halothane (HAL) anesthesia. Eight healthy dogs were given atropine and acepromazine, and anesthesia was induced with thiamylal and maintained with 1.5 minimal alveolar concentration of MOF or HAL for 1 hour during controlled ventilation. Eight treatments were given with each anesthetic: 3 with MEP (0.5, 1.0, and 2.0 mg/kg, IV), 3 with oxymorphone (OXY; 0.05, 0.1, and 0.2 mg/kg, IV), and 2 placebos with sterile water. Test drugs were given at the end of anesthesia when early signs of recovery were evident. Minimal threshold stimulus/response nociception was assessed by use of an inflatable soft plastic colonic balloon. Blood pressures and pulse rate were measured with a noninvasive monitor. Meperidine and OXY were found to be effective analgesics and could be reversed with naloxone. Intravenous administration of 2.0 mg of MEP/kg provided analgesia for 36 +/- 6 minutes and 39 +/- 15 minutes after MOF and HAL, respectively. In contrast, OXY was effective at all 3 doses with effects of IV administration of 0.2 mg of OXY/kg lasting 154 +/- 13 minutes and 152 +/- 12 minutes, after MOF and HAL, respectively. Analgesia could not be demonstrated after anesthesia for acepromazine, MOF, or HAL. Blood pressure was not changed by either anesthetic nor was it influenced by MEP or OXY. Pulse rate was significantly depressed by the higher doses of OXY following HAL, but was not changed by MEP following either anesthetic. This study demonstrated the longer duration of analgesia of OXY. In addition, we could not find that analgesia was provided by either MOF or HAL following recovery from anesthesia.

We investigated the influence of parasympathetic tone on the arrhythmogenicity of graded dobutamine infusions in horses anesthetized under clinical conditions. Six horses were used in 9 trials. Two consecutive series of graded dobutamine infusions were given IV; each continuous graded dobutamine infusion was administered for 20 minutes. The dobutamine infusion dosage (5, 10, 15, and 20 microgram/kg of body weight/min) was increased at 5-minute intervals. Isovolumetric saline solution vehicle (v) or atropine (A; 0.04 mg(kg) was administered IV, or bilateral vagotomy (VG) was performed as a treatment before the second series of dobutamine infusions. Treatment was not administered prior to the first dobutamine infusion. Significant interaction between treatment and dosage of dobutamine infusion existed for differences from baseline for mean arterial pressure, systolic arterial pressure, diastolic arterial pressure, heart rate, and cardiac index at dosages of 5 and 10 micrograms of dobutamine/kg/min, given IV and for heart rate at dosage of 15 micrograms of dobutamine/kg/min, given IV. Results for group-V horses were different from those for group-A and group-VG horses, but were not different between group-A and group-VG horses in all aforementioned cases, except for heart rate and cardiac index at dosage of 5 micrograms of dobutamine/kg/min, given IV. Normal sinus rhythm, second-degree atrioventricular block, and bradyarrhythmias predominated during low dobutamine infusion rates during the first infusion series (nontreated horses) and in group-V horses during the second infusion series. Only tachyarrhythmias were observed during the second infusion series in the horses of the A and VG groups. The modulating influence of parasympathetic nervous system activity on hemodynamics and development of arrhythmia was conspicuous during low dobutamine infusion rates. Significant differences were not observed in hemodynamic responses to dobutamine, with respect to parasympathetic influence at high dobutamine infusion rates.

The effect of xylazine on the arrhythmogenic dose of epinephrine (ADE) was studied in 9 horses. Anesthesia was induced by administration of guaifenesin (50 mg/kg of body weight, IV) followed by thiamylal (4 to 6 mg/kg, IV) and was maintained at 1 minimal alveolar concentration MAC) of halothane (0.89%). Base apex ECG and facial artery pressure were recorded. Epinephrine was infused in a sequence of arithmetically spaced increasing rates (initial rate 0.25 (Lg/kg/min) for a maximum of 10 minutes. The ADE was defined as the lowest epinephrine infusion rate to the nearest 0.25 microgram/kg/min at which at least 4 premature ventricular depolarizations occurred in a 15-second period. Xylazine (1.1 mg/kg, IV) was administered after the control ADE was determined. Xylazine did not significantly alter the ADE (control, 1.12 +/- 0.38 microgram/kg/min; xylazine, 1.21 +/- 0.46 microgram/kg/min). Blood pressure increased transiently for 8 minutes after xylazine administration. Baseline systolic and diastolic arterial pressures and heart rate were not significantly different from control baseline pressures and heart rate 15 minutes after xylazine administration. Blood pressure and heart rate increased significantly during control and xylazine ADE determinations. Significant differences in pH, PaO2, PaCO2, or base excess were not observed between baseline and ADE in the control or xylazine groups. One horse developed atrial fibrillation, and 2 horses developed ventricular fibrillation during ADE determinations.

Eighteen rats were anesthetized with xylazine/ketamine and placed in right lateral recumbency, and a small incision was made in the skin of the left hemithorax. A 21-gauge, 1-inch, short-beveled hypodermic needle, attached directly to a pressure transducer filled with degassed saline solution, was advanced through the incision into the left ventricle and then advanced through the septum into the right ventricle. High-fidelity tracings of right and left ventricular pressures and their derivatives were obtained through this approach in 13 rats. In 5 rats, measurements of right ventricular pressures were obtained by additional right ventricular puncture through the incision in the left hemithorax. Right and left ventricular pressures were recorded on single occasions in 18 rats, twice at 2-week intervals in 6 rats, and 3 times at 2-week intervals in 3 rats. Minimal hemopericardium was observed, but most rats had evidence of hemorrhage on the visceral pericardium. Left and right ventricular pressures can be measured rapidly, safely, and repeatedly in anesthetized rats by this method.