Exogenously administered vasopressors (sympathomimetics) were evaluated in halothane-anesthetized dogs to determine the effects of these drugs on cardiovascular function before and after hemorrhage. Six dogs were anesthetized with thiamylal sodium (20 mg/kg of body weight) and halothane (1.25 minimal alveolar concentration) in 100% oxygen. After instrumentation, cardiac output, systemic arterial blood pressure (SAP), heart rate (HR), left ventricular pressure, pulmonary arterial pressure, and an index of cardiac contractility (dP/dT) were measured. Stroke volume, cardiac index (CI), stroke index (SI), rate-pressure product, and systemic vascular resistance (SVR) were calculated. Epinephrine (0.1, 0.3, and 0.5 micrograms/kg/min [low, medium, and high doses, respectively]) and dobutamine (1, 5, and 10 micrograms/kg/min [low, medium, and high doses, respectively]) were infused. Methoxamine was given in a bolus of 0.22 mg/kg, IV. All measurements were taken at 2.5 minutes after infusion, and were repeated after removal of 40% of the estimated blood volume. Dobutamine administered at the low dose before hemorrhage increased SAP and dP/dT. At the high and medium dose, dobutamine significantly increased CI, dP/dT, and SAP with no significant change in HR or SVR. The medium dose of epinephrine was the most effective dose of epinephrine at increasing key variables (CI, SI, dP/dT). The response of CI and SI to this dose was not significantly different from the changes seen with high-dose administration of dobutamine. The dP/dT was significantly lower with epinephrine than with dobutamine, and SVR and HR were unchanged with epinephrine, except at the low dose, which decreased SVR. Methoxamine significantly decreased CI, SVR, and HR, whereas SVR and SAP were increased significantly. After hemorrhage, the only variables that had a significant change in the absolute magnitude of the response to a drug, relative to the response before hemorrhage, were a significantly reduced ability of dobutamine and methoxamine to increase SAP, and a significantly decreased ability of methoxamine to decrease CI. We concluded that dobutamine and epinephrine provide beneficial short-term support of the cardiovascular system in the halothane-anesthetized dog during acute hypovolemia.

Baroreflex sensitivity (BS) was used to quantitatively assess the effects of halothane and isoflurane on the heart rate/arterial pressure relationship during steady-state (10 minutes) and dynamic pressure changes in adult horses. Arterial pressure was decreased in response to nitroglycerin or sodium nitroprusside and increased in response to phenylephrine HCl. Mean (+/- SEM) BS in awake horses was 28.9 +/- 2.6 and 13.2 +/- 2.0 ms/mm of Hg during steady-state decreases and increases in systolic arterial pressure (SAP), respectively. Halothane and isoflurane either significantly (P < 0.05) decreased or eliminated BS during steady-state decreases in SAP, with no significant differences detected between anesthetic agents. During steady-state decreases in SAP, significant (P < 0.05) correlation between R-R interval and arterial pressure was not observed for 6 of 10 and 4 of 11 halothane and isoflurane anesthesia periods, respectively. Halothane significantly (P < 0.05) decreased BS during steady-state increases in SAP to 7.9 +/- 0.6 and 6.5 +/- 1.1 ms/mm of Hg during low and high minimal alveolar concentration (MAC) multiples, respectively. Isoflurane decreased BS during steady-state increases in SAP to 9.6 +/- 1.5 and 6.6 +/- 1.1 ms/mm of Hg during low and high MAC anesthesia, respectively, with high MAC of isoflurane decreasing BS significantly (P < 0.05), compared with awake and low MAC values. Plasma catecholamine (epinephrine and norepinephrine) concentrations increased significantly (P < 0.05), compared with baseline values during steady-state vasodilator infusions in halothane- and isoflurane-anesthetized horses. Steady-state infusions of phenylephrine in anesthetized horses resulted in arrhythmia development, with premature atrial and ventricular complexes seen in halothane-anesthetized horses and increased heart rate and atrial premature complexes seen less frequently in isoflurane-anesthetized horses. Dynamic BS was 25.0 +/- 4.5 and 20.1 +/- 2.8 ms/mm of Hg for decreasing and increasing SAP, respectively, in awake horses. The R-R interval and SAP were linearly correlated during dynamic decreases in SAP in 7 of 9 halothane and 8 of 10 isoflurane anesthesia periods. Baroreflex sensitivity decreased to 15.0 +/- 6.8 and 13.3 +/- 3.5 ms/mm of Hg during anesthesia with low MAC of halothane and isoflurane, respectively. High MAC of halothane and isoflurane significantly (P < 0.05) decreased BS during dynamic decreases in SAP in 7.8 +/- 1.8 and 7.2 +/- 1.3 ms/mm of Hg, respectively. There were no significant differences in BS depression between halothane and isoflurane.

Exogenously administered vasopressors (sympathomimetics were evaluated in isoflurane-anesthetized dogs to determine the effects of these drugs on cardiovascular function before and after hemorrhage. Six dogs were anesthetized with thiamylal sodium (20 mg/kg of body weight) and isoflurane (1.25 minimal alveolar concentration) in 100% oxygen. After instrumentation, cardiac output, systemic arterial blood pressure, heart rate (HR), left ventricular pressure, pulmonary arterial pressure, and an index of cardiac contractility (dP/dT) were measured. Stroke volume, cardiac index (CI), stroke index (SI), rate-pressure product, and systemic vascular resistance (SVR) were calculated. Epinephrine (0.1, 0.3, and 0.5 micrograms/kg/min [low, medium, and high doses, respectively]) and dobutamine (1, 5, and 10 micrograms/kg/min [low, medium, and high doses, respectively]) were infused. Methoxamine was given in a bolus of 0.22 mg/kg, IV. All measurements were taken at 2.5 minutes after infusion, and were repeated after removal of 40% of the estimated blood volume. Before hemorrhage, administration of high doses of dobutamine and medium and high doses of epinephrine were equally effective at increasing CI and SI. The dP/dT was increase to the greatest degree by administration of high doses of dobutamine. Administration of the low dose of dobutamine increased dP/dT, whereas administration of the low dose of epinephrine increased CI, HR, and SI, and decreased SVR. The HR and SVR were not increased by administration of any dose of dobutamine or of the medium and high doses of epinephrine. However, methoxamine increased SVR and decreased HR. Methoxamine decreased CI, SI, and dP/dT, but increased systemic arterial pressure to the same degree as that attributed to administration of high doses of dobutamine and epinephrine. After hemorrhage, effectiveness of the drugs in eliciting a response was unchanged, except for a decreased ability of dobutamine to increase rate-pressure product. Further, when the results of this study were compared with those of an earlier halothane study, there were no significant differences in the response of a variable to drug infusion on the basis of the anethetic. The drugs were equally effective with halothane or isoflurane anesthesia. Results inidcated that dobutamine and ephinephrine are effective short-term treatments for hypovolemia during volume resuscitation, and that they work equally well with halothane or isoflurane anesthesia.

Hemodynamic effects of spontaneous ventilation, intermittent positive-pressure ventilation (IPPV), and high-frequency oscillatory ventilation (HFOV) were compared in 6 dogs during halothane anesthesia. Anesthesia was induced with IV thiamylal Na and was maintained with halothane (end-tidal concentration, 1.09%). During placement of catheters, dogs breathed spontaneously through a conventional semiclosed anesthesia circuit. Data were collected, and dogs were mechanically ventilated, using IPPV or HFOV in random order. Ventilation was adjusted to maintain PaCO2 between 38 and 43 mm of Hg during IPPV and HFOV. Cardiac index, aortic blood pressure, and maximum rate of increase of left ventricular pressure were significantly (P less than 0.05) less during HFOV than during spontaneous ventilation, whereas right atrial and pulmonary artery pressure were significantly greater during HFOV than during spontaneous ventilation. During IPPV, only the maximum rate of increase of left ventricular pressure was significantly less than that during spontaneous ventilation.

Lateral cecal arterial blood flow, carotid arterial pressure, heart rate, and mechanical activity of the circular and longitudinal muscle layers of the cecal body were measured in 7 conscious healthy horses during IV infusion of physiologic saline solution for 60 minutes (control), during a 60-minute IV infusion of dopamine (at dosages of 1, 2.5, and 5 microgram/kg/min), and for 60 minutes after IV infusion of dopamine. The mean values for lateral cecal arterial blood flow during IV infusion of dopamine at a dosage of either 1 or 2.5 microgram/kg/min were not significantly different from the mean values for lateral cecal arterial blood flow during IV infusion of saline solution. The mean values for lateral cecal arterial blood flow, however, were significantly greater during IV infusion of dopamine at a dosage of 5 microgram/kg/min than the mean values for lateral cecal arterial blood flow during IV infusion of saline solution. Intravenous infusion of dopamine at 1 and 2.5 microgram/kg/min did not significantly change the mean values for carotid arterial pressure. In contrast, the mean values for carotid arterial pressure were significantly less during IV infusion of dopamine at dosages of 2.5 and 5 microgram/kg/min than during infusion of saline solution. The mean values for heart rate were not significantly altered by infusion of dopamine at a dosage of either 1 or 2.5 microgram/kg/min, but infusion of dopamine at a dosage of 5 microgram/kg/min significantly increased heart rate. Intravenous infusion of dopamine at dosages of either 1 or 5 microgram/kg/min did not significantly change the mechanical activity of the circular muscle layer of the cecal body, as measured by the area under the strain gauge deflection curve. Conversely, the mechanical avtivity of the circular muscle layer of the cecal body was significantly reduced by IV infusion of dopamine at a dosage of 2.5 microgram/kg/min. This reduction of circular muscle mechanical activity by dopamine infusion was attributable to a significant decrease in the total duration of contractions. The mechanical activity of the longitudinal muscle layer was not significantly altered by infusion of dopamine at any dose. These results suggest that IV infusion of dopamine at a dosage of 5 microgram/kg/min increased lateral cecal arterial blood flow by either increasing cardiac output or dilating the lateral cecal artery, an effect most likely mediated by dopaminergic or beta-adrenergic receptors. In addition, dopamine had a biphasic effect on contractile activity of the equine cecum.

We studied 6 singly caged adult female rhesus monkeys to determine whether increased cage size had any effect on behavior or heart rate. Two monkeys at a time were placed in cages 40% larger than their standard cage for 1 week on 2 occasions, using a counter-balanced design. Direct behavioral observations were performed 75 minutes/week on each monkey. Heart rate and general activity were monitored 35 hours/week by a telemetry system. Statistically significant differences were not found in aggressive, submissive, abnormal, or self-abusive behavior, nor in time spent in the front half of the cage, duration of grooming, looking at the observer, or stereotyped or nonstereotyped locomotion. Vocalizations increased the first time in the larger cage, but not the second, and decreased upon the second return to the standard cage. Differences with respect to cage size were not found in heart rate or activity level, although there were significant variations at different times of day. We conclude that modest increases in cage size are unlikely to enrich the environment of singly caged laboratory primates.

Oxymorphone was administered IV to dogs 4 times at 20-minute intervals (total dosage, 1 mg/kg of body weight, IV) on 2 separate occasions. Minute ventilation, mixed-expired carbon dioxide concentration, arterial and mixed-venous pH and blood gas tensions, arterial, central venous, pulmonary arterial, and pulmonary wedge pressures, and cardiac output were measured. Physiologic dead space, base deficit, oxygen transport, and vascular resistance were calculated before and at 5 minutes after the first dose of oxymorphone (0.4 mg/kg) and at 15 minutes after the first and the 3 subsequent doses of oxymorphone (0.2 mg/kg). During 1 of the 2 experiments in each dog, naloxone was administered 20 minutes after the last dose of oxymorphone; during the alternate experiment, naloxone was not administered. In 5 dogs, naloxone was administered IV in titrated dosages (0.005 mg/kg) at 1-minute intervals until the dogs were able to maintain sternal recumbency, and in the other 5 dogs, naloxone was administered IM as a single dose (0.04 mg/kg). Naloxone (0.01 mg/kg, IV or 0.04 mg/kg, IM) transiently reversed most of the effects of oxymorphone. Within 20 to 40 minutes after IV naloxone administration and within 40 to 70 minutes after IM naloxone administration, most variables returned to the approximate values measured before naloxone administration. The effects of oxymorphone outlasted the effects of naloxone; cardiovascular and pulmonary depression and sedation recurred in all dogs. Four hours and 20 minutes after the last dose of oxymorphone, alertness, responsiveness, and coordination improved in all dogs after IM administration of naloxone. Cardiac arrhythmia, hypertension, or excitement was not observed after naloxone administration.

The arrhythmogenic dose of epinephrine (ADE) was determined in heartworm-infected and noninfected (control) dogs during thiamylal-induced and halothane-maintained anesthesia to assess the myocardial sensitization. The ADE in heartworm-infected dogs (2.42 +/- 0.26 micrograms/kg of body weight) was significantly lower than that for the controls (3.36 +/- 0.29 micrograms/kg). After 2 weeks, ADE was determined again in these dogs after atropine treatment. Atropine treatment lowered the ADE to 1.76 +/- 0.33 micrograms/kg and 1.77 +/- 0.19 micrograma/kg in heartworm-positive and negative dogs, respectively. After 2 weeks more the ADE was determined after administration of prazosin, an alpha 1-antagonist. Only 2 of 6 controls and 3 of 6 heartworm-positive dogs had arrhythmias after a threefold increase of ADE. The mean ADE in the dogs that responded to treatment were 7.4 micrograms/kg and 7.2 micrograms/kg for heart worm-positive and negative dogs, respectively. The findings of this study indicated that ADE in heartworm-infected dogs were lower than those in the control dogs, which makes the heartworm-infected dogs more vulnerable to arrhythmia during anesthesia. Atropine did not protect the dogs of either group. However, prazosin protected the dogs of both groups by significantly increasing the threshold of the ADE. On the basis of our findings, to reduce the risk of arrhythmia, we suggest that routine screening of dogs for heartworm infection be done before anesthetics are used.

Eight adult Holstein cows were used to compare the effects of lumbar segmental epidural analgesia (SEA) and lumbar segmental subarachnoid analgesia (SSA). A modified 17-gauge Huber point (Tuohy) needle was used to place a catheter with stylet into either the epidural space at the thoracolumbar (T13-L1) intervertebral space or the tubarachnoid space at the lumbosacral intervertebral junction. The catheters were advanced so that their tips lay at the anterior lumbar (L1-L2) epidural space or at the thoracolumbar (T-13-L1) subarachnoid space. The position of the catheter was confirmed radiographically. A 5% solution of procaine HCl was used at mean doses of 300 mg (6 ml) to induce SEA and 84.4 +/- 12.9 mg (1.7 +/-0.3 ml) to induce SSA. Onset of analgesia to superficial and deep muscular pinprick stimulation was significantly (P less than 0.05) faster in cows with SSA than in those with SEA (10.4 +/- 2.3 minutes vs 15.9 +/- 3.8 minutes). Maximal thoracolumbar analgesia extended from spinal cord segments T12 to L4 on one or both sides of the vertebral column during SEA and from T10 to L3 on one or both sides during SSA. Duration of analgesia lasted significantly (P less than 0.05) longer in cows with SEA than in those with SSA (76.2 +/- 16.2 minutes vs 53.7 +/- 14.3 minutes). The advantages and disadvantages of the SEA catheter technique are discussed.

Effects of ketamine, xylazine, and a combination of ketamine and xylazine were studied in 12 male Pekin ducks (7 to 12 weeks old; mean [+/- SD] body weight, 3.1 +/- 0.3 kg). After venous and arterial catheterization and fixation of a temperature probe in the cloaca, each awake duck was confined, but not restrained, in an open box in a dimly lit room. Blood pressure and lead-II ECG were recorded. Three arterial blood samples were collected every 15 minutes over a 45-minute period (control period) and were analyzed for pHa, Paco2 and Pao2. After the control period, each duck was assigned at random to 1 of 3 drug groups: (1) ketamine (KET; 20 mg/kg of body weight, IV), (2) xylazine (XYL; 1 mg/kg, IV), and (3) KET + XYL (KET 20 mg/kg and XYL, 1 mg/kg; IV). Measurements were made at 1, 5, 10, 15, 30, 45, 60, and 90 minutes after drug administration. All ducks survived the drug study. Cloacal temperature was significantly (P less than or equal to 0.05) increased above control cloacal temperature at 90 minutes after the administration of ketamine, and from 10 through 90 minutes after administration of ketamine plus xylazine. In ducks of the KET group, pHa, Paco2, and Pao2, remained unchanged after administration of the drug. In ducks of the XYL group, pHa and Pao2 decreased significantly (P less than or equal to 0.05) from control values for all time points up to and including 15 minutes after drug administration. In ducks of the KET + XYL group, pHa and Pa02 were significantly (P less than or equal to 0.05) decreased at all time points up to and including 45 and 15 minutes, respectively, after administration of the drugs. In ducks of the XYL group, Paco2 increased significantly (P less than 0.05) during the first 15 minutes after drug administration, and for 45 minutes after administration of KET + XYL. Results indicated that ketamine when given alone to ducks, was not associated with pulmonary depression. There was drug-associated respiratory depression after IV administration of XYL or KET + XYL.