The oxytocic effect of xylazine on the canine uterus.

The effect of xylazine on intrauterine pressure was compared to that of prostaglandin and oxytocin in seven diestrual bitches. Microtipped pressure transducers were surgically implanted in the uteri of four bitches at 30 d diestrus and in three bitches at 60 d diestrus. Uterine contractile force was measured in the awake bitches on Day 1 and Day 2 following implantation. Uterine responses to intravenous prostaglandin (5 mug/kg), oxytocin (0.05 USP units/kg), and xylazine (0.22 mg/kg) were measured. In the 30-d diestrual bitches, prostaglandin and oxytocin increased intrauterine pressure to 67 and 69 mmHg, with the duration of action being 16 and 14 min, respectively. Xylazine increased intra-uterine pressure to 49 mmHg and had a duration of action of 8 min. All results were decreased but similar in the 60-d diestrual bitches. These findings indicate that xylazine, given intravenously, produces a transitory increase in intrauterine pressure in the diestrual bitch.

Hemodynamic effects of calcium gluconate administered to conscious horses.

Calcium gluconate was administered to conscious horses at 3 different rates (0.1, 0.2, and 0.4 mg/kg/min for 15 minutes each). Serum calcium concentrations and parameters of cardiovascular function were evaluated. All 3 calcium administration rates caused marked increases in both ionized and total calcium concentrations, cardiac index, stroke index, and cardiac contractility (dP/dtmax). Mean arterial pressure and right atrial pressure were unchanged; heart rate decreased markedly during calcium administration. Ionized calcium concentration remained between 54% and 57% of total calcium concentration throughout the study. We conclude that calcium gluconate can safely be administered to conscious horses at 0.1 to 0.4 mg/kg/min and that administration will result in improved cardiac function.

Alterations in epinephrine-induced arrhythmogenesis after xylazine and subsequent yohimbine administration in isoflurane-anesthetized dogs.

Effects of xylazine (1.1 mg/kg of body weight, IV bolus, plus 1.1 mg/kg/h infusion) and subsequent yohimbine (0.125 mg/kg, IV bolus) administration on the arrhythmogenic dose of epinephrine (ADE) in isoflurane (1.8% end-tidal)-anesthetized dogs were evaluated. The ADE was defined as the total dose of epinephrine that induced greater than or equal to 4 premature ventricular contractions within 15 seconds during a 3-minute infusion period or within 1 minute after the end of infusion. Total ADE values during isoflurane anesthesia, after xylazine administration, and after yohimbine injection were 36.6 +/- 8.45 micrograms/kg, 24.1 +/- 6.10 micrograms/kg, and 45.7 +/- 6.19 micrograms/kg, respectively. Intravenous xylazine administration significantly (P less than 0.05) increased blood pressure and decreased heart rate, whereas yohimbine administration induced a significant (P less than 0.05) decrease in blood pressure. induced a significant (P less than 0.05) decrease in blood pressure. After yohimbine administration, the ADE significantly (P less than 0.05) increased above that after isoflurane plus xylazine administration. After yohimbine administration, blood pressure measured immediately before epinephrine-induced arrhythmia was significantly (P less than 0.05) less than the value recorded during isoflurane plus xylazine anesthesia. Heart rate was unchanged among treatments immediately before epinephrine-induced arrhythmia. Seemingly, yohimbine possessed a protective action against catecholamine-induced arrhythmias in dogs anesthetized with isoflurane and xylazine.

Anesthetic potency of nitrous oxide in young swine (Sus scrofa).

Determination of nitrous oxide (N2O) potency was accomplished by extrapolation using the concepts of minimum alveolar concentration (MAC) and additivity among inhalation anesthetics. Halothane and isoflurane anesthetic requirement (alveolar concentration) necessary to achieve MAC in 9 pigs decreased with each successive increase in the percentage of inspired N2O (25%, 50%, 75%). Halothane and isoflurane MAC was determined to be 0.94 +/- 0.03 and 1.75 +/- 0.01 volumes percent, respectively. Halothane and isoflurane requirements decreased to 0.74 +/- 0.02, 0.66 +/- 0.02, and 0.58 +/- 0.02; and to 1.56 +/- 0.02, 1.38 +/- 0.02, and 1.08 +/- 0.03 volumes percent with 25%, 50%, and 75% N2O, respectively. The line of best fit derived from regression analysis of the combined data (isoflurane and halothane MAC values) had a correlation coefficient of 0.987 and an X intercept equivalent to 195% N2O. The potency of N2O in pigs was similar to that of other domesticated mammals and reduced halothane and isoflurane anesthetic requirements by approximately 50% of the reduction observed in human beings.

Halothane-catecholamine arrhythmias in swine (Sus scrofa).

The arrhythmogenic dose of epinephrine (ADE) was determined in 6 pigs during steady-state anesthesia (1.5% halothane in O2) and steady-state anesthesia plus xylazine (1.1 mg X kg-1 X hr-1; IV infusion) and after either prazosin (alpha 1) or metoprolol (beta 1) adrenergic blockade during halothane-xylazine (H-X) anesthesia. A constant infusion (1, 2, 3, 5, and 10 micrograms X kg-1 X min-1) of freshly mixed epinephrine (100 micrograms X ml-1 in saline solution) was used to determine ADE. The ADE was defined as the total dose of epinephrine which produced 4 or more continuous or intermittent, premature, ventricular contractions within a 15-s period. The mean epinephrine total dose values during 1.5% halothane anesthesia, H-X anesthesia alone, or H-X anesthesia after either prazosin (0.1 mg X kg-1) or metoprolol (0.5 mg X kg-1) adrenergic blockade were 3.60 +/- 0.844, 2.68 +/- 0.402, 11.85 +/- 3.804, and 5.17 +/- 0.587 micrograms X kg-1, respectively. Xylazine administration did not significantly decrease ADE, although mean arterial pressure significantly increased. Prazosin administration significantly increased ADE and was associated with an increased heart rate and a decreased mean arterial pressure. We conclude that alpha 1-blockade with prazosin is more protective to epinephrine-induced arrhythmias in H-X-anesthetized pigs than is beta 1-blockade with metoprolol.

Cardiopulmonary responses of swine to intravenous infusion of guaifenesin, ketamine, and xylazine.

Swine were anesthetized with a 5% solution of dextrose in water containing 50 mg of guaifenesin, 1 mg of ketamine, and 1 mg of xylazine X ml-1 (G-K-X) infused IV at a rate of 2.2 ml X kg-1 X hr-1. Mean arterial blood pressure and systemic vascular resistance were significantly increased from base-line values throughout the 2 hours of G-K-X infusion. Cardiac index decreased significantly initially, but returned to near base line at 30 minutes. Fifteen minutes after G-K-X infusion was discontinued, cardiac index was not significantly different from base line. Heart rate decreased significantly from base line 90 minutes after infusion of G-K-X began and remained so throughout the study. However, the mean heart rate remained within the acceptable range for swine. Rate-pressure product was not significantly altered. The PaCO2 decreased, and arterial pH increased significantly from base line, supporting our clinical impression that pigs breathe well when anesthetized with G-K-X. We conclude that G-K-X is a satisfactory combination of drugs for induction and maintenance of surgical anesthesia in healthy swine for a period of 2 hours.

Alterations in the arrhythmogenic dose of epinephrine after adrenergic receptor blockade with prazosin, metoprolol, or yohimbine in halothane-xylazine-anesthetized dogs.

Recent evidence has linked alpha-receptor and beta-receptor activations with ventricular arrhythmia genesis. In order to assess the relative contribution of specific adrenoceptors (alpha 1, alpha 2, beta 1) on ventricular arrhythmogenic activity during xylazine (1.1 mg X kg-1 X hr-1)-halothane (1.35%) anesthesia, the arrhythmogenic dose of epinephrine (ADE) was repeatedly determined before and after prazosin (alpha 1 antagonist; 0.1 mg X kg-1), metoprolol (beta 1 antagonist; 0.5 mg X kg-1), and yohimbine (alpha 2 antagonist; 0.125 mg X kg-1) administration in 6 dogs. The ADE was expressed as infusion rate and total dose. The ADE was defined as the dose which produced 4 or more intermittent premature ventricular contractions within 15 s during a 3-minute infusion period or within 1 minute from end of infusion. Control ADE was 2.69 +/- 0.372 (micrograms X kg-1 X min-1) and 4.17 +/- 0.544 (micrograms X kg X -1) for infusion rate and total dose, respectively. The ADE significantly increased after prazosin (P less than 0.005), metoprolol (P less than 0.005), and yohimbine (P less than 0.05) administration. The ADE values increased to 5.42 +/- 1.22 (rate) and 8.10 +/- 1.95 (dose) after alpha 2 blockade, but were significantly less than the alpha 1 and beta 1 blockade ADE values. In conclusion, although both alpha- and beta-adrenoceptor blockade depressed ventricular arrhythmia genesis in xylazine-halothane-anesthetized dogs, alpha 2 blockade, which was achieved with the recommended dose of yohimbine for reversal of anesthetic-induced CNS depression, was not as protective as alpha 1 (prazosin) or beta 1 (metoprolol) blockade.

Organ blood flow and distribution of cardiac output in hypocapnic ketamine-anesthetized swine.

Organ blood flow and distribution of cardiac output (CO) were determined in 9 awake (control) and ketamine-anesthesized swine (4 mg/kg bolus followed by continuous infusion of 0.3 mg/kg/min, IV), using 15 micron diameter radionuclide-labeled microspheres. Absolute values of blood flow (per 100 g basis) were determined for various organs and peripheral tissues. Internal organs of the swine, which constituted 8.25 +/- 0.79% of the total body mass, received 55.83 +/- 5.13% of the CO. The fraction of CO received by brain, heart, kidneys, liver (via hepatic artery), and gastrointestinal tract was 1.10%, 2.67%, 19.84%, 11.81%, and 16.84%, respectively. During ketamine anesthesia, the fraction of CO perfusing the kidneys and liver (hepatic artery) increased from control and values for brain, heart, and splanchnic organs remained unchanged. Blood flow (per unit weight) of brain, cardiac, and splanchnic organs decreased; kidney and skeletal muscle blood flow was unaltered; and hepatic arterial blood flow increased from the awake (control) values. The hyperdynamic state often associated with ketamine anesthesia was not evident in these pigs during intermittent positive-pressure ventilation resulting in hypocapnia.

Physiologic effects of succinylcholine chloride in mechanically ventilated horses anesthetized with halothane in oxygen.

Succinylcholine chloride, administered to horses anesthetized with halothane in oxygen and mechanically ventilated, caused slight but significant (P less than 0.01) increases in heart rate. Significant alteration in mean arterial blood pressure did not occur, and there were clinically insignificant increases in serum K+ and C1- concentration. Cardiac dysrhythmia and myoglobinuria did not occur. Thus, effects of halothane anesthesia and mechanical ventilation prevented cardiac dysrhythmia and hypertension and greatly reduced the tachycardia generally associated with siccinylcholine administration.

Hemodynamic response of calves to tiletamine-zolazepam-xylazine anesthesia.

Six healthy Holstein calves were anesthesized with isoflurane in O2 and instrumented for hemodynamic studies. A saphenous artery was catheterized for measurement of blood pressure and withdrawal of blood for determination of the partial pressure of carbon dioxide (PaCO2), oxygen (PaO2), and arterial pH (pHa). Respiration was controlled throughout the study. The ECG and EEG were monitored continuously. A thermodilution catheter was passed via the right jugular vein into the pulmonary artery for determination of cardiac output and measurement of central venous pressure, pulmonary arterial pressure, and pulmonary capillary wedge pressure. Baseline values (time 0) were recorded following recovery from isoflurane. Tiletamine-zolazepam (4 mg/kg)-xylazine (0.1 mg/kg) were administered IV immediately after recording baseline values. Values were again recorded at 5, 10, 20, 30, 40, 50, and 60 minutes after injection. Changes in left ventricular stroke work index, PaCO2, and pHa were insignificant. Arterial blood pressure and systemic vascular resistance increased above baseline at 5 minutes and then gradually decreased below baseline at 40 minutes, demonstrating a biphasic response. Values for pulmonary capillary wedge pressure, pulmonary arterial pressure, central venous pressure, and PaO2 were increased above baseline from 5 to 60 minutes. Stroke volume, stroke index, and right ventricular stroke work index were increased from 20 or 30 minutes to 60 minutes. Pulmonary vascular resistance increased at 10 minutes, returned to baseline at 20 minutes, and was increased again at 60 minutes. Heart rate, cardiac output, cardiac index, and rate pressure product were decreased at 5 minutes, and with the exception of cardiac output, remained so for 60 minutes. Cardiac output returned to the baseline value at 30 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of nifedipine on xylazine-induced acute pressor response in halothane-anesthetized dogs.

Effects and interaction of nifedipine (Ca channel blocker) and xylazine (mixed alpha agonist) during halothane anesthesia were examined in 6 dogs. After achievement of steady-state halothane (1.35%) anesthesia, blood pressure (BP) and heart rate (HR) were recorded in these dogs during 3-minute saline or nifedipine (20 micrograms/kg) infusion periods. Seven minutes after the end of saline or nifedipine infusion, xylazine (1.1 mg/kg of body weight) was infused over a 2-minute period. After saline pretreatment, xylazine administration increased diastolic BP (33.67 +/- 3.91 mm of Hg) and decreased HR. Nifedipine infusion induced a transient reduction in BP, accompanied by a more persistent increase in HR. Compared with saline pretreatment, nifedipine pretreatment significantly decreased the acute increase in diastolic BP (33.67 +/- 3.91 vs 14.00 +/- 2.94 mm of Hg) which occurred during xylazine injection. After saline and nifedipine infusions, xylazine administration decreased HR 30 +/- 15.02 and 36.5 +/- 10.36 beats/min, respectively. A pronounced sinus arrhythmia and/or 2nd-degree atrioventricular block developed in all dogs during xylazine injection after saline infusion. Arrhythmias were not observed in the dogs after nifedipine infusion. Nifedipine's Ca blocking action depressed xylazine-induced acute vasoconstriction and concomitant increase in diastolic BP. Because alpha 2-, but not alpha 1-adrenoceptor-mediated vasoconstriction is Ca-dependent, these results indicate that a portion of the acute pressor response induced by IV xylazine in halothane-anesthetized dogs may be alpha 2-mediated. Seemingly, nifedipine-induced hypotension and damping of xylazine-induced increases in BP attenuated xylazine's actions on cardiac rate and rhythm.

Cardiopulmonary effects of an intravenous infusion of guaifenesin, ketamine, and xylazine in dogs.

A 5% solution of dextrose in water containing 50 mg of guaifenesin, 0.25 mg of xylazine, and 1 mg of ketamine/ml was infused IV at the rate of 2.2 ml X kg-1 X hour-1 in dogs. Heart rate, systemic vascular resistance, mean arterial blood pressure, rate-pressure product, and arterial oxygen tension were not altered significantly from baseline values during 2 hours of anesthesia. Cardiac index was significantly (P less than 0.05) decreased from base-line values. Hypoventilation resulted in increased arterial carbon dioxide tension and decreased arterial pH. After the dogs were given glycopyrrolate, cardiac index returned to base line, and heart rate, mean arterial pressure, and rate-pressure product were significantly greater (P less than 0.05) than base-line values.

Cardiopulmonary effects of continuous intravenous infusion of guaifenesin, ketamine, and xylazine in ponies.

Eight ponies were anesthetized with a solution containing 50 mg of guaifenesin, 1 mg of ketamine, and 0.5 mg of xylazine X ml-1 of 5% dextrose in water. Anesthesia was induced by IV injection (1.1 ml X kg-1), followed by continuous IV infusion at 2.75 ml X kg-1 X hr-1. Heart rate, rate-pressure product, mean pulmonary artery pressure, and standard bicarbonate were not significantly changed throughout the study. Systolic, diastolic, and mean arterial pressures and left ventricular stroke work index were significantly decreased at 5 and 15 minutes after a bolus of the anesthetic solution was injected. Systolic blood pressure returned to within the base-line range at 30 minutes, but diastolic and mean arterial pressures were significantly decreased throughout the study. Cardiac index and arterial pH were decreased at 5 minutes only. Systemic vascular resistance was significantly decreased 60 minutes after bolus injection was given. Hypoventilation, as indicated by increased PaCO2, occurred 5 minutes after bolus injection was given.

Alterations in the arrhythmogenic dose of epinephrine after xylazine or medetomidine administration in halothane-anesthetized dogs.

Eight dogs (12.5 to 21.5 kg) were assigned at random to each of 3 groups that were not given glycopyrrolate (HS, HX, HM) and to each of 3 groups that were given glycopyrrolate (HGS, HGX, HGM). Dogs were anesthetized with halothane (1.31% end-tidal concentration), and ventilation was controlled (PCO2 35 to 40 mm of Hg end-tidal concentration). Glycopyrrolate was administered IV and IM at a dosage of 11 micrograms/kg of body weight, each. Saline solution, xylazine (1.1 mg/kg, IM), or medetomidine (15 micrograms/kg, IM) was administered 10 minutes after baseline arrhythmogenic dose of epinephrine (ADE) determination. Redetermination of the ADE at the same infusion rate was started 10 minutes after drug administration. Arrhythmogenic dose was determined by constant infusion of epinephrine at rates of 1.0 and 2.5 micrograms/kg/min. The ADE was defined as the total dose of epinephrine inducing at least 4 ectopic ventricular depolarizations within 15 seconds during a 3-minute infusion or within 1 minute after the end of the infusion. Total dose was calculated as the product of infusion rate and time to arrhythmia. Statistical analysis of the differences between baseline ADE and posttreatment ADE for groups HS, HX, and HM was performed by use of one-way ANOVA.(ABSTRACT TRUNCATED AT 250 WORDS)

Alterations in the arrhythmogenic dose of epinephrine after xylazine or medetomidine administration in isoflurane-anesthetized dogs.

Eight dogs (body weight, 12.5 to 21.5 kg) were assigned at random to each of 3 treatment groups (IS, IX, IM) that were not given glycopyrrolate and to each of 3 groups that were given glycopyrrolate (IGS, IGX, IGM). Dogs were anesthetized with isoflurane (1.95% end-tidal concentration), and ventilation was controlled (PCO2, 35 to 40 mm of Hg end-tidal concentration). Glycopyrrolate was administered IV and IM at a dosage of 11 micrograms/kg of body weight, each. Saline solution, xylazine (1.1 mg/kg, IM), or medetomidine (15 micrograms/kg, IM) was administered 10 minutes after baseline ADE determination. Redetermination of the ADE at the same infusion rate was started 10 minutes after drug administration. Arrhythmogenic dose was determined by constant infusion of epinephrine at rates of 1.0, 2.5, and 5.0 micrograms/kg/min. The ADE was defined as the total dose of epinephrine that induced at least 4 ectopic ventricular depolarizations within 15 seconds during a 3-minute infusion, or within 1 minute after the end of the infusion. Total dose was calculated as the product of infusion rate and time to arrhythmia. Statistical analysis of the differences between baseline and treatment ADE values was performed by use of one-way ANOVA. Mean +/- SEM baseline ADE values for groups IS, IX, and IM were 1.55 +/- 0.23, 1.61 +/- 0.28, and 1.95 +/- 0.65 micrograms/kg, respectively. Differences for groups IS, IX, and IM were -0.12 +/- 0.05, -0.31 +/- 0.40, and -0.17 +/- 0.26, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of yohimbine on xylazine-induced hypoinsulinemia and hyperglycemia in mares.

Serum insulin and plasma glucose concentrations were determined in 8 mares. Four IV treatments were studied: xylazine (1.1 mg/kg of body weight); yohimbine (0.125 mg/kg); yohimbine (0.125 mg/kg) followed 5 minutes later by xylazine (1.1 mg/kg); and 5 ml of isotonic saline solution as a control. Blood samples were collected before (time 0) and at 5, 15, 30, 60, 120, and 180 minutes after drug administration. Serum insulin concentration decreased and plasma glucose concentration increased in mares given xylazine. Plasma glucose concentration was unchanged in control mares and in mares given yohimbine or yohimbine followed by xylazine. Serum insulin concentration was unchanged in mares given saline solution, but transiently increased in mares given yohimbine alone. Treatment with yohimbine prevented xylazine-induced hypoinsulinemia and hyperglycemia.

Intravenous administration of lenperone and glycopyrrolate followed by continuous infusion of sufentanil in dogs: cardiovascular effects.

Cardiopulmonary effects of IV administration of lenperone (0.44 mg/kg) and glycopyrrolate (0.11 mg/kg) were determined in 6 healthy adult (2 to 5 years) Pointers during controlled ventilation with oxygen. Sufentanil was then administered as a loading dose (5 micrograms/kg, IV) and continually infused (0.1 microgram/kg/min) for 120 minutes. Lenperone-glycopyrrolate did not significantly affect heart rate, but induced a significant decrease in systemic vascular resistance, rate-pressure product, and mean arterial pressure, and significantly increased cardiac index. Administration of sufentanil did not significantly affect mean arterial pressure. Heart rate and rate-pressure product were significantly decreased during sufentanil infusion. Systemic vascular resistance gradually increased during the 2-hour sufentanil infusion and was not significantly different from base-line values at end of study. Cardiac index was not significantly different from baseline values during sufentanil infusion, except at 90 and 120 minutes, when it was significantly less. As administered in the present study, lenperone, glycopyrrolate, and sufentanil are safe and efficacious in adult dogs.

Hemodynamic and analgesic effects of propofol infusion in medetomidine-premedicated dogs.

Hemodynamic and analgesic effects of medetomidine (30 micrograms/kg of body weight, IM), atropine (0.044 mg/kg, IM), and propofol (2 mg/kg, IV, as a bolus, and 165 micrograms/kg/min, IV, for 60 minutes, as an infusion) were evaluated in 6 healthy adult Beagles. Catheters were placed while the dogs were anesthetized with isoflurane in oxygen. Administration of isoflurane was then discontinued, and dogs were allowed to breath oxygen until end-tidal isoflurane concentration was < or = 0.5%. At this time, baseline measurements were recorded and medetomidine and atropine were administered. Ten minutes later, the bolus of propofol was given and the infusion was begun. Analgesia was evaluated with a tail clamp test and by use of a direct-current nerve stimulator. Sinoatrial and atrioventricular blockade developed in all 6 dogs within 2 minutes of administration of medetomidine and atropine, but disappeared within 10 minutes. Apnea did not develop after administration of propofol. Analgesia was strong and consistent throughout the entire 60-minute period of propofol infusion. Medetomidine significantly (P < 0.05) increased systemic vascular resistance and decreased cardiac output, compared with baseline values. Propofol infusion appeared to alleviate medetomidine-induced vasoconstriction. Recovery was smooth and uncomplicated. All dogs were able to walk normally at a mean time (+/- SEM) of 88.2 +/- 20.6 minutes after termination of propofol infusion. It was concluded that medetomidine, atropine, and propofol, as given in the present study, is a safe combination of anesthetic drugs for use in healthy Beagles.

Duration of nonresponse to noxious stimulation after intramuscular administration of butorphanol, medetomidine, or a butorphanol-medetomidine combination during isoflurane administration in dogs.

OBJECTIVE: To assess duration of actions of butorphanol, medetomidine, and a butorphanol-medetomidine combination in dogs given subanesthetic doses of isoflurane (ISO). ANIMALS: 6 healthy dogs. PROCEDURE: Minimum alveolar concentration (MAC) values for ISO were determined. for each dog. Subsequently, 4 treatments were administered to each dog (saline [0.9% NaCl] solution, butorphanol [0.2 mg/kg of body weight], medetomidine [5.0 microg/kg], and a combination of butorphanol [0.2 mg/kg] and medetomidine [5.0 microg/kg]). All treatments were administered IM to dogs concurrent with isoflurane; treatment order was determined, using a randomized crossover design. Treatments were given at 7-day intervals. After mask induction with ISO and instrumentation with a rectal temperature probe, end-tidal CO2 and anesthetic gas concentrations were analyzed. End-tidal ISO concentration was reduced to 90% MAC for each dog. A tail clamp was applied 15 minutes later. After a positive response, 1 of the treatments was administered. Response to application of the tail clamp was assessed at 15-minute intervals until a positive response again was detected. RESULTS: Duration of nonresponse after administration of saline solution, butorphanol, medetomidine, and butorphanol-medetomidine (mean +/- SD) was 0.0+/-0.0, 1.5+/-1.5, 2.63+/-0.49, and 5.58+/-2.28 hours, respectively. Medetomidine effects were evident significantly longer than those for saline solution, whereas effects for butorphanol-medetomidine were evident significantly longer than for each agent administered alone. CONCLUSION AND CLINICAL RELEVANCE: During ISO-induced anesthesia, administration of medetomidine, but not butorphanol, provides longer and more consistent analgesia than does saline solution, and the combination of butorphanol-medetomidine appears superior to the use of medetomidine or butorphanol alone.

Radiographic characterization of diaphragmatic excursion in halothane-anesthetized ponies: spontaneous and controlled ventilation systems.

A radiograph technique for identification of diaphragmatic segments and quantitation of their contribution to total diaphragmatic function was developed. five anesthetized ponies were studied on 3 separate occasions. Studies were made of the ponies in left lateral recumbency at 2 anesthetic levels (1 and 2 minimal alveolar anesthetic concentrations; halothane) and under spontaneous and controlled ventilation systems. General pattern of diaphragmatic displacement was unchanged by increased depth of anesthesia. Controlled ventilation altered the pattern of diaphragmatic displacement. Diaphragmatic displacement and regional volume changes were a function of active contraction or passive movement.