Effects of saffan on cardiopulmonary function in healthy cats.

The effects of saffan on cardiopulmonary function were evaluated in eight healthy adult cats. Measured values were cardiac output by thermodilution, heart rate by electrocardiogram, arterial blood gases, respiratory rate and systolic, diastolic and mean arterial blood pressures by arterial catheterization. Calculated values included cardiac index, stroke volume and systemic vascular resistance. Statistical analysis employed paired t-tests comparing pre saffan anesthetic induction and post saffan anesthetic parameters over a 120 minute time sequence. Thirty min after saffan induction, significant depression in cardiac output was evident while stroke volume was significantly depressed at 45 and 60 min, systolic blood pressure at 15 min and respiratory rate at 5, 10 and 15 min. No significant changes occurred in cardiac index, heart rate, arterial blood gases, diastolic and mean arterial blood pressure or systemic vascular resistance. It was concluded that saffan causes significant depression of cardiopulmonary function in normal adult cats.     

Doxapram: cardiopulmonary effects in the horse

The cardiopulmonary effects of 3 dosages of doxapram hydrochloride (0.275 mg/kg, 0.55 mg/kg, and 1.1 mg/kg, IV) were studied in 6 adult horses. Doxapram given IV significantly (P less than 0.05) decreased PaCO2 and increased respiratory rate, cardiac output arterial blood pressures (systolic, mean, and diastolic) arterial pH, and PaO2 at 1 minute after each dose was administered. Heart rate and mean and diastolic pulmonary arterial blood pressure were significantly (P less than 0.05) increased 1 minute after the 2 larger dosages of doxapram were given (0.55 mg/kg and 1.1 mg/kg, IV), but not after the smallest dosage was given. All measurements, except heart rate and cardiac output, had returned to base line by 5 minutes after each dosing. Heart rate remained significantly (P less than 0.05) increased 10 minutes after the 0.55 mg/kg dosage was given and 30 minutes after the 1.1 mg/kg dosage. Cardiac output remained significantly (P less than 0.05) increased at 10 minutes, 5 minutes, and 30 minutes after the 0.275, 0.55, and 1.1 mg/kg dosages, respectively, were given.     

Comparative cardiovascular, analgesic, and sedative effects of medetomidine, medetomidine-hydromorphone, and medetomidine-butorphanol in dogs

OBJECTIVE: To compare sedative, analgesic, and cardiopulmonary effects after IV administration of medetomidine (20 microg/kg), medetomidine-hydromorphone (20 microg of medetomidine/kg and 0.1 mg of hydromorphone/kg), and medetomidine-butorphanol (20 microg of medetomidine/kg and 0.2 mg of butorphanol tartrate/kg) in dogs. ANIMALS: 6 dogs healthy mixed-breed dogs. PROCEDURE: Instruments were surgically inserted, and heart rate (HR), respiratory rate (RR), systolic arterial pressure (SAP), mean arterial pressure (MAP), diastolic arterial pressure (DAP), mean pulmonary arterial pressure (MPAP), pulmonary capillary wedge pressure (PCWP), central venous pressure (CVP), core body temperature, and cardiac output (CO) were measured 0, 5, 10, 15, 30, 45, and 60 minutes after injection. Cardiac index (CI), stroke volume (SV), stroke index (SI), systemic vascular resistance (SVR), and pulmonary vascular resistance (PVR) were calculated. Arterial samples for blood gas analysis were collected 0, 15, and 45 minutes after injection. Intensity of analgesia, degree of sedation, and degree of muscle relaxation were evaluated at aforementioned time points and 75, 90, 120, 150, 180, and 210 minutes after injection. RESULTS: Administration of medetomidine, medetomidine-hydromorphone, and medetomidine-butorphanol was associated with increases in SAP, MAP, DAP, MPAP, PCWP, CVP, SVR, PVR, core body temperature, and PaCO2 and decreases in HR, CO, CI, SV, SI, RR, pH, and PaO2. Clinically important differences were not detected among treatments. Medetomidine-hydromorphone and medetomidine-butorphanol provided a longer duration of sedation and better quality of analgesia, compared with medetomidine alone. CONCLUSIONS AND CLINICAL RELEVANCE: Medetomidine-hydromorphone or medetomidine-butorphanol is associated with improved analgesia and sedation but has cardiopulmonary effects comparable to those for medetomidine alone.     

Effect of xylazine on heart rate and arterial blood pressure in conscious dogs, as influenced by atropine, 4-aminopyridine, doxapram, and yohimbine

The effects of xylazine on heart rate (HR) and mean arterial blood pressure (ABP) were studied in 5 conscious male dogs. An IV injection of xylazine (1 mg/kg) caused a decrease in HR, which was accompanied by sinus arrhythmia. Xylazine administration also caused an initial increase in ABP, which was followed by a decrease. Atropine sulfate (0.045 mg/kg, IM) increased both the ABP and HR, but prevented xylazine-induced bradycardia only in 3 of 5 dogs. The other 2 dogs had to be given a supplemental dose of atropine sulfate (0.01 mg/kg, IV) before xylazine-induced bradycardia was antagonized. In addition, atropine sulfate potentiated xylazine-induced hypertension for 60 minutes. Yohimbine, an alpha 2-adrenoreceptor blocking agent, given IV at a dosage of 0.1 mg/kg, antagonized hypertension, hypotension, and bradycardia induced by xylazine. In addition, doxapram HCl, given IV at a dosage of 5.5 mg/kg, antagonized bradycardia but potentiated xylazine-induced hypertension, and an IV injection of 4-aminopyridine at a dosage of 0.5 mg/kg did not affect the cardiovascular actions of xylazine. It was concluded that atropine sulfate at the IM dosage of 0.045 mg/kg may be insufficient to antagonize xylazine-induced bradycardia but may potentiate xylazine-induced hypertension, and yohimbine may be useful in antagonizing these untoward reactions associated with xylazine administration. Doxapram and 4-aminopyridine were not found to be beneficial.     

Cardiopulmonary effects of a halothane/oxygen combination in healthy cats.

The effects of a halothane/oxygen combination on the cardiopulmonary function of 11 healthy cats were studied. Test parameters included cardiac output, measured via thermo-dilution, heart rate, respiratory rate, arterial blood pressure (systolic, diastolic and mean) and blood gas analysis. Values for systemic vascular resistance, cardiac index and stroke volume were calculated from these data. Cardiac output, cardiac index, heart rate, stroke volume, arterial blood pressure (systolic, diastolic and mean) and arterial blood pH were significantly decreased (p less than 0.001). Respiratory rate was also significantly decreased (p less than 0.007) with arterial CO2 tension being significantly increased (p less than 0.001). Statistically significant changes, where seen, persisted for the duration of the anesthetic period. Arterial O2 tension and systemic vascular resistance remained unchanged. All parameters returned to near pretest values within 30 minutes following cessation of halothane anesthesia.     

七氟醚氟烷异氟醚对犬心脏功能影响的临床比较

为评价七氟醚对心脏功能的影响。并与氟烷和异氟醚作比较，对动物医院就诊、心肺功能正常、拟作手术治疗的8例患犬进行麻醉试验，所有犬均以l-美散痛和安定和为麻醉前给药，分别以1.5%七氟醚、1.0%七氟醚与66.7%笑气、1.0%氟烷、1.5%异氟醚维持手术麻醉，并作人工呼吸，各组均未观察到心律异常，手术麻醉期间，七氟醚组犬心率降幅（4.73%）低于异氟醚组（9.74%)或氟烷组（10.23%)。七氟醚组、氟烷组和异氟醚组的收缩压/舒张压轻度升高（七氟醚3.38%/11.93%氟烷6.09%/9.09%，异氟醚4.82%/6.25%)。而七氟醚与笑气组的收缩压/舒张压则降低（6.84%/5.73%)。证实七氟醚应为临床首选的吸入麻醉剂。     

Cardiopulmonary effects of a ketamine hydrochloride/acepromazine combination in healthy cats.

The effect of a ketamine hydrochloride/acepromazine combination on the cardiopulmonary function of 11 healthy cats was studied. Test parameters included cardiac output, measured by thermodilution, heart rate, respiratory rate, arterial blood pressure (systolic, diastolic and mean) and arterial blood gas analysis. Values for systemic vascular resistance, cardiac index and stroke volume were calculated. The cardiac output, cardiac index, stroke volume, arterial blood pressure and arterial blood pH decreased significantly (p less than 0.006). The arterial CO2 increased significantly (p less than 0.006). All changes occurred during the five to 45 minute postinduction time period. The heart rate, respiratory rate, arterial O2 and systemic vascular resistance were not significantly altered. The anesthetic regime maintained an adequate plane of surgical anesthesia for 30-45 minutes.     

Comparative hemodynamic effects of halothane and halothane-acepromazine at equipotent doses in dogs.

The purpose of this study was to compare the cardiovascular effects of halothane when used alone at increasing doses (1.2, 1.45 and 1.7 minimum alveolar concentration, MAC) to those produced with equipotent doses of halothane after potentiation of the anesthetic effect with acepromazine (ACP) sedation (45% reduction of halothane MAC). Six healthy mature dogs were used on three occasions. The treatments were halothane and intramuscular (IM) saline (1.0 mL), halothane and ACP (0.04 mg/kg IM), or halothane and ACP (0.2 mg/kg IM). Anesthesia was induced and maintained with halothane in oxygen and the dogs were prepared for the collection of arterial and mixed venous blood and for the determination of heart rate, systolic, diastolic and mean arterial pressure, mean pulmonary arterial pressure (PAP), central venous pressure and cardiac output. Following animal preparation the saline or ACP was administered and positive pressure ventilation instituted. Twenty-five minutes later the dogs were exposed to the first of three anesthetic levels, with random assignment of the sequence of administration. At each anesthetic level, measurements were obtained at 20 and 35 min. Calculated values included cardiac index, stroke index, left ventricular work, systemic vascular resistance, arterial oxygen content, mixed venous oxygen content, oxygen delivery and oxygen consumption. Heart rate was significantly higher with halothane alone than with both halothane-ACP combinations and was significantly higher with high dose ACP compared to low dose ACP. Systolic and mean blood pressures were lowest with halothane alone and highest with 0.2 mg/kg ACP, the differences being significant for each treatment. Oxygen uptake and PAP were significantly lower in dogs treated with ACP. It was concluded that ACP does not potentiate the cardiovascular depression that accompanies halothane anesthesia when the resultant lower dose requirements of halothane are taken into consideration.     

Hemodynamic Effects of Atropine and Glycopyrrolate in Isoflurane-Xylazine-Anesthetlzed Dogs

Alterations in parasympathetic tone are partially responsible for xylazine's hemodynamic effects. The purpose of this study was to evaluate and compare the hemodynamic changes caused by the administration of intravenous (IV) atropine or glycopyrrolate after IV xylazine in isoflurane-anesthetized dogs. Six healthy beagles (8.2 to 10.7 kg) were used in two trials separated by 7 days. Anesthesia was induced and maintained with isoflurane in 100% oxygen with controlled ventilation. Once constant end-tidal isoflurane (1.8%) and arterial partial pressure of carbon dioxide (35 to 45 mm Hg) values were reached, baseline data were recorded and xylazine (0.5 mg/kg, IV) was given. In trial 1 atropine (0.1 mg/kg, IV) was given 5 minutes after xylazine, and in trial 2 glycopyrrolate (0.025, mg/kg, IV), was given 5 minutes after xylazine. Hemodynamic variables were recorded 3 minutes after xylazine and 3 minutes after anticholinergic administration. In trial 2, bilateral vagotomies were performed 10 minutes after glycopyrrolate, and hemodynamic variables were recorded 3 minutes later. Heart rate, cardiac index, and stroke index decreased; arterial pressure and systemic vascular resistance increased after xylazine. Heart rate, cardiac index, and rate pressure product increased after anticholinergic administration. Significant differences between atropine and glycopyrrolate were not observed in any of the hemodynamic parameters. Similarly, significant differences between glycopyrrolate and bilateral vagotomy were not observed. The authors conclude that intravenous atropine and glycopyrrolate have equivalent hemodynamic actions during the increased pressure phase after IV xylazine in isoflurane-anesthetized dogs; that intravenous atropine and glycopyrrolate produce comparable increases in heart rate and that both may increase the risk of myocardial hypoxia associated with an increase in rate pressure product; and that vagal blockade produced by high-dose glycopyrrolate (.025 mg/kg, IV) is similar to that produced by bilateral vagotomy.     

Cardiopulmonary and anesthetic effects of ketamine and its enantiomers in dogs

Dogs were used to determine cardiopulmonary and chemical restraining effects of racemic ketamine and its enantiomers. Levorotatory ketamine induced the shortest duration of unconsciousness and recumbency when compared with effects of dextrorotatory and racemic ketamine. Administration of racemic ketamine or either of its enantiomers (30 mg/kg of body weight, IV) to dogs recovering from isoflurane anesthesia induced transient, but significant (P less than 0.05), decreases in arterial blood pressure, left ventricular contractility, cardiac output, and total peripheral vascular resistance. Arterial blood pressure and left ventricular contractility significantly (P less than 0.05) increased at later times after ketamine administration. Arterial pH and the PO2 values decreased after IV administration of racemic ketamine or its enantiomers. Significant differences in cardiopulmonary variables were not observed between groups given ketamine or its enantiomers.     

Oxymorphone: cardiovascular, pulmonary, and behavioral effects in dogs

Cardiovascular, pulmonary, and behavioral effects of multiple doses of oxymorphone in 10 nonanesthetized, spontaneously breathing, healthy dogs were studied. Oxymorphone (0.4 mg/kg of body weight) was administered IV, and at 20, 40, and 60 minutes after the first injection was given, 0.2 mg of oxymorphone/kg was administered. Cardiovascular and pulmonary variables were measured before (base line) and at 5, 15, 35, 55, 75, 100, 120, 150, 180, 210, 240, 270, and 300 minutes after the first oxymorphone injection. Degree of sedation and behavioral effects also were recorded. Naloxone (0.04 mg/kg, IV) was administered 4.5 hours after the 4th oxymorphone injection, and behavioral changes were recorded. Oxymorphone induced mild respiratory depression. After transient apnea developed, respiratory rate increased to a pant, tidal volume decreased, and minute ventilation increased, but these values were not significantly (P = 0.05) different from base line. The PaCO2, physiologic dead space, and base deficit increased; alveolar tidal volume decreased; and alveolar minute ventilation did not change. The PaO2 decreased, hemoglobin and arterial O2 content increased, and O2 transport did not change. Venous admixture transiently increased. Oxymorphone induced minimal cardiovascular depression. Mean arterial blood pressure, stroke volume, central venous pressure, pulmonary artery pressure, and pulmonary wedge pressure increased. Heart rate decreased, systemic vascular resistance transiently increased, and cardiac output transiently decreased. Because the dogs moved spontaneously, responded to sound with sudden, vigorous movements, and breathed with excessive effort, oxymorphone alone was considered inadequate as a general anesthetic.     

Evaluation of 25%, 50%, and 67% Nitrous Oxide with Halothane-Oxygen for General Anesthesia in Horses

Twenty-five percent, 50%, and 67% nitrous oxide was administered to 12 horses anesthetized with halothane and oxygen. Compared to halothane-oxygen alone, there was no significant difference in heart rate, systolic, diastolic, or mean blood pressure values, arterial pH, PaCO2, or plasma bicarbonate values when nitrous oxide was included. A significant linear reduction in PaO2 values could be correlated with N2O:O2 concentrations. The halothane level required to maintain surgical anesthesia was reduced when nitrous oxide was administered, but it was not affected by changing the nitrous oxide concentrations. Nitrous oxide concentrations greater than 25% provide no additional reduction in halothane requirement and may be accompanied by PaO2 values that pose risk to the horse.     

Cardiopulmonary effects of thiopental/lidocaine combination during anesthetic induction in the dog

The cardiopulmonary effects and tendencies to produce ventricular arrhythmias were evaluated in 13 dogs given a surgical plane of anesthesia by thiopental (IV) or a combination of thiopental and lidocaine (IV). Thiopental (22 mg/kg of body weight) was compared with a combination of thiopental (11 mg/kg) and lidocaine (8.8 mg/kg). Preanesthetic agents were not given. Both methods for IV anesthesia provided a smooth induction suitable for easy intubation. The thiopental/lidocaine combination had a shorter duration, produced no arrhythmias, and resulted in less cardiopulmonary depression than did thiopental alone. Bigeminy developed after intubation during 19 of 20 thiopental inductions as compared with that in 0 of 22 thiopental/lidocaine inductions. The bigeminies were preceded by systemic hypertension and tachycardia which developed as the trachea was being intubated. The increase in aortic pressure and heart rate was minimal after intubation during the thiopental/lidocaine inductions. Five minutes after administration of thiopental alone, increases in heart rate, aortic pressure, total peripheral vascular resistance, and left ventricular systolic and end-diastolic pressures were observed. When these increases in rate, preload, and afterload were considered in relation to a stabile maximum positive first derivative of left ventricular pressure, left ventricular contractility was considered to be decreased. Mild respiratory acidosis and hypoxemia were present at 5 and 10 minutes after thiopental induction. Because the combination of thiopental/lidocaine had less cardiopulmonary depressive effects and protected against arrhythmias, it would appear to be a good method for anesthetic induction of the patient with cardiopulmonary disease. In the patient with normal cardiopulmonary function, thiopental produces only a moderate and reversible depression.     

Ketamine in dogs

The cardiopulmonary consequences of ketamine (10 mg/kg, IV) were evaluated in 18 dogs. Heart rate, cardiac output, systemic blood pressure, left ventricular work, oxygen transport, oxygen consumption, carbon dioxide production, and core temperature increased. Breathing rate, minute ventilation, and arterial partial pressure of oxygen transiently decreased. Arterial partial pressure of carbon dioxide, alveolar-arterial oxygen gradient, and venous admixture transiently increased. The duration of action of ketamine for surgical anesthesia was short. Muscle tone and salivation were excessive, and spontaneous muscular activity was prominent.     

Hemodynamic effects of nitrous oxide in isoflurane-anesthetized cats

OBJECTIVE: To determine the hemodynamic effects of nitrous oxide in isoflurane-anesthetized cats. ANIMALS: 12 healthy adult domestic shorthair cats. PROCEDURE: Cats were anesthetized by administration of isoflurane in oxygen. After instruments were inserted, end-tidal isoflurane concentration was set at 1.25 times the individual minimum alveolar concentration, and nitrous oxide was administered in a Latin-square design at 0, 30, 50, and 70%. Each concentration was administered for 25 minutes before measurements were obtained to allow for stabilization. Heart rate; systemic and pulmonary arterial pressures; central venous pressure; pulmonary artery occlusion pressure; cardiac output; body temperature; arterial and mixed-venous pH, PCO2, PO2, and hemoglobin concentrations; PCV; and total protein and lactate concentrations were measured before and during noxious stimulation for each nitrous oxide concentration. Arterial and mixed-venous bicarbonate concentrations and oxygen saturation, cardiac index, stroke index, rate-pressure product, systemic and pulmonary vascular resistance indices, left and right ventricular stroke work indices, arterial and mixed-venous oxygen contents, oxygen delivery, oxygen consumption, oxygen extraction ratio, alveolar-to-arterial oxygen difference, and venous admixture were calculated. RESULTS: Arterial pressure, central venous pressure, pulmonary arterial pressure, rate-pressure product, systemic and pulmonary vascular resistance indices, arterial PCO2, and PCV increased during administration of 70% nitrous oxide. Arterial and mixed-venous pH, mixed-venous PO2, and alveolar-to-arterial oxygen difference decreased during administration of 70% nitrous oxide. Results before and during noxious stimulation were similar. CONCLUSIONS AND CLINICAL RELEVANCE: Administration of 70% nitrous oxide to isoflurane-anesthetized cats resulted in improved arterial pressure, which was related to a vasoconstrictive effect.     

Cardiopulmonary effects of etomidate in hypovolemic dogs.

Cardiopulmonary effects of etomidate administration were studied in hypovolemic dogs. Baseline cardiopulmonary data were recorded from conscious dogs after instrumentation. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. Blood pressure was maintained at 60 mm of Hg for 1 hour, by further removal or replacement of blood. One milligram of etomidate/kg of body weight was then administered IV to 7 dogs, and the cardiopulmonary effects were measured 3, 15, 30, and 60 minutes later. After blood withdrawal and prior to etomidate administration, heart rate, arterial oxygen tension, and oxygen utilization ratio increased. Compared with baseline values, the following variables were decreased: mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, mixed venous oxygen content, and arterial carbon dioxide tension. Three minutes after etomidate administration, central venous pressure, mixed venous and arterial carbon dioxide tension, and venous admixture increased, and heart rate, arterial and venous pH, and arterial oxygen tension decreased, compared with values measured immediately prior to etomidate administration. Fifteen minutes after etomidate injection, arterial pH and heart rate remained decreased. At 30 minutes, only heart rate was decreased, and at 60 minutes, mean arterial pressure was increased, compared with values measured before etomidate administration. Results of this study indicate that etomidate induces minimal changes in cardiopulmonary function when administered to hypovolemic dogs.     

Cardiopulmonary effects of medetomidine, oxymorphone, or butorphanol in selegiline-treated dogs

OBJECTIVES: To determine if chronic selegiline HCl administration affects the cardiopulmonary response to medetomidine, oxymorphone, or butorphanol in dogs. STUDY DESIGN: Prospective randomized experimental study. ANIMALS: Twenty-eight adult, random source, hound dogs weighing 21-33 kg. METHODS: Dogs were assigned to the following treatment groups: selegiline + medetomidine (MED; n = 6); placebo + MED (n = 6), selegiline + oxymorphone (OXY; n = 6); placebo + OXY (n = 6); selegiline + butorphanol (BUT; n = 7) or placebo + BUT (n = 6). Nine dogs were treated with two of the three pre-medicants. Dogs were treated with selegiline (1 mg kg(-1) PO, q 24 hours) or placebo for at least 44 days prior to pre-medicant administration. On the day of the experiment, arterial blood for blood gas analysis, blood pressure measurements, ECG, cardiac ultrasound (mM-mode, 2-D, and continuous wave Doppler), and behavioral observations were obtained by blinded observers. An IV injection of MED (750 micro g m(-2)), OXY (0.1 mg kg(-1)) or BUT (0.4 mg kg(-1)) was given. Cardiopulmonary and behavioral data were collected at 1, 2, 5, 15, 30, and 60 minutes after injection. RESULTS: Selegiline did not modify responses to any of the pre-medicant drugs. Medetomidine caused a significant decrease in heart rate (HR), cardiac output (CO), and fractional shortening (FS). Mean arterial pressure (MAP), systemic vascular resistance (SVR), and central venous pressure (CVP) were increased. Level of consciousness and resistance to restraint were both decreased. Oxymorphone did not affect MAP, CO, CVP, or SVR, but RR and PaCO(2) were increased. Level of consciousness and resistance to restraint were decreased. BUT decreased heart rate at 1 and 5 minutes. All other cardiovascular parameters were unchanged. BUT administration was associated with decreased arterial pH and increased PaCO(2). BUT decreased level of consciousness and resistance to restraint. CONCLUSIONS AND CLINICAL RELEVANCE: Although pre-medicants themselves altered cardiopulmonary and behavioral function, selegiline did not affect the response to medetomidine, oxymorphone, or butorphanol in this group of normal dogs.     

Evaluation of hemodynamic measurements, including lithium dilution cardiac output, in anesthetized dogs undergoing ovariohysterectomy

OBJECTIVE: To measure cardiac output in healthy female anesthetized dogs by use of lithium dilution cardiac output and determine whether changes in mean arterial pressure were caused by changes in cardiac output or systemic vascular resistance. DESIGN: Prospective clinical study. ANIMALS: 20 healthy female dogs. PROCEDURE: Dogs were anesthetized for ovariohysterectomy. Ten dogs breathed spontaneously throughout anesthesia, and 10 dogs received intermittent positive-pressure ventilation. Cardiovascular and respiratory measurements, including lithium dilution cardiac output, were performed during anesthesia and surgery. RESULTS: Mean arterial pressure and systemic vascular resistance index were low after induction of anesthesia and just prior to surgery and increased significantly after surgery began. Cardiac index (cardiac output indexed to body surface area) did not change significantly throughout anesthesia and surgery. CONCLUSIONS AND CLINICAL RELEVANCE: Results provide baseline data for cardiac output and cardiac index measurements during clinical anesthesia and surgery in dogs. Changes in mean arterial pressure do not necessarily reflect corresponding changes in cardiac index.     

Cardiovascular and respiratory effects of thiopental administration in hypovolemic dogs

The cardiopulmonary effects of thiopental sodium were studied in hypovolemic dogs from completion of until 1 hour after administration of the drug. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. After stabilization at this pressure for 1 hour, 8 mg of thiopental/kg of body weight was administered IV to 7 dogs, and cardiopulmonary effects were measured. After blood withdrawal and prior to thiopental administration, heart rate and oxygen utilization ratio increased, whereas mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, and mixed venous oxygen content decreased from baseline. Three minutes after thiopental administration, heart rate, mean arterial pressure, mean pulmonary arterial pressure, pulmonary vascular resistance, and mixed venous oxygen tension increased, whereas oxygen utilization ratio and arterial and mixed venous pH decreased from values measured prior to thiopental administration. Fifteen minutes after thiopental administration, heart rate was still increased; however by 60 minutes after thiopental administration, all measurements had returned to values similar to those obtained prior to thiopental administration.     

Xylazine and xylazine-ketamine in dogs

The cardiopulmonary consequences of IV administered xylazine (1.0 mg/kg) followed by ketamine (10 mg/kg) were evaluated in 12 dogs. Xylazine caused significant decreases in heart rate, cardiac output, left ventricular work, breathing rate, minute ventilation, physiologic dead space, oxygen transport, mixed venous partial pressure of oxygen, and oxygen concentration. It caused significant increases in systemic blood pressure, central venous pressure, systemic vascular resistance, tidal volume, and oxygen utilization ratio. The subsequent administration of ketamine was associated with significant increases in heart rate (transient increase), cardiac output, the alveolar-arterial PO2 gradient and venous admixture (transient increase), and arterial PCO2 (transient increase). It caused significant decreases in stroke volume (transient decrease), left ventricular stroke work (transient decrease), effective alveolar ventilation, arterial PO2 and oxygen content (transient decrease).