We investigated changes in hemostatic function after infusion of 6% dextran 70 (high molecular weight dextran) at 2 rates. Six healthy dogs underwent 3 regimens: 20 ml of dextran/kg of body weight administered in 1 hour (trial A), 20 ml of dextran/kg administered in 30 minutes (trial B), and 0.9% sodium chloride solution as a control administered over 1 hour to achieve hemodilution equivalent to that for 20 ml of dextran/kg (trial C). Before and at 2, 4, 8, and 24 hours after the start of trials A and B, we measured PCV, total solids (TS) concentration, amount of von Willebrand factor antigen (vWf:Ag), factor VIII coagulant activity (VIII:C), prothrombin time, activated partial thromboplastin time (APTT), platelet retention in a glass bead column, and buccal mucosa bleeding time (BMBT). Values were not obtained at 8 and 24 hours for trial C. Saline-induced changes in hemostasis were significant (P less than 0.05) from baseline throughout the sample collection period. Significant differences (P less than 0.05) between trial A and control were observed for vWf:Ag, VIII:C, BMBT, APTT, TS, and PCV values at 2 hours, and for VIII:C at 4 hours. Significant differences (P less than 0.05) between trial B and control were observed for APTT, TS, and PCV values at 2 hours, and for vWf:Ag, VIII:C, BMBT, APTT, TS, and PCV values at 4 hours. During trials A and B, mean values of analytes infrequently deviated from reference intervals, and clinical signs of bleeding were not observed in any dog.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

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.

Animals↗

PubMed1992

Cardiovascular and respiratory effects of propofol administration in hypovolemic dogs.

Cardiopulmonary effects of propofol were studied in hypovolemic dogs from completion of, until 1 hour after administration. 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, 6 mg of propofol/kg of body weight was administered IV to 7 dogs, and cardiopulmonary effects were measured. After blood withdrawal and prior to propofol administration, oxygen utilization ratio increased, whereas mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary capillary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, and mixed venous oxygen content decreased from baseline. Three minutes after propofol administration, mean pulmonary arterial pressure, pulmonary vascular resistance, oxygen utilization ratio, venous admixture, and arterial and mixed venous carbon dioxide tensions increased, whereas mean arterial pressure, arterial oxygen tension, mixed venous oxygen content, arterial and mixed venous pH decreased from values measured prior to propofol administration. Fifteen minutes after propofol administration, mixed venous carbon dioxide tension was still increased; however by 30 minutes after propofol administration, all measurements had returned to values similar to those measured prior to propofol administration.

Animals↗

PubMed1991

Effects of a highly concentrated hypertonic saline-dextran volume expander on cardiopulmonary function in anesthetized normovolemic horses.

Conventional fluid resuscitation is unsatisfactory in a small percentage of equine emergency surgical cases because the large volumes of fluids required cannot be given rapidly enough to adequately stabilize the horse. In anesthetized horses, the volume expansion and cardiopulmonary effects of a small volume of highly concentrated hypertonic saline-dextran solution were evaluated as an alternative initial fluid choice. Seven halothane-anesthetized, laterally recumbent, spontaneously ventilating, normovolemic horses were treated with a 25% NaCl-24% dextran 70 solution (HSD) at a dosage of 1.0 ml/kg of body weight, IV, infused over 10 minutes, and the effects were measured for 120 minutes after infusion. Plasma volume expansion was rapid and significant (from 36.6 +/- 4.6 ml/kg to 44.9 +/- 4.8 ml/kg), and remained significantly expanded for the duration of the experiment. Packed cell volume, total blood hemoglobin, and plasma protein concentrations significantly decreased, confirming rapid and sustained volume expansion with hemodilution. Cardiac index and stroke index immediately increased and remained high for the entire study (from 69.6 +/- 15.3 ml/min/kg to 106.6 +/- 28.4 ml/min/kg, and from 1.88 +/- 0.49 ml/beat/kg to 2.50 +/- 0.72 ml/beat/kg, respectively). Systemic vascular resistance significantly decreased immediately after HSD infusion and remained decreased for the duration of the study (from 1.41 +/- 0.45 mm of Hg/ml/min/kg to 0.88 +/- 0.22 mm of Hg/ml/min/kg). Arterial and venous blood oxygen content decreased significantly because of hemodilution, but actual oxygen transport transiently increased at the 10-minute measurement before returning toward baseline.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗

PubMed1991

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.

Anesthesia↗

PubMed1990

Ketamine in hypovolemic dogs.

The cardiopulmonary consequences of hemorrhagic hypovolemia and the subsequent administration of ketamine were evaluated in eight dogs; five additional dogs served as controls. Heart rate (HR), systemic vascular resistance, breathing rate, minute ventilation (VE), PaO2, alveolar-arterial oxygen tension gradient, and oxygen extraction ratio increased, while arterial and pulmonary pressures, CVP, cardiac output, oxygen transport, PVO2 PaCO2, mixed venous oxygen content, bicarbonate, and base deficit decreased in response to hypovolemia. Ketamine administration was associated with a significant increase in HR, arterial and pulmonary BP, and PaCO2, and a significant decrease in VE (transient), PaO2 (transient), and pH. Ketamine supported cardiovascular function well, did not impair tissue oxygenation, and caused only transient respiratory depression in these hypovolemic dogs.

Acid-Base Equilibrium↗

PubMed1990

Effects of epinephrine and ritodrine in dogs with acute hyperkalemia.

As plasma potassium concentrations, whether normal or elevated, can be reduced by intravenous administration of either epinephrine or ritodrine, the effects of these drugs were examined during acute hyperkalemia. Six anesthetized dogs were studied every 2 wk, on 18 separate occasions. Hyperkalemia was induced by intravenous infusion of potassium chloride, resulting in plasma potassium concentrations of 9.6 +/- 0.3 mEq/L (mean +/- SEM), bradycardia, and idioventricular rhythm. Dogs were then given slow intravenous injections every 30 min of either saline (controls), epinephrine, or ritodrine. Epinephrine doses were 0.01, 0.1, 1.0, 10, or 100 micrograms/kg; ritodrine doses were 0.1, 1.0, 10, 100, or 1000 micrograms/kg. At the highest does, both epinephrine and ritodrine caused clinically important decreases in plasma potassium, reducing concentrations to below 7.0 mEq/L. Ritodrine had a significantly greater effect than epinephrine. Side effects included hypertension and dysrhythmias with epinephrine, serious hypotension with ritodrine, and tachycardia with both drugs. For both drugs, the doses that caused a decrease in plasma potassium also caused an increase in heart rate and there was a correlation between plasma potassium levels and heart rate. Epinephrine and ritodrine may be useful in treating acute hyperkalemia, but cardiovascular side effects may occur. Increased heart rate could be used as an indicator of therapeutic effect and the magnitude of the increase in heart rate may be helpful in predicting the level of response.

Animals↗

PubMed1989

Monitoring the critically ill patient.

Monitoring is the key to a successful critical care endeavor. It is the only way in which we know if we did a good thing and if we did enough of it (or too much). Oftentimes, the decision to treat or not to treat is made difficult by the paucity of information available. The secret is to make an intuitive decision and then monitor the patient to see if it was the right or the wrong decision. Most wrong decisions can be caught and corrected long before the patient has suffered the consequences. Go forth, and monitor!

Animals↗

PubMed1989

Naloxone reversal of oxymorphone effects in dogs.

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.

Animals↗

PubMed1988

Comparison of PO2, PCO2, and pH in blood collected from the femoral artery and a cut claw of cats.

A technique for collection of blood samples from the cut claw of the cat was developed. Forty-six blood samples were collected simultaneously from the cut claw and the femoral artery of 7 healthy cats. Blood gas and pH values were measured and compared. There was no difference between sample pairs for blood PO2 and PCO2, but the pH values were significantly (P less than 0.001) higher in the capillary samples (7.432 +/- 0.033) than in the samples from the femoral artery (7.419 +/- 0.031).

Animals↗

PubMed1988

A simple fluid therapy planning guide.

Explore the source record for details and available documents.

Animals↗

PubMed1988

Effects of mizoribine on canine renal allograft recipients.

Heterotopic renal allograft transplantation and bilateral nephrectomies were performed on 12 mixed-breed dogs. Histoincompatibility was confirmed by serologically defined and lymphocyte-defined antigen testing. Mizoribine (5 mg/kg, q 24 h) was administered orally starting the day of surgery. Body weights, blood cell counts, serum biochemical and electrolyte values, immunoglobulin concentration, and serum mizoribine concentrations were determined. Complete urinalyses, including bacteriologic culturing and lymphocyte stimulation assays were performed. The mean survival time for the allograft recipients was 20 +/- 14 days; significantly longer than nontreated historic controls surviving 8.1 +/- 0.6 days (P = 0.0098). Death was attributed to the combined effects of renal allograft rejection and development of a mizoribine-dependent gastroenteritis. Serum mizoribine concentrations were greater in dogs undergoing rapid allograft rejection because of compromised renal excretion of the drug. This resulted in a rapid onset of gastroenteritis. There were no complications resulting from infection, myelosuppression, or hepatotoxicosis.

Alanine Transaminase↗

PubMed1987

Use of analgesics postoperatively and in a small animal intensive care setting.

Explore the source record for details and available documents.

Analgesics↗

PubMed1987

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.

Animals↗