Vasopressor therapy using vasopressin prior to crystalloid resuscitation in irreversible hemorrhagic shock under isoflurane anesthesia in dogs

In the present study, we tested the hypothesis that vasopressin administration prior to crystalloid resuscitation can be used to improve hemodynamic and oxygen delivery functions. Hemorrhagic shock was experimentally induced by maintaining mean arterial pressure at 60 mmHg for 30 min in sixteen healthy dogs weighing from 8 to 10.6 kg. Vasopressin was administered and then volume resuscitation was performed for the 6 dogs of V-C group, while vasopressin was administered at the end of volume resuscitation in the 5 dogs of C-V group. The control group (n=5) was administered 0.4 IU/kg of vasopressin after induction of shock without fluid resuscitation. In all groups, hemodynamic parameters were measured pre- and post-hemorrhage and for 60 min after fluid resuscitation. The dogs in V-C group had substantially increased systolic arterial pressure (SAP) for 60 min and improved pulmonary capillary wedge pressure (PCWP), cardiac output (CO), oxygen delivery, and oxygen consumption indexes compared with C-V and control groups. Diastolic pressure and systemic vascular resistance was significantly lower in the V-C group than those in the C-V and control groups (P<0.05). In the V-C group, there was effective and rapid restoration of the SAP, CO, PCWP, and oxygen delivery parameters after treatment. This study indicates that vasopressin administration before crystalloid resuscitation is a more efficient way of improving hemodynamic and oxygen delivery functions in hemorrhagic shock in dogs.     

Hemodynamic characteristics of vasopressin in dogs with severe hemorrhagic shock

The effect of vasopressin was compared with that of the established vasopressor epinephrine in experimentally induced hemorrhagic shock. After rapid crystalloid resuscitation in a ratio of three volumes of 0.9% saline to one volume of blood (3:1 crystalloid resuscitation), six dogs were given 0.4 IU/kg vasopressin and another six dogs were given 0.1 mg/kg epinephrine. Five dogs in the control group were given fluid resuscitation in the same manner as above without administration of any drugs. Administration of vasopressin increased diastolic arterial pressure (DAP) from 45.0 +/- 4.9 to 91.2 +/- 9.6 mmHg within 5 min, compared with epinephrine from 46 +/- 4.0 to 51.8 +/- 7.7, and control from 47.3 +/- 7.5 to 46.3 +/- 7.3. Systolic arterial pressure (SAP) did not increase significantly following vasopressin compared with epinephrine and control group. Results of DAP and systemic vascular resistance index (SVRI) suggested that vasopressin administration was vasoconstrictive after fluid resuscitation in decompensatory hemorrhagic shock in dogs, whereas epinephrine did not compared with control. In addition, epinephrine did not affect the cardiac index (CI) and SVRI, while a significant decrease in CI and increase in SVRI were observed in vasopressin group. The pressor effect of epinephrine in the vascular system was abrupt and only lasted a short period of time (within 5 min), while that of vasopressin was steady and lasted for more than 1 hr, especially regard to in DAP. When compared with epinephrine, vasopressin can be a more effective and safer choice in patients with severe hemorrhagic shock.     

Effects of lactated Ringer solution and prednisolone sodium succinate on dogs with induced hemorrhagic shock.

Hemorrhagic shock was induced in nonsplenectomized dogs by removing 41% of their blood volume over a 15-minute period. Hemodynamic and metabolic variables were determined prior to and for 3 hours after completion of hemorrhage. One group of 5 dogs was not treated. After the 30-minute sample was collected, a second group of 5 dogs was given lactated Ringer solution (LRS) at 88 ml/kg of body weight, IV. A third group of 5 dogs was given LRS (88 ml/kg, IV) and prednisolone sodium succinate (11 mg/kg, IV) 30 minutes after hemorrhage. The IV administration of LRS was completed within 15 minutes. The glucocorticoid was administered as an IV bolus after 500 ml of LRS had been given. The large volume and administration of LRS significantly (P = 0.05) improved many of the hemodynamic and metabolic effects of acute hemorrhage and hemorrhagic shock. At one time or another during the 2.5-hour observation period after the initiation of treatment, mean arterial pressure, cardiac index, systemic vascular resistance, heart rate, respiratory rate, lactate, glucose, and arterial and venous blood gas values were significantly (P = 0.05) improved, compared with baseline values. The addition of prednisolone sodium succinate to the treatment regimen improved the effectiveness of LRS alone only in some dogs at random sampling times. Significant trends were not observed except, possibly, the improvement of venous pH and A-V pH and PCO2 differences.     

Determination of optimal dose of arginine vasopressin in hemorrhagic shock in dogs

The hemodynamic effects of vasopressin of high/low doses on dogs were investigated using experimentally induced hemorrhagic shock model. Experimental groups were categorized according to administered doses of vasopressin (0.1, 0.4 and 1.6 IU/kg) and hemodynamic parameters were measured before and after the graded-dose administration of vasopressin. Administration of high- and middle-dose vasopressin (0.4 and 1.6 IU/kg) showed superior increase in blood pressure and systemic vascular resistance, compared with those of low-dose one (0.1 IU/kg). Results of systolic arterial pressure and mean arterial pressure in 1.6 IU/kg-administered group revealed lower efficacy than that in 0.4 IU/kg group in spite of administration of higher dose. This study demonstrates that 0.4 IU/kg of vasopressin can be used as the most effective dose for improving hemodynamic condition in the decompensatory phase of hemorrhagic shock in dogs.     

Hepatic effects of halothane, isoflurane or sevoflurane anaesthesia in dogs

The effects of halothane, isoflurane and sevoflurane anaesthesia on hepatic function and hepatocellular damage were investigated in dogs, comparing the activity of hepatic enzymes and bilirubin concentration in serum. An experimental study was designed. Twenty-one clinically normal mongrel dogs were divided into three groups and accordingly anaesthetized with halothane (n = 7), isoflurane (n = 7) and sevoflurane (n = 7). The dogs were 1-4 years old, and weighed between 13.5 and 27 kg (18.4 +/- 3.9). Xylazine HCI (1-2 mg/kg) i.m. was used as pre-anaesthetic medication. Anaesthesia was induced with propofol 2 mg/kg i.v. The trachea was intubated and anaesthesia maintained with halothane, isoflurane or sevoflurane in oxygen at concentrations of 1.35, 2 and 3%, respectively. Intermittent positive pressure ventilation (tidal volume, 15 ml/kg; respiration rate, 12-14/min) was started immediately after intubation and the anaesthesia lasted for 60 min. Venous blood samples were collected before pre-medication, 24 and 48 h, and 7 and 14 days after anaesthesia. Serum level of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and gamma-glutamyltransferase (GGT), lactate dehydrogenase (LDH GGT) activities and bilirubin concentration were measured. Serum AST, ALT and GGT activities increased after anaesthesia in all groups. In the halothane group, serum AST and ALT activities significantly increased all the time after anaesthesia compared with baseline activities. But in the isoflurane group AST and ALT activities increased only between 2 and 7 days, and in the sevoflurane group 7 days after anaesthesia. GGT activity was increased in the halothane group between 2 and 7 days, and in the isoflurane and sevoflurane groups 7 days after anaesthesia. All dogs recovered from anaesthesia without complications and none developed clinical signs of hepatic damage within 14 days. The results suggest that the use of halothane anaesthesia induces an elevation of serum activities of liver enzymes more frequently than isoflurane or sevoflurane from 2 to 14 days after anaesthesia in dogs. The effects of isoflurane or sevoflurane anaesthesia on the liver in dogs is safer than halothane anaesthesia in dogs.     

Evaluation of hemostatic analytes after use of hypertonic saline solution combined with colloids for resuscitation of dogs with hypovolemia.

The effects of hypertonic saline solution (HTSS) combined with colloids on hemostatic analytes were studied in 15 dogs. The analytes evaluated included platelet counts, one-stage prothrombin time, activated partial thromboplastin time, von Willebrand's factor antigen (vWf:Ag), and buccal mucosa bleeding times. The dogs were anesthetized, and jugular phlebotomy was used to induced hypovolemia (mean arterial blood pressure = 50 mm of Hg). Treatment dogs (n = 12) were resuscitated by infusion (6 ml/kg of body weight) of 1 of 3 solutions: HTSS combined with 6% dextran 70, 6% hetastarch, or 10% pentastarch. The control dogs (n = 3) were autotransfused. Hemostatic analytes were evaluated prior to induction of hypovolemia (baseline) and then after resuscitation (after 30 minutes of sustained hypovolemia) at 0.25, 0.5, 1, 6 and 24 hours. All treatment dogs responded rapidly and dramatically to resuscitation with hypertonic solutions. Clinically apparent hemostatic defects (epistaxis, petechiae, hematoma) were not observed in any dog. All coagulation variables evaluated, with the exception of vWf:Ag, remained within reference ranges over the 24-hour period. The vWf:Ag values were not statistically different than values from control dogs, and actual values were only slightly lower than reference ranges. Significant (P < or = 0.04) differences were detected for one-stage prothrombin time, but did not exceed reference ranges. The results of this study suggested that small volume HTSS/colloid solutions do not cause significant alterations in hemostatic analytes and should be considered for initial treatment of hypovolemic or hemorrhagic shock.     

Effects of naloxone in treating hemorrhagic shock in dogs with maintained baroreceptor responsiveness

The efficacy of treating hemorrhagic shock with naloxone in conjunction with fluids, compared with fluid therapy alone, was studied. Previously instrumented dogs were anesthetized with 0.04 mg of fentanyl/kg + 2.2 mg of droperidol/kg and pentobarbital sodium (to effect). Blood was withdrawn from each animal to achieve and maintain a mean arterial blood pressure of 40 to 50 mm of Hg for the first 2 hours of the experiment (t = 0 to 120 minutes). At t = 120 minutes, IV fluid administration was begun (all dogs) and continued for 1 hour (lactated Ringer's solution at a dosage of 70 ml/kg/hr). Hypothermia was corrected. Control dogs were given no other treatment. Dogs in the naloxone plus fluids group were given an IV bolus of naloxone (1 mg/kg) at t = 120 minutes and 1 mg of naloxone/kg/hr in the fluids from t = 120 to t = 180 minutes. Treatment (either naloxone plus fluids or fluids alone) was stopped at t = 180 minutes, and measuring of response was continued for an additional hour (posttherapeutic period). Significant differences were not seen in mean arterial pressures, left ventricular peak systolic pressures, dP/dt max, time constant T (a measure of left ventricular elasticity), and mean pulmonary arterial pressures between the dogs given naloxone and fluid therapy and those given fluid therapy alone. All dogs in both groups survived the procedure.     

Lack of efficacy of low-dose spironolactone as adjunct treatment to conventional congestive heart failure treatment in dogs

Aldosterone plays an important role in the pathophysiology of heart failure. Aldosterone receptor blockade has been shown to reduce morbidity and mortality in human patients with advanced congestive left ventricular heart failure. This study was designed to assess the efficacy and tolerance of long-term low-dose spironolactone when added to conventional heart failure treatment in dogs with advanced heart failure. Eighteen client-owned dogs with advanced congestive heart failure due to either degenerative valve disease (n=11) or dilated cardiomyopathy (n=7) were included in this prospective, placebo-controlled, double-blinded, randomized clinical study. After initial stabilization including furosemide, angiotensin-converting enzyme inhibitors, pimobendan and digoxin, spironolactone at a median dose of 0.52 mg/kg (range 0.49-0.8 mg/kg) once daily (n=9) or placebo (n=9) was added to the treatment, and the dogs were reassessed 3 and 6 months later. Clinical scoring, echocardiography, electrocardiogram, systolic blood pressure measurement, thoracic radiography, sodium, potassium, urea, creatinine, alanine aminotransferase, aldosterone and aminoterminal atrial natriuretic propeptide were assessed at baseline, 3 and 6 months. Survival times were not significantly different between the two treatment groups. Spironolactone was well tolerated when combined with conventional heart failure treatment.     

Cardiopulmonary effects of medetomidine or midazolam in combination with ketamine or tiletamine/zolazepam for the immobilisation of captive cheetahs (Acinonyx jubatus)

Captive cheetah (Acinonyx jubatus) scheduled for either general health examination or dental surgery were immobilised with combinations of medetomidine-ketamine (K/DET, n = 19), midazolam-ketamine (K/MID, n = 4) or medetomidine-tiletamine-zolazepam (Z/DET, n = 5). Induction time and arterial blood pressure was not statistically significantly (P > 0.05) different between treatment groups. Transient seizures were observed in the K/DET treated animals during induction. Hypertension was present in all groups during anaesthesia with mean (+/- SD) systolic pressure of 30.7 +/- 5.0 kPa for the K/DET group, 27.7 +/- 2.7 kPa for the K/MID group, and 33.1 +/- 4.6 kPa for the Z/DET group. Heart rate was statistically significantly (P < 0.05) lower in the K/DET group (69 +/- 13.2 beats/min) compared to the K/MID group (97 +/- 22.6 beats/min), and ventilation rate was statistically significantly (P < 0.05) lower in the K/MID group (15 +/- 0.0 breaths/min) compared with the K/DET group (21 +/- 4.6). A metabolic acidosis and hypoxia were observed during anaesthesia when breathing air. Oxygen (O2) administration resulted in a statistically significant (P < 0.05) increase in the arterial partial pressure of carbon dioxide (hypercapnoea), arterial partial pressure of O2, and % oxyhaemoglobin saturation.     

Hypertonic saline/dextran resuscitation of dogs with experimentally induced gastric dilatation-volvulus shock.

We investigated small-volume (5 ml/kg) 7% NaCl in 6% dextran 70 (HS/D70) as an alternative to large-volume (60 ml/kg) 0.9% NaCl for treatment of experimentally induced canine gastric dilatation-volvulus (GDV) shock. The stomach was surgically displaced and then distended with an intragastric balloon in 11 dogs anesthetized with pentobarbital. All dogs were subjected to GDV for 180 minutes before partial decompression and resuscitation. Hemodynamic values, blood gas values, and plasma volume were measured during control, shock, and resuscitation periods. Resuscitation started with 1 group (n = 6) receiving 5 ml of HS/D70/kg, iv, over 5 minutes, and the other group (n = 5) receiving 60 ml of 0.9% NaCl/kg, IV, over 60 minutes. Both groups received a surgical maintenance dosage (20 ml/kg/h) of 0.9% NaCl after initial resuscitation. Resuscitative effects of small-volume HS/D70 were similar to large-volume 0.9% NaCl during the first hour of treatment; however, cardiac output was significantly higher in the HS/D70 group for the last 2 hours of resuscitation. Changes in heart rate, left ventricular pressure change, and systemic vascular resistance appeared to be responsible for improved perfusion. Mixed venous oxygen partial pressure data supported improved perfusion in the HS/D70 group. Packed cell volume remained higher in the HS/D70 group, indicating less hemodilution and improved oxygen delivery. Resuscitation of this GDV-induced shock model was better sustained with small-volume HS/D70, compared with conventional large-volume 0.9% NaCl.     

Treatment of Dogs in Hemorrhagic Shock by Intraosseous Infusion of Hypertonic Saline and Dextran

Under isoflurane anesthesia, 50% of the calculated blood volume was removed from 11 dogs. After 30 minutes, five dogs were treated with hypertonic saline and dextran (HSD) (5 mL/kg) followed by isotonic saline solution (2 mL/kg) intraosseously. Six dogs (controls) received isotonic saline (7 mL/kg) intraosseously. All treatments were administered through the medullary cavity of the tibia over a 30-minute period. Cardiac output, mean arterial pressure, central venous pressure, packed cell volume, total protein, and blood gases were monitored for 4 hours. Cardiac output, mean arterial pressure, and circulating volume (indicated by packed cell volume and total protein) were significantly improved after administration of HSD. We conclude that intraosseous infusion of HSD is efficacious in treating hemorrhagic shock and believe the technique may prove to be useful in clinical situations when intravenous lines cannot be established rapidly.     

Dose effect and benefits of glycopyrrolate in the treatment of bradycardia in anesthetized dogs.

This study evaluated the effectiveness of glycopyrrolate (0.005 or 0.01 mg/kg body weight (BW)) in anesthetized dogs (n = 40) for reversal of bradycardia (< 65 beats/min). Following random intravenous (i.v.) treatment, heart rate was determined at 5 min and, if it was < or = 70 beats/min, the lower dose was repeated. A 2-way analysis of variance considered dose and animal size (< or = 10 kg, > 10 kg) effects (P < 0.05). Glycopyrrolate produced a significant increase in heart rate and infrequent tachycardia (< or = 150 beats/min), which was not dose-related. The size of the dog produced a significant effect on baseline heart rate (higher in small), rate following the first dose (lower in small), and requirement for retreatment (47% in small, 13% in large). In a separate group of anesthetized dogs (n = 20), the blood pressure effect of glycopyrrolate (0.01 mg/kg BW, i.v.) treatment of bradycardia (65-85 beats/min, weight-adjusted) was studied. A significant increase in systolic, diastolic, and mean blood pressure was produced. In conclusion, the effective dose of glycopyrrolate treatment is size-related and produces a beneficial effect on blood pressure.     

High volume continuous venovenous haemofiltration (HV-CVVH) in an equine endotoxaemic shock model

Equine acute abdominal disease is often associated with shock. Important aspects in the onset of this complication include hypovolaemia, the translocation of endotoxins from the gut and the subsequent activation of the cytokine network. The clinical efficacy of high volume continuous venovenous haemofiltration (HV-CVVH) and the clearance of cytokines were therefore investigated in an equine endotoxaemic model. Ten male Shetland ponies received a slow infusion of LPS (2 microg/kg bwt) under general anaesthesia. The treatment group (n = 5) received HV-CVVH (2 ml/kg bwt/min) using a 75 kD polymethylmethacrylate (PMMA filter). Haemodynamic, blood variable and cytokine (TNF, IL-1 and IL-6) measurements were performed every 30 min for a 6 h period. The ponies showed a typical reaction in mean pulmonary arterial pressure, blood chemical and haematological markers after LPS challenge. No significant differences were found between the treatment group and the control group. Only a slight increase in cardiac index and no marked decrease in mean arterial pressure were seen. A clear cytokine response was found in all ponies, though substantially different in magnitude between individuals. The clearance of cytokines from the blood increased in time, but did not lead to significant decrease in serum levels. In this study, HV-CVVH with a PMMA filter did not prove to have a significant beneficial effect on the course of experimental endotoxaemia in horses. However, in a more severe model, better efficacy might be obtained. Testing additional filters might lead to a more suitable therapy for horses.     

Association of systemic hypertension with renal injury in dogs with induced renal failure

Systemic hypertension is hypothesized to cause renal injury to dogs. This study was performed on dogs with surgically induced renal failure to determine whether hypertension was associated with altered renal function or morphology. Mean arterial pressure (MAP), heart rate (HR), systolic arterial pressure (SAP), and diastolic arterial pressure (DAP) were measured before and after surgery. Glomerular filtration rate (GFR) and urine protein:creatinine ratios (UPC) were measured at 1, 12, 24, 36, and 56-69 weeks after surgery, and renal histology was evaluated terminally. The mean of weekly MAP, SAP, and DAP measurements for each dog over the 1st 26 weeks was used to rank dogs on the basis of MAP, SAP, or DAP values. A statistically significant association was found between systemic arterial pressure ranking and ranked measures of adverse renal responses. When dogs were divided into higher pressure and lower pressure groups on the basis of SAP, group 1 (higher pressure, n = 9) compared with group 2 (lower pressure, n = 10) had significantly lower GFR values at 36 and 56-69 weeks; higher UPC values at 12 and 56-69 weeks; and higher kidney lesion scores for mesangial matrix, tubule damage, and fibrosis. When dogs were divided on MAP and DAP values, group 1 compared with group 2 had significantly lower GFR values at 12, 24, 36, and 56-69 weeks; higher UPC values at 12 and 56-69 weeks; and higher kidney lesion scores for mesangial matrix, tubule damage, fibrosis, and cell infiltrate. These results demonstrate an association between increased systemic arterial pressure and renal injury. Results from this study might apply to dogs with some types of naturally occurring renal failure.     

Cardiovascular effects of tramadol in dogs anesthetized with sevoflurane

Cardiovascular effects of tramadol were evaluated in dogs anesthetized with sevoflurane. Six beagle dogs were anesthetized twice at 7 days interval. The minimum alveolar concentration (MAC) of sevoflurane was earlier determined in each dog. The dogs were then anesthetized with sevoflurane at 1.3 times of predetermined individual MAC and cardiovascular parameters were evaluated before (baseline) and after an intravenous injection of tramadol (4 mg/kg). The administration of tramadol produced a transient and mild increase in arterial blood pressure (ABP) (P=0.004) with prolonged increase in systemic vascular resistance (SVR) (P<0.0001). Compared with baseline value, mean ABP increased significantly at 5 min (119% of baseline value, P=0.003), 10 min (113%, P=0.027), and 15 min (111%, P=0.022). SVR also increased significantly at 5 min (128%, P<0.0001), 10 min (121%, P=0.026), 30 min (114%, P=0.025), 45 min (113%, P=0.025) and 60 min (112%, P=0.048). Plasma concentrations of tramadol were weakly correlated with the percentage changes in mean ABP (r=0.642, P<0.0001) and SVR (r=0.646, P<0.0001). There was no significant change in heart rate, cardiac output, cardiac index, stroke volume, pulmonary arterial pressure, right atrial pressure and pulmonary capillary wedge pressure. In conclusion, the administration of tramadol produces a prolonged peripheral vascular constriction in dogs anesthetized with sevoflurane, which is accompanied with a transient and mild increase in arterial blood pressure. It also indicated that the degree of vasoconstriction might depend on the plasma concentration of tramadol.     

The effect of differing rates and injection sites on the amount of protamine delivered before detection of hemodynamic alterations in dogs

OBJECTIVES: To determine the effect of the route and rate of protamine administration on the amount of protamine that could be delivered before a hemodynamic reaction occurred in dogs. STUDY DESIGN: Prospective randomized experimental study. ANIMALS: Twenty adult mixed-breed dogs weighing 25.1+/-2.5 kg. METHODS: Before vascular surgery, the dogs were heparinized to reach an activated clotting time (ACT) of 300 seconds. After completion of the vascular surgery, protamine was administered intravenously until a hemodynamic reaction was recorded. The 4 groups of dogs were given protamine at 5 mg/min (slow) or 10 mg/min (fast) via the cephalic or the jugular veins. Systemic and pulmonary arterial pressures, central venous pressure (CVP), and pulmonary arterial occlusion pressure (PAOP) were recorded before and after protamine administration. The dose of protamine was recorded when a reaction occurred, which was defined as mean arterial pressure (MAP) <60 mm Hg or mean pulmonary arterial pressure (MPAP) >20 mm Hg or more than double the baseline value. RESULTS: Significant decreases in systolic arterial pressure (SAP), MAP, and diastolic arterial pressure (DAP) and significant increases in systolic (SPAP), mean (MPAP), and diastolic (DPAP) pulmonary arterial pressures were recorded after protamine administration. The cephalic slow group had significantly fewer protamine reactions than other groups (chi-square = 8.57, P = .03, df = 3). Significantly more protamine could be delivered from the cephalic vein (52.5+/-14.5 mg) compared with the jugular vein (37.6+/-16 mg) before a reaction occurred (P = .048). CONCLUSION: The rate of administration did not have an effect on the amount of protamine delivered. Adverse reactions were minimized when protamine was administered via the cephalic vein at a slow rate. CLINICAL RELEVANCE: We would recommend delivering protamine after cardiopulmonary bypass or vascular surgery through a peripheral venous route.     

Vasopressin therapy in dogs with dopamine-resistant hypotension and vasodilatory shock

Objective: To describe the therapeutic use of vasopressin in dogs with dopamine‐resistant hypotension and vasodilatory shock. Series summary: We report the effects of intravenous vasopressin therapy on mean arterial blood pressure and central venous pressure (CVP) in 5 dogs with dopamine‐resistant hypotension from vasodilatory shock. All subjects had documented hypotension and vasodilation, despite adequate intravascular volume and catecholamine therapy. There was an increase in mean arterial pressure following vasopressin administration. No cardiac arrhythmias were noted, nor were there clinically significant changes in CVP. New information provided: Mean arterial blood pressure increased following vasopressin therapy in all of the dogs. Vasopressin may prove useful in the treatment of vasodilatory shock, however further research is warranted.     

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.     

Cardiovascular effects of doxacurium chloride in isoflurane-anaesthetised dogs

The cardiovascular effects of doxacurium were studied in 6 isoflurane-anaesthetised dogs. Each dog was anaesthetised twice, receiving doxacurium (0.008 mg/kg bwt) or placebo iv. Dogs were ventilated to normocapnia. Heart rate, cardiac index, systolic, diastolic, and mean arterial blood pressures, stroke volume, pulmonary vascular resistance, pulmonary artery wedge pressure, systemic vascular resistance, and pulmonary arterial pressure were determined. Neuromuscular blockade was assessed using the train-of-four technique. After recording baseline values, dogs randomly received either doxacurium or placebo iv, and data were recorded at 5, 10, 15, 30, 45, 60, 75, 90, 105 and 120 min. At 120 min, dogs treated with doxacurium received edrophonìum (0.5 mg/kg bwt iv) to antagonise neuromuscular blockade; dogs treated with placebos received saline iv. No statistically significant differences were detected after doxacurium compared to placebo. In both the doxacurium and placebo groups, significant increases in systolic arterial blood pressure, cardiac index, and stroke volume and a significant decrease in systemic vascular resistance occurred with time. Doxacurium depressed twitch tension 100% in all dogs (time to maximal twitch depression, 11 ± 7 min). First twitch tension was less than 10% of baseline values in all dogs at the time (120 min) of edrophonium administration. Additional edrophonium (1.0 ± 0.4 mg/kg iv) was required to obtain a fourth twitch to first twitch ratio of greater than 0.70. In conclusion, doxacurium is a long-acting neuromuscular blocking agent with no significant cardiovascular effects in isoflurane-anesthetised dogs. In dogs, doxacurium is indicated primarily for long surgical procedures requiring neuromuscular blockade and cardiovascular stability.     

Cardiovascular effects of topical ophthalmic 10% phenylephrine in dogs

Objective To evaluate the effect of topical ophthalmic 10% phenylephrine on systolic arterial pressure (SAP), diastolic arterial pressure (DAP), mean arterial pressure (MAP), pulse rate (PR) and electrocardiogram (ECG) in dogs. Animals studied Nine clinically normal dogs. Procedure Arterial catheters were placed in the dorsal pedal artery of awake dogs and ECG leads were attached. After a 15‐min acclimatization period, baseline PR, SAP, DAP and MAP were recorded every 5 min for 20 min. Two treatment groups (eight dogs each) were studied. Group I: one drop of phenylephrine was placed in each eye once. Group II: one drop of phenylephrine was placed in each eye three times at 5‐min intervals. Following treatment, PR, SAP, DAP and MAP were recorded every 5 min for 90 min. The mixed procedure of the SAS system was used to perform a repeated measures analysis of variance to test for linear and quadratic trends across time. Results Group I: There was a significant quadratic decrease in PR across time (P = 0.0051). Systolic arterial pressure increased linearly with time (P = 0.0002), MAP increased linearly with time (P = 0.0131), and DAP increased linearly with time (P = 0.0001). Group II: There was a significant quadratic decrease in PR across time (P = 0.0023). There was a significant quadratic increase in SAP (P = 0.0324), MAP (P = 0.0103) and DAP (P = 0.0131) across time. Conclusions Topical ophthalmic application of 10% phenylephrine in normal dogs results in elevation of arterial blood pressure and reflex bradycardia.