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.     

The use of vasopressin for treating vasodilatory shock and cardiopulmonary arrest

Objective – To discuss 3 potential mechanisms for loss of peripheral vasomotor tone during vasodilatory shock; review vasopressin physiology; review the available animal experimental and human clinical studies of vasopressin in vasodilatory shock and cardiopulmonary arrest; and make recommendations based on review of the data for the use of vasopressin in vasodilatory shock and cardiopulmonary arrest. Data Sources – Human clinical studies, veterinary experimental studies, forum proceedings, book chapters, and American Heart Association guidelines. Human and Veterinary Data Synthesis – Septic shock is the most common form of vasodilatory shock. The exogenous administration of vasopressin in animal models of fluid‐resuscitated septic and hemorrhagic shock significantly increases mean arterial pressure and improves survival. The effect of vasopressin on return to spontaneous circulation, initial cardiac rhythm, and survival compared with epinephrine is mixed. Improved survival in human patients with ventricular fibrillation, pulseless ventricular tachycardia, and nonspecific cardiopulmonary arrest has been observed in 4 small studies of vasopressin versus epinephrine. Three large studies, though, did not find a significant difference between vasopressin and epinephrine in patients with cardiopulmonary arrest regardless of initial cardiac rhythm. No veterinary clinical trials have been performed using vasopressin in cardiopulmonary arrest. Conclusion – Vasopressin (0.01–0.04 U/min, IV) should be considered in small animal veterinary patients with vasodilatory shock that is unresponsive to fluid resuscitation and catecholamine (dobutamine, dopamine, and norepinephrine) administration. Vasopressin (0.2–0.8 U/kg, IV once) administration during cardiopulmonary resuscitation in small animal veterinary patients with pulseless electrical activity or ventricular asystole may be beneficial for myocardial and cerebral blood flow.     

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.     

Effects of acepromazine on the cardiovascular actions of dopamine in anesthetized dogs

OBJECTIVE: To evaluate the effects of acepromazine maleate on the cardiovascular changes induced by dopamine in isoflurane-anesthetized dogs. STUDY DESIGN: Prospective, randomized cross-over experimental design. ANIMALS: Six healthy adult spayed female dogs weighing 16.4 +/- 3.5 kg (mean +/- SD). METHODS: Each dog received two treatments, at least 1 week apart. Acepromazine (0.03 mg kg(-1), IV) was administered 15 minutes before anesthesia was induced with propofol (7 mg kg(-1), IV) and maintained with isoflurane (1.8% end-tidal). Acepromazine was not administered in the control treatment. Baseline cardiopulmonary parameters were measured 90 minutes after induction. Thereafter, dopamine was administered intravenously at 5, 10, and 15 microg kg(-1) minute(-1), with each infusion rate lasting 30 minutes. Cardiopulmonary data were obtained at the end of each infusion rate. RESULTS: Dopamine induced dose-related increases in cardiac index (CI), stroke index, arterial blood pressure, mean pulmonary arterial pressure, oxygen delivery index (DO(2)I) and oxygen consumption index. In the control treatment, systemic vascular resistance index (SVRI) decreased during administration of 5 and 10 microg kg(-1) minute(-1) of dopamine and returned to baseline with the highest dose (15 microg kg (-1) minute(-1)). After acepromazine treatment, SVRI decreased from baseline during dopamine administration, regardless of the infusion rate, and this resulted in a smaller increase in blood pressure at 15 microg kg (-1) minute(-1). During dopamine infusion hemoglobin concentrations were lower following acepromazine and this contributed to significantly lower arterial O(2) content. CONCLUSIONS: Acepromazine prevented the return in SVRI to baseline and reduced the magnitude of the increase in arterial pressure induced by higher doses of dopamine. However, reduced SRVI associated with lower doses of dopamine and the ability of dopamine to increase CI and DO(2)I were not modified by acepromazine premedication. CLINICAL RELEVANCE: Previous acepromazine administration reduces the efficacy of dopamine as a vasopressor agent in isoflurane anesthetized dogs. Other beneficial effects of dopamine such as increased CO are not modified by acepromazine.     

Cardiopulmonary resuscitation with vasopressin in a dog

That endogenous vasopressin levels in successfully resuscitated human patients were significantly higher than in patients who died pointed to the possible benefit of administering vasopressin during cardiopulmonary resuscitation (CPR). Several CPR studies in pigs showed that vasopressin improved blood flow to vital organs, cerebral oxygen delivery, resuscitability and neurological outcome when compared with epinephrine. In a small clinical study, vasopressin significantly improved short-term survival when compared with epinephrine indicating its potential as an alternative pressor to epinephrine during CPR in human beings. As there was little clinical data available at that time, its recommended use was limited to adult human beings with shock-refractory ventricular fibrillation. In this report, we present the case of a dog in which the successful management of intraoperative asystolic cardiac arrest involved vasopressin. Unexpected cardiac arrest occurred during anaesthesia for the surgical removal of multiple mammary adenocarcinomata in a 11-year-old Yorkshire terrier. Despite an ASA physical status assignation of III, the dog was successfully resuscitated with external chest compressions, intermittent positive pressure ventilation and vasopressin (2 doses of 0.8 IU kg(-1)) and was discharged 3 days later without signs of neurological injury. We believe vasopressin contributed to restoring spontaneous circulation. It may prove increasingly useful in perioperative resuscitation in dogs.     

Effects of isovolemic resuscitation with hemoglobin-based oxygen carrier Hemoglobin glutamer-200 (bovine) on systemic and mesenteric perfusion and oxygenation in a canine model of hemorrhagic shock: a comparison with 6% hetastarch solution and shed blood

OBJECTIVE: To study Hemoglobin glutamer-200 bovine (Hb-200), 6% hetastarch (HES) and shed whole blood (WB) resuscitation in canine hemorrhagic shock. STUDY DESIGN: Prospective laboratory investigation. Animals Twelve adult dogs [29 +/- 1 kg (mean +/- SD)]. METHODS: Anesthetized dogs were instrumented for recording systemic and mesenteric hemodynamic parameters and withdrawal of arterial, mixed and mesenteric venous blood, in which hematological, oxygenation, blood gas and acid-bases variables were determined. Recordings were made before [baseline (BL)], after 1 hour of hypovolemia and immediately and 3 hours post-resuscitation with 30 mL kg(-1) of either Hb-200, HES, or WB. RESULTS: Blood withdrawal (average 34 +/- 2 mL kg(-1)) caused significant hemodynamic changes, metabolic acidosis and hyperlactatemia characteristic for hemorrhagic shock. Only WB transfusion restored all variables. Hemoglobin glutamer-200 bovine infusion returned most hemodynamic parameters including cardiac output and mesenteric arterial blood flow to BL but increased mean arterial pressure above BL (p < 0.05). However, Hb-200 failed to restore total Hb and arterial oxygen content (CaO2), leaving systemic (DO2I) and mesenteric O2 delivery (DO2Im) below BL (p < 0.05). Nevertheless, acid-base variables recovered completely after Hb-200 resuscitation, and met-hemoglobin (Met-Hb) levels increased (p < 0.05). Hetastarch resuscitation returned hemodynamic variables to or above BL but further decreased total Hb and CaO2, preventing recovery of sDO2I and mDO2I (p < 0.05). Thus, systemic and mesenteric O2 extraction stayed above BL (p < 0.05) while acid-base variables recovered to BL, although slower than in Hb-200 and WB groups (p < 0.05). CONCLUSIONS AND CLINICAL RELEVANCE: Resuscitation with Hb-200 seemed to resolve metabolic acidosis and lactatemia more rapidly than HES, but not WB; yet it is not superior to HES in improving DO2I and DO2Im. The hyperoncotic property of solutions like Hb-200 that results in rapid volume expansion with more homogenous microvascular perfusion and the ability to facilitate diffusive O2 transfer accelerating metabolic recovery may be the key mechanisms underlying their beneficial effects as resuscitants.     

Clinical evaluation of the Surgivet V60046, a non invasive blood pressure monitor in anaesthetized dogs

OBJECTIVE: To compare the performance of the Surgivet Non-Invasive Blood Pressure (NIBP) monitor V60046 with an invasive blood pressure (IBP) technique in anaesthetized dogs. STUDY DESIGN: A prospective study. ANIMALS: Thirty-four dogs, anaesthetized for a variety of procedures. METHODS: Various anaesthetic protocols were used. Invasive blood pressure measurement was made using a catheter in the femoral or the pedal artery. A cuff was placed on the contralateral limb to allow non invasive measurements. Recordings of arterial blood pressures (ABPs) were taken at simultaneous times for a range of pressures. For analysis, three pressure levels were determined: high [systolic blood pressure (SAP) > 121 mmHg], normal (91 mmHg < SAP < 120 mmHg) and low (SAP < 90 mmHg). Comparisons between invasive and non invasive measurements were made using Bland-Altmann analysis. RESULTS: The NIBP monitor consistently underestimated blood pressure at all levels. The lowest biases and greatest precision were obtained at low and normal pressure levels for SAP and mean arterial pressure (MAP). At low blood pressure levels, the biases +/- 95% confidence interval (CI) were 1.9 +/- 2.96 mmHg (SAP), 8.3 +/- 2.41 mmHg diastolic arterial pressure (DAP) and 3.5 +/- 2.09 mmHg (MAP). At normal blood pressure levels, biases and CI were: 1.2 +/- 2.13 mmHg (SAP), 5.2 +/- 2.32 mmHg (DAP) and 2.1 +/- 1.54 mmHg (MAP). At high blood pressure levels, the biases and CI were 22.7 +/- 5.85 mmHg (SAP), 5.5 +/- 3.13 mmHg (DAP) and 9.4 +/- 3.52 mmHg (MAP). In 90.6% of cases of hypotension (MAP < 70 mmHg), the low blood pressure was correctly diagnosed by the Surgivet. CONCLUSIONS: Measurement of blood pressure with the indirect monitor allowed detection of hypotension using either SAP or MAP. The most accurate readings were determined for MAP at hypotensive and normal levels. The monitor lacked accuracy at high pressures. CLINICAL RELEVANCE: When severe challenges to the cardiovascular system are anticipated, an invasive method of recording ABP is preferable. For routine usage, the Surgivet monitor provided a reliable and safe method of NIBP monitoring in dogs, thereby contributing to the safety of anaesthesia by providing accurate information about the circulation.     

Effects of high-volume, rapid-fluid therapy on cardiovascular function and hematological values during isoflurane-induced hypotension in healthy dogs

The objective of this study was to determine the effects of the administration of a high volume of isotonic crystalloid at a rapid rate on cardiovascular function in normovolemic, isoflurane-anesthetized dogs during induced hypotension.Using a prospective study, 6 adult dogs were induced to general anesthesia and cardiovascular and hematological values were measured while the dogs were maintained at 3 hemodynamic states: first during light anesthesia with 1.3% end-tidal isoflurane (ETI); then during a hypotensive state induced by deep anesthesia with 3% ETI for 45 min while administered 1 mL/kg body weight (BW) per minute of isotonic fluids; and then decreased to 1.6% ETI while receiving 1 mL/kg BW per minute of fluids for 15 min. End-tidal isoflurane (ETI) at 3.0 ± 0.2% decreased arterial blood pressure (ABP), cardiac index (CI), and stroke volume index (SVI), and increased stroke volume variation (SVV) and central venous pressure (CVP). Fluid administration during 3% ETI decreased only SVV and systemic vascular resistance index (SVRI), while CVP increased progressively. Decreasing ETI to 1.6 ± 0.1% returned ABP and SVI to baseline (ETI 1.3 ± 0.1%), while CI and heart rate increased and SVV decreased. There was significant progressive clinical hemodilution of hemoglobin (Hb), packed cell volume (PCV), total protein (TP), colloid osmotic pressure (COP), arterial oxygen content (CaO₂), and central-venous oxygen content (CcvO₂).High-volume, rapid-rate administration of an isotonic crystalloid was ineffective in counteracting isoflurane-induced hypotension in normovolemic dogs at a deep plane of anesthesia. Cardiovascular function improved only when anesthetic depth was reduced. Excessive hemodilution and its adverse consequences should be considered when a high volume of crystalloid is administered at a rapid rate.     

Inadequacy of low-volume resuscitation with hemoglobin-based oxygen carrier hemoglobin glutamer-200 (bovine) in canine hypovolemia

Stroma-free hemoglobin-based oxygen carriers (HBOC) have been developed to overcome problems associated with transfusion of allogeneic blood. We have studied the efficacy of the first licensed veterinary blood substitute, hemoglobin glutamer-200 bovine (Oxyglobin; Biopure, Cambridge, MA, USA, Hb-200), in a canine model of acute hypovolemia and examined whether clinically commonly used criteria are adequate to guide fluid resuscitation with this product. Twelve anesthetized dogs were instrumented for measurements of physiological variables including hemodynamic, oxygenation, and blood gas and acid-base parameters. Dogs were bled to a mean arterial pressure (MAP) of 50 mmHg for 1 h followed by resuscitation with either shed blood (controls) or Hb-200 until heart rate (HR), MAP and central venous pressure (CVP) returned to baseline. Recordings were repeated immediately and 3 h after termination of fluid resuscitation. Hemorrhage (average 32 mL/kg) caused significant decreases in total hemoglobin (Hb), mean pulmonary arterial pressure (PAP), cardiac output (CO) and oxygen delivery (DO2I), increases in HR and systemic vascular resistance (SVRI), and lactic acidosis. In controls, only re-transfusion of all shed blood returned HR, MAP and CVP to prehemorrhage values, whereas in other dogs this endpoint was reached with infusion of 10 mL/kg Hb-200. Unlike blood transfusion, Hb-200 infusion failed to return CI and DO2I to baseline and to increase arterial oxygen content (CaO2) and total Hb; SVRI further increased. Thus, commonly used criteria (HR, MAP, CVP) to guide transfusion therapy in patients posthemorrhage prove insufficient when HBOCs with pronounced vasoconstrictive action are used and lead to inadequate volume repletion.     

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.     

Effect of the proteinase inhibitor aprotinin in the management of hemorrhagic shock in the dog.

Aprotinin, a proteinase inhibitor, was evaluated as a pharmacologic aid in dogs subjected to lethal hemorrhagic shock. Survival time, hemodynamic changes, and plasma enzyme analysis were measured as criteria for drug effects. Mixed-breed dogs (n = 14) were divided into 2 groups of 7 each: nontreated dogs in shock (group 1) and aprotinin-treated dogs in shock (group 2). One of 7 dogs in group 1 and 2 of 7 dogs in group 2 survived. Survival time, for the remaining dogs in group 1 (190 min, n = 6) and group 2 (188 min, n = 5) were not significantly different. There was no significant difference in mean arterial pressure, mean pulmonary arterial pressure, cardiac output, or left ventricle systolic pressure associated with aprotinin treatment at any time after hemorrhagic shock. There was no significant difference in plasma lactic acid, aspartate aminotransferase, alanine aminotransferase, creatine phosphokinase, alpha-amylase, and beta-glucuronidase associated with treatment at any time; however, there were significant (P less than 0.05) increases with time. The gastrointestinal tract was the site of most obvious lesions found at necropsy. Lesions varied considerably in extent and severity without apparent correlation to the treatment regimen. These experiments did not show beneficial effects of aprotinin in dogs subjected to hemorrhagic shock, but neither did they completely rule out some valuable actions that may have been obscured by the type of model used.     

Cardiovascular effects of desflurane following acute hemorrhage in dogs

Objective: To determine the cardiovascular effects of desflurane in dogs following acute hemorrhage. Design: Experimental study. Animals: Eight mix breed dogs. Interventions: Hemorrhage was induced by withdrawal of blood until mean arterial pressure (MAP) dropped to 60 mmHg in conscious dogs. Blood pressure was maintained at 60 mmHg for 1 hour by further removal or replacement of blood. Desflurane was delivered by facemask until endotracheal intubation could be performed and a desflurane expiratory end‐tidal concentration of 10.5 V% was maintained. Measurements and main results: Systolic, diastolic, and mean arterial blood pressure (SAP, DAP and MAP), central venous pressure (CVP), cardiac output (CO), stroke volume (SV), cardiac index (CI), systemic vascular resistance (SVR), heart rate (HR), respiratory rate (RR), partial pressure of carbon dioxide in arterial blood (PaCO₂), and arterial pH were recorded before and 60 minutes after hemorrhage, and 5, 15, 30, 45 and 60 minutes after intubation. Sixty minutes after hemorrhage, SAP, DAP, MAP, CVP, CO, CI, SV, PaCO₂, and arterial pH decreased, and HR and RR increased when compared with baselines values. Immediately after intubation, MAP and arterial pH decreased, and PaCO₂ increased. Fifteen minutes after intubation SAP, DAP, MAP, arterial pH, and SVR decreased. At 30 and 45 minutes, MAP and DAP remained decreased and PaCO₂ increased, compared with values measured after hemorrhage. Arterial pH increased after 30 minutes of desflurane administration compared with values measured 5 minutes after intubation. Conclusions: Desflurane induced significant changes in blood pressure and arterial pH when administered to dogs following acute hemorrhage.     

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.     

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.     

Variance of indirect blood pressure measurements and prevalence of hypertension in clinically normal dogs

In a series of 3 studies, indirect blood pressure measurements were obtained to define normal variance, identify hypertension, and estimate the prevalence of hypertension in apparently healthy dogs. In part 1, we measured values in 5 clinically normal dogs twice weekly for 5 weeks in a home setting. Mean +/- SD systolic arterial pressure (SAP) and diastolic arterial pressure (DAP) was 150 +/- 16 and 86 +/- 13 mm of Hg, respectively. The DAP significantly (P less than 0.01) decreased with repeated measurements over the 5-week period. In part 2, we assessed the variation between blood pressures measured in a clinic vs those measured in the home. Within a 2-week period, measurements were obtained from 10 clinically normal dogs in a private veterinary clinic and again in their home. Significant differences were not observed between clinic and home measurements of SAP and DAP; however, heart rate was significantly (P less than 0.05) higher in the clinic. In part 3, SD about the SAP and DAP mean values were determined in 102 clinically normal dogs. Canine hypertensive status was determined, using statistical methods and data from 102 clinically normal dogs. Values of SAP greater than 202 mm of Hg and DAP greater than 116 mm of Hg were determined to be 2 SD beyond the mean and, therefore, were interpreted to be hypertensive. Approximately 10% of the 102 apparently healthy dogs measured in this study were considered hypertensive on the basis of these criteria. In addition, a border zone of suspected hypertension was estimated, using the mean + 1.282 SD. The SAP border zone was between 183 and 202 mm of Hg, whereas the DAP border zone was between 102 and 113 mm of Hg. Of the 102 dogs, 12 had values within these zones of suspected hypertension.     

The cardiopulmonary effects of a peripheral alpha‐2‐adrenoceptor antagonist,MK‐467, in dogs sedated with a combination of medetomidine and butorphanol

ObjectiveTo compare the cardiopulmonary effects of intravenous (IV) and intramuscular (IM) medetomidine and butorphanol with or without MK-467.Study designProspective, randomized experimental cross-over.AnimalsEight purpose–bred beagles (two females, six males), 3–4 years old and weighing 14.5 ±1.6 kg (mean ± SD).MethodsAll dogs received four different treatments as follows: medetomidine 20 μg kg^?1 and butorphanol tartrate 0.1 mg kg^?1 IV and IM (MB), and MB combined with MK-467,500 μg kg^?1 (MBMK) IV and IM. Heart rate (HR), arterial blood pressures (SAP, MAP, DAP), central venous pressure (CVP), cardiac output, respiratory rate (f_R), rectal temperature (RT) were measured and arterial blood samples were obtained for gas analysis at baseline and at 3, 10, 20, 30, 45 and 60 minutes after drug administration. The cardiac index (CI), systemic vascular resistance index (SVRI) and oxygen delivery index (DO₂I) were calculated. After the follow-up period atipamezole 50 μg kg^?1 IM was given to reverse sedation.ResultsHR, CI and DO₂I were significantly higher with MBMK after both IV and IM administration. Similarly, SAP, MAP, DAP, CVP, SVRI and RT were significantly lower after MBMK than with MB. There were no differences in f_R between treatments, but arterial partial pressure of oxygen decreased transiently after all treatments. Recoveries were uneventful following atipamezole administration after all treatments.Conclusions and clinical relevanceMK-467 attenuated the cardiovascular effects of a medetomidine-butorphanol combination after IV and IM administration.     

Ventricular arrhythmogenic dose of epinephrine in dogs and cats anesthetized with tiletamine/zolazepam and halothane

The ventricular arrhythmogenic dose of epinephrine (ADE) was determined in 6 dogs anesthetized with halothane alone or with halothane after injection of tiletamine/zolazepam (TZ). Respiratory rate and tidal volume were controlled and sodium bicarbonate was administered to maintain arterial pH and blood gas values within reference range. Heart rate and arterial blood pressure were recorded during determination of the ADE. The ADE (mean +/- SD) was no different during anesthesia with use of halothane alone (8.9 +/- 4.3) than it was when injections of TZ preceded administration of halothane (6.7 +/- 2.8). Tiletamine/zolazepam was also administered IV immediately after determination of the ADE during halothane-induced anesthesia. The TZ administered in this manner did not alter the ADE. Blood pressure and heart rate were significantly greater during infusion of epinephrine than immediately prior to infusion. The administration of TZ did not alter blood pressure response. The ADE was also determined in 6 cats anesthetized with halothane preceded by administration of TZ. The ADE (mean +/- SD) was 0.7 +/- 0.23 micrograms/kg, a value similar to that reported for cats during anesthesia with halothane alone.     

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.     

Effects of thoracolumbar epidural anesthesia with lidocaine on the systemic hemodynamics and hepatic blood flow in propofol anesthetized dogs

General anesthesia reduces hepatic blood flow (HBF) from circulatory depression. Total intravenous anesthesia (TIVA) is associated with decreased circulatory depression compared to inhalation anesthesia, and epidural anesthesia using local anesthetics increases blood flow by blocking the sympathetic nerves and expanding blood vessels. We investigated the effects of thoracolumbar epidural anesthesia with TIVA on HBF in dogs. Six Beagle dogs had epidural catheters placed between T13 and L1 and were anesthetized with propofol and vecuronium. Physiological saline (control) or 2% lidocaine (0.2 ml/kg, followed by 0.2 ml/kg/hr) was administered at 1–2 weeks intervals. Heart rate (HR), cardiac index (CI), mean arterial pressure (MAP), and systemic vascular resistance index (SVRI) were recorded at 10-min intervals from before epidural injections (T0) to 110 min. Indocyanine green test was used to measure HBF during the awake state and until 90 min after epidural injections. HR and CI did not differ between treatments. MAP and SVRI after lidocaine were significantly lower than those of controls, and the lowest MAP value was 65 ± 11 mmHg at T10. Compared to T0, after lidocaine treatment, HBF was significantly higher at T30, T60 and T90 (P<0.05); while, after control treatment, no significant change was evident at any time point. Despite a decrease in MAP by this technique, HBF was either maintained at pre-anesthetic levels or increased in comparison to controls, probably due to vasodilation of the hepatic artery induced by the selective blockade sympathetic ganglia.     

Does cortisol inhibit vasopressin secretion in sheep?

Glucocorticoids inhibit the plasma vasopressin responses to hemorrhage and hypoxia in dogs. Attempts to demonstrate glucocorticoid inhibition of vasopressin secretion in fetal sheep have been unsuccessful, suggesting the possibility that there is an influence of development on the expression of this interaction, or that the interaction cannot be demonstrated in all mammalian species. This study was designed to investigate these two possibilities. Adult ewes chronically prepared with carotid arterial loops, were subjected to 5 hr infusions of cortisol at a rate of 6 ug/kg min or vehicle (5% ethanol in saline). The infusion of cortisol increased plasma cortisol concentration from 26 +/- 3 to 46 +/- 8 ng/ml, while vehicle infusion was associated with a decrease in plasma cortisol concentration from 23 +/- 4 to 15 +/- 3 ng/ml. One hr after the end of the cortisol or vehicle infusions, vasopressin secretion was stimulated by arterial hypotension produced by 10 min infusions of sodium nitroprusside (20 ug/kg min). Nitroprusside decreased arterial blood pressure equally in both groups. Plasma vasopressin concentrations were increased to peak concentrations of 92 +/- 33 and 116 +/- 20 pg/ml in the vehicle- and cortisol-infused groups, responses which were not significantly different as tested by ANOVA. We conclude that increases in plasma cortisol concentration, equal to those observed during responses to stressors, do not inhibit vasopressin secretion in this species.