Objective—To assess the microcirculatory effects of IV fluid administration in healthy anesthetized dogs undergoing elective ovariohysterectomy. Animals—49 client-owned dogs. Procedures—Dogs were sedated, and anesthesia was induced with propofol and diazepam and maintained with isoflurane in oxygen. Dogs received lactated Ringer's solution (LRS) IV at rates of 0, 10, or 20 mL/kg/h. Videomicroscopy was used to assess and record effects of LRS administration on microcirculation in the buccal mucosa. Measurements of microcirculatory (total vessel density, proportion of perfused vessels, microcirculatory flow index, and perfused vessel density by vessel size [< 20 μm, ≥ 20 μm, and all diameters]) and other physiologic variables (heart rate, Doppler-measured blood pressure, oxygen saturation as measured by pulse oximetry, capillary refill time, and body temperature) were compared among groups at baseline (immediately after anesthetic induction), 30 and 60 minutes afterward, and overall. Results—Neither the proportion of perfused vessels nor microcirculatory flow index varied among treatment groups at any time point, regardless of vessel size. For vessels < 20 μm in diameter and for all vessels combined, total and perfused vessel density were similar among groups. For vessels ≥ 20 μm in diameter, total vessel density was significantly greater in the 20 mL/kg/h group than in other groups, and perfused vessel density was significantly greater in the 20 mL/kg/h group than in the 0 mL/kg/h group, when all time points were considered. Other physiologic variables were similar among groups. Conclusions and Clinical Relevance—Total and perfused vessel density of vessels ≥ 20 μm in diameter (mostly venules) were greatest in dogs that received 20 mL of LRS/kg/h. Further research is required to evaluate clinical importance of these findings.

Objective-To determine whether increasing the viscosity of a standard hemoglobin-based oxygen-carrying solution (HBOC) would offset its associated vasoconstrictive effects and result in improved microvascular perfusion in healthy splenectomized dogs with experimentally induced hemorrhagic shock. Animals-12 male American Foxhounds. Procedures-Each dog underwent anesthesia and splenectomy. Shock was induced by controlled hemorrhage until a mean arterial blood pressure of 40 mm Hg was achieved and maintained for 60 minutes. Dogs were then randomly assigned to receive either a standard or hyperviscous HBOC (6 dogs/group). Sidestream dark-field microscopy was used to assess the effects of shock and HBOC administration on the microcirculation of the buccal mucosa and the jejunal serosa. Video recordings of the microcirculation were collected before shock was induced (baseline) and at intervals up to 180 minutes following HBOC administration. Vascular analysis software was used to compute microcirculatory variables. Results-Compared with baseline findings, hemorrhagic shock resulted in decreases in all microvascular variables in the buccal mucosa and the jejunal serosa. At all time points following HBOC administration, microvascular variables were similar to initial values and no significant differences between treatment groups were detected. At all time points following HBOC administration, blood and plasma viscosities in dogs treated with the hyperviscous solution were significantly higher than values in dogs receiving the standard solution. Conclusions and Clinical Relevance-In splenectomized dogs with experimentally induced hemorrhagic shock, administration of a hyperviscous HBOC did not significantly affect microvascular variables, compared with effects of a standard HBOC. Microcirculatory flow returned to baseline values in both treatment groups, suggesting that marked HBOC-associated vasoconstriction did not occur.

Objective-To evaluate tissue oxygen saturation (Sto2) by use of near-infrared spectroscopy in experimental acute hemorrhagic shock and resuscitation in dogs. Animals-14 healthy adult purpose-bred Beagles. Procedures-Dogs were anesthetized with isoflurane via facemask, anesthesia was maintained with propofol and rocuronium bromide, and dogs were mechanically ventilated to maintain normocapnia. Dogs were studied under normovolemia (baseline), hypovolemia with target mean arterial blood pressure < 40 mm Hg achieved and maintained steady for 10 minutes (hypovolemia T1), then 20 minutes later (hypovolemia T2), following resuscitation with shed blood (after transfusion), and after administration of 20 mL of hetastarch/kg (hypervolemia). Conditions were executed sequentially during a single anesthetic episode, allowing stabilization between states (10 minutes). Hemoglobin concentration, mean arterial blood pressure, arterial blood gas concentrations, cardiac index, oxygen delivery indexed to body surface area, and Sto2 were monitored. Results-From baseline to hypovolemia T1, there was a significant reduction in mean +/- SD oxygen delivery index (619 ± 257 mL/min/m2 to 205 ± 76 mL/min/m2) and StO2 (94 ± 4.4% to 78 ±12.2%). Following resuscitation, Sto2 (80 ± 8.5% vs 92 ± 6.45%) and oxygen delivery index (211 ± 73 mL/min/m2 vs 717 ± 221 mL/min/m2) significantly increased, returning to baseline values. Hypervolemia had no effect on Sto2 or oxygen delivery index. A strong correlation (r = 0.97) was detected between mean oxygen delivery index and Sto2 across all time points. Conclusions and Clinical Relevance-Under the conditions of this study, there was a strong correlation between Sto2 and oxygen delivery, suggesting that Sto2 may be used to estimate oxygen delivery.

Objective- To assess the accuracy of an ultrasound velocity dilution cardiac output (UDCO) method, compared with that of the lithium dilution cardiac output (LiDCO) method, for determination of cardiac output (CO) in juvenile horses with experimentally induced hypovolemia. Animals- 12 anesthetized 2- to 6-month-old horses. Procedures- For each anesthetized horse, CO was determined by the LiDCO and UDCO methods prior to any intervention (baseline state), after withdrawal of approximately 40% of the horse's blood volume (low CO state), after maintenance of hypovolemia and infusion of norepinephrine until mean arterial blood pressure was equal to baseline value (high CO state), and after further infusion of norepinephrine and back-transfusion of withdrawn blood (posttransfusion state). For each of the 4 hemodynamic situations, CO and calculated cardiac index (CI) values were obtained by each method in duplicate (8 pairs of measurements/horse); mean values for each horse and overall mean values across all horses were calculated. Agreement between CI determined by each method (96 paired values) was assessed by Bland-Altman analysis. Results- For the UDCO method–derived CI measurements among the 12 horses, mean ± SD bias was −4 ± 11.3 mL/kg/min (95% limits of agreement, −26.1 to 18.2 mL/kg/min) and mean relative bias was −10.4 ± 21.5% (95% limits of agreement, −52.6% to 31.8%). Conclusions and Clinical Relevance- Results indicated that, compared with the LiDCO method, the UDCO method has acceptable clinical usefulness for determination of CO in foals.

Objective-To assess effects of body position on direct measurements of intra-abdominal pressure (IAP) and abdominal perfusion pressure (APP) in horses anesthetized with total intravenous anesthesia (TIVA). Animals-9 healthy adult horses. Procedures-Instrumentation in unsedated standing horses involved insertion of an arterial catheter for blood pressure measurements and 3 intraperitoneal cannulas (left flank, right flank, and ventral abdomen) for IAP measurements. Baseline values were measured for heart rate, respiratory rate, systolic arterial blood pressure, mean arterial blood pressure (MAP), diastolic arterial blood pressure, and IAP. Horses were medicated with xylazine, and pressures were measured again. Anesthesia was induced with ketamine-diazepam and maintained with a ketamine-guaifenesin infusion. Horses were positioned twice into left lateral recumbency, right lateral recumbency, or dorsal recumbency. Hemodynamic pressures and accessible abdominal pressures were measured for each recumbency position. The APP was calculated as MAP - IAP. Differences in IAP, MAP, APP and sedation (standing horses) or body position (anesthetized horses) were compared by means of repeated-measures ANOVA or paired t tests. Results-Baseline hemodynamic and IAPs were not different after xylazine administration. Ventral abdomen IAP and MAP were lower for horses in dorsal recumbency than in right or left lateral recumbency. Ventral abdomen APP remained unchanged. For lateral recumbencies, flank IAP was lower and APP was higher than pressure measurements at the same sites during dorsal recumbency. Conclusions and Clinical Relevance-Body position affected IAP and APP in healthy anesthetized horses. These effects should be considered when developing IAP acquisition methods for use in horses with abdominal disease.

Objective-To evaluate the cardiorespiratory effects of IV administration of propofol (4 mg/kg), ketamine hydrochloride and propofol (2 mg/kg each; K-P), or ketamine hydrochloride (5 mg/kg) and diazepam (0.2 mg/kg; K-D) before and after induction of anesthesia (IoA) in dogs sedated with acepromazine maleate and oxymorphone hydrochloride. Animals-10 healthy adult Beagles. Procedures-Each dog was randomly allocated to receive 2 of 3 treatments (1-week interval). For instrumentation prior to each treatment, each dog was anesthetized with isoflurane. After full recovery, acepromazine (0.02 mg/kg) and oxymorphone (0.05 mg/kg) were administered IV. Fifteen minutes later (before IoA), each dog received treatment IV with propofol, K-P, or K-D. Cardiorespiratory and arterial blood gas variables were assessed before, immediately after, and 5 minutes after IoA. Results-Compared with findings before IoA, dogs receiving the K-P or K-D treatment had increased cardiac output, oxygen delivery, and heart rate 5 minutes after IoA; K-P administration did not change mean arterial blood pressure or stroke volume and decreased systemic vascular resistance. Propofol decreased mean arterial blood pressure and systemic vascular resistance immediately after IoA but did not change heart rate, cardiac output, or oxygen delivery. All treatments caused some degree of apnea, hypoventilation, and hypoxemia (Pao2 < 80 mm Hg). Conclusions and Clinical Relevance-In dogs, K-P treatment maintained mean arterial blood pressure better than propofol alone and increased heart rate, cardiac output, or oxygen delivery, as did the K-D treatment. Supplemental 100% oxygen should be provided during IoA with all 3 treatments.

Objective—To compare the effects of 2 NSAIDs (phenylbutazone and meloxicam) on renal function in horses. Animals—9 Thoroughbred or Standardbred mares (mean ± SD age, 5.22 ± 1.09 years [range, 2 to 12 years]; mean body weight, 470 ± 25 kg [range, 442 to 510 kg]). Procedures—A randomized blinded placebo-controlled crossover study was conducted to examine the effects of treatment with phenylbutazone, meloxicam, or a placebo (control solution) on renal responses to the administration of furosemide, dobutamine, and exercise (15 minutes at 60% of maximum heart rate). Renal function was assessed by use of bilateral ureteral catheterization for simultaneous determination of creatinine clearance, sodium excretion, and urine flow rate. Results—Both phenylbutazone and meloxicam attenuated diuresis and natriuresis and reduced glomerular filtration rate, compared with results for the control solution, when horses were treated with furosemide. Mean arterial blood pressure, urine flow rate, and glomerular filtration rate were increased during or after (or both) dobutamine infusion. Both NSAIDs reduced urine flow rate and sodium excretion associated with dobutamine infusion and exercise but had no effect on glomerular filtration rate. Conclusions and Clinical Relevance—Responses to meloxicam, a cyclooxygenase (COX)-2 preferential agent, appeared comparable to those detected after phenylbutazone treatment, which suggested that COX-2 was the mediator of prostanoid-induced changes to renal function in horses and indicated that COX-2–preferential agents would be likely to have adverse renal effects similar to those for nonselective COX inhibitors in volume-depleted horses.