peer reviewed | Techniques of cost-effectiveness analyses were applied to determine whether or not it is economically efficient to measure the packed cell volume (PCV) on a colic horse before deciding on abdominal surgery. The effects of this decision of uncertainty on the estimated values of the parameters (probability of survival after surgery, surgery costs, PCV positive predictive value, and length of survival after surgery) were considered along with the monetary values of collecting additional information on those parameters. The effects of uncertainty on the incremental net benefits of each alternative were depicted by tornado diagrams, cost-effectiveness acceptability curves, and posterior probability distributions. The worth of additional information was computed as the expected values of perfect and sampling information. Given previously published results, the best PCV cut-off point to distinguish between survivors and nonsurvivors was at 44%. At this threshold, the most economically effective alternative is to measure PCV before surgery providing the owner is willing to pay less than €672 for each year the horse survives. Uncertainty on probability of survival after surgery largely influenced the decision whether or not to measure the PCV, but one should spend at most €381 in research to reduce this uncertainty. A study of postoperative survival of 500 colic horses would ensure an expected gain of €370 associated with a reduction in uncertainty.

Thirty healthy male horses were allotted to 3 groups and treated blindly during 4 days. Group-1 horses received unfractioned calcium heparin (100 IU/kg of body weight, SC, q 12 h). Group-2 horses received a single dose of a low-molecular-weight heparin (50 anti-Xa IU/kg, SC) every morning, and a similar volume of saline solution every evening. Group-3 horses received the vehicle (saline solution), SC, every 12 hours. Citrated and EDTA-anticoagulated blood samples were collected before starting the medication (T-0) and once daily 3 hours after each morning injection (T-3, T-27, T-51, and T-75). The PCV, hemoglobin concentration, RBC and platelet counts, and clotting times (activated partial thromboplastin time and thrombin time) were determined, and a microscopic examination to detect hemagglutination was performed. Plasma concentration of heparin was measured by use of the antifactor Xa activity assay. Bleeding time was determined on the first and fourth days, using a double-template method. The horses given unfractioned heparin had marked agglutination of erythrocytes after the first injection that became more pronounced as treatment progressed. Also, significant decrease in PCV, hemoglobin concentration, and RBC count was observed during treatment. Platelet count was significantly decreased after the first day, and clotting times were significantly prolonged. In contrast to the horses given unfractioned heparin, those given low-molecular-weight heparin did not have any agglutination of erythrocytes during the 4 days of treatment, and there were no significant changes in PCV, hemoglobin concentration, or RBC and platelet counts. Activated partial thromboplastin time increased slightly in the horses given low-molecular-weight heparin, although the values remained within reference range. Both groups of horses achieved adequate concentrations of heparin in plasma for prophylactic purposes, but those given low-molecular-weight heparin achieved those values after the first injection. Bleeding times were not significantly different between heparin-treated horses and horses given saline solution during treatment. We conclude that low-molecular-weight heparin may be used more safely and conveniently in horses, because it does not affect equine erythrocytes, platelets, or clotting and bleeding times.

Arterial blood samples were obtained at rest, just before, and 5 minutes after a 704-m race, to quantify changes in hematologic variables, plasma electrolyte and protein concentrations, osmolality, and acid/base variables. Changes in plasma volume were estimated from the change in plasma protein concentration. Immediately prior to the race, plasma volume decreased by 10% from rest and total circulating RBC volume increased by 60%, attributable to increased RBC number rather than size. Increases in blood volume (VB) by 24% and PCV by 29% also were detected before the race. Five minutes after the race, plasma volume was 21% below the resting value and total circulating RBC volume had increased 73% above the resting value, resulting in a 40% increase in PCV. Contraction of the spleen appeared responsible for increased PCV and VB before the race and maintenance of VB after the race. Plasma chloride concentration was the same before and after the race; the chloride content of the plasma decreased by the same fraction (22%) as did the plasma volume, indicating Cl- loss from the plasma. Plasma Na+ content decreased by a smaller fraction (13%), causing Na+ concentration to increase from 151 mEq/L at rest to 167 mEq/L after the race. Assuming that Na+ concentration was the same throughout the extracellular fluid, H20 likely moved into the intracellular compartment. As a consequence of these changes, the inorganic strong ion difference in plasma increased by about 16 mEq/L, tending to minimize the acid/base disturbance induced by the 33 mEq/L increase in lactate concentration. Results indicated that the physiologic changes taking effect during strenuous sprint exercise in Greyhounds enhance blood volume and aid in acid/base homeostasis, both of which are adaptive for this type of exercise.

Starling forces and hemodynamics in the digits of 5 horses were studied during early laminitis induced by oral administration of an aqueous extract of black walnut (Juglans nigra). The black walnut extract was prepared from heartwood shavings and was administered by nasogastric tube. Heart and respiratory rates, rectal temperature, central venous and arterial pressures, digital pulses, and signs of lameness were monitored. Blood samples were collected for determination of WBC count, hemoglobin concentration, and PCV and for endotoxin and tumor necrosis factor assays. Total WBC count and central venous pressure were monitored until they decreased by 30 or 20%, respectively. These decreases in WBC count and central venous pressure were observed 2 to 3 hours after dosing with black walnut extract. Respiratory and heart rates, body temperature, systolic and diastolic blood pressures, PCV, and hemoglobin concentration did not change significantly. Anesthesia was induced, heparin (500 IU/kg of body weight) was administered IV, and a pump-perfused extracorporeal digital preparation was established. Digital arterial and venous pressures were maintained at 100 and 30 mm of Hg, respectively. Blood flow, capillary pressure, lymph and plasma protein concentrations, and weight of the isolated digit during rapid increase in venous pressure were measured. Isogravimetric capillary filtration coefficient, vascular compliance, vascular and tissue oncotic pressures, tissue pressure, osmotic reflection coefficient, and precapillary and postcapillary resistances were calculated. Mean digital blood flow was 14 ml/min/100 g, capillary pressure was 52 mm of Hg, and vascular compliance was 0.06 ml/mm of Hg. The vascular and tissue oncotic pressures were 21.49 and 4.93 mm of Hg, respectively. The osmotic reflection coefficient was 0.71, and tissue pressure was 41 mm of Hg. The precapillary and postcapillary resistances were 7 and 2 mm of Hg/ml, respectively. Capillary permeability to proteins was not significantly different from that previously measured in healthy horses, suggesting that the increased capillary filtration coefficient reflected increased capillary hydrostatic pressure and perfusion of previously nonperfused capillaries. Neither endotoxin nor serum tumor necrosis factor activity was detected in any samples. The hemodynamic and Starling forces observed in this study were similar to those observed after laminitis was induced by administration of a carbohydrate gruel. Significant differences between the 2 models were detected for total vascular resistance, postcapillary resistance, and capillary filtration coefficient. It is likely that these differences were identified because the horses administered the black walnut extract were at an earlier stage in the disease process. The findings of this study suggest that the increase in capillary pressure causes transvascular fluid movement, resulting in increased tissue pressure and edema. We hypothesize that further increases in tissue pressure may collapse capillary beds and lead to tissue ischemia.

To study behavioral and cardiopulmonary characteristics of horses recovering from inhalation anesthesia, 6 nonmedicated horses were anesthetized under laboratory conditions on 3 different days, with either halothane or isoflurane in O2. Anesthesia was maintained at constant dose (1.5 times the minimum alveolar concentration [MAC]) of halothane in O2 for 1 hour (H1), halothane in O2 for 3 hours (H3), or isoflurane in O2 for 3 hours (13). The order of exposure was set up as a pair of Latin squares to account for horse and trial effects. Circulatory (arterial blood pressure and heart rate) and respiratory (frequency, PaCO2, PaO, pHa) variables were monitored during anesthesia and for as long as possible during the recovery period. End-tidal percentage of the inhaled agent was measured every 15 seconds by automated mass spectrometry, then by hand-sampling after horses started moving. Times of recovery events, including movement of the eyelids, ears, head, and limbs, head lift, chewing, swallowing, first sternal posture and stand attempts, and the number of sternal posture and stand attempts, were recorded. The washout curve or the ET ratio (end-tidal percentage of the inhaled agent at time t to end-tidal percentage of the inhaled agent at the time the anesthesia circuit was disconnected from the tracheal tube) plotted against time was similar for HI and H3. The slower, then faster (compared with halothane groups) washout curve of isoflurane was explainable by changes in respiratory frequency as horses awakened and by lower blood/gas solubility of isoflurane. The respiratory depressant effects of isoflurane were marked and were more progressive than those for halothane at the same 1.5 MAC dose. During the first 15 minutes of recovery, respiratory frequency for group-13 horses increased significantly (P < 0.05), compared with that for the halothane groups. For all groups, arterial blood pressure increased throughout the early recovery period and heart rate remained constant. Preanesthesia temperament of horses and the inhalation agent used did not influence the time of the early recovery events (movement of eyelids, ears, head, and limbs), except for head lift. For events that occurred at anesthetic end-tidal percentage < 0.20, or when horses were awake, temperament was the only factor that significantly influenced the nature of the recovery (chewing P = 0.04, extubation P = 0.001, first stand attempt P = 0.008, and standing P = 0.005). The quality of the recoveries did not differ significantly among groups (H1, H3, I3) or horses; however 5 of 6 horses recovering from the H1 exposure had ideal recovery. During recovery, the anesthetic end-tidal percentage did not differ significantly among groups. However, when concentrations were compared on the basis of anesthetic potency (ie, MAC multiple) a significantly (P < 0.05) lower MAC multiple of isoflurane was measured for the events ear movement, limb movement, head lift, and first attempt to sternal posture, compared with that for horses given halothane, indicating that isoflurane may be a more-potent sedative than halothane in these horses.

Four hours prior to exercise on a high-speed treadmill, 4 dosages of furosemide (0.25, 0.50, 1.0, and 2.0 mg/kg of body weight) and a control treatment (10 ml of 0.9% NaCl) were administered IV to 6 horses. Carotid arterial pressure (CAP), pulmonary arterial pressure (PAP), and heart rate were not different in resting horses before and 4 hours after furosemide administration. Furosemide at dosage of 2 mg/kg reduced resting right atrial pressure (RAP) 4 hours after furosemide injection. During exercise, increases in treadmill speed were associated with increases in RAP, CAP, PAP, and heart rate. Furosemide (0.25 to 2 mg/kg), administered 4 hours before exercise, reduced RAP and PAP during exercise in dose-dependent manner, but did not influence heart rate. Mean CAP was reduced by the 2-mg/kg furosemide dosage during exercise at 9 and 11 m/s, but not at 13 m/s. During recovery, only PAP was decreased by furosemide administration. Plasma lactate concentration was not significantly influenced by furosemide administration. Furosemide did not influence PCV or hemoglobin concentration at rest prior to exercise, but did increase both variables in dose-dependent manner during exercise and recovery. However, the magnitude of the changes in PCV and hemoglobin concentration were small in comparison with changes in RAP and PAP, and indicate that furosemide has other properties in addition to its diuretic activities. Furosemide may mediate some of its cardiopulmonary effects by vasodilatory activities that directly lower pulmonary arterial pressure, but also increase venous capacitance, thereby reducing venous return to the atria and cardiac filling.

Hematologic and rheologic changes were examined in 49 Thoroughbreds before and after competitive racing. Mean postrace values for RBC count, hemoglobin concentration, and PCV increased by 58 to 61%, whereas blood viscosity increased 2 to 3 times. Postrace echinocyte numbers were 162% greater than prerace values. Smaller, but statistically significant, changes were found for mean corpuscular hemoglobin concentration, red cell distribution width, plasma total protein concentration, total WBC count, neutrophil count, and lymphocyte count. Variables measured did not predict whether a horse was a bleeder not treated with furosemide, a bleeder treated with furosemide, or a nonbleeder.

The temporal response of blood and serum proteins to chronic plasmapheresis was determined in 8 horses used in a commercial antibody enterprise. Plasmapheresis of between 4 and 11 L induced significant decreases in total protein, albumin, and IgG values. With the exception of a high hematocrit value for the first postplasmapheresis blood sample, there were no changes in erythrocyte or leukocyte measurements, and no changes in the proportions of serum protein in an electrophoretic profile. Regression equations generated for recovery of proteins after plasmapheresis indicated a return to preplasmapheresis values of total protein and albumin at approximately 1 month. Complications of repeated plasmapheresis were not detected when plasma extractions were done between 7 and 19 times at 30-day intervals.

Blood constituents and vascular volume indices were determined in 5 standing horses by use of 2-period crossover experimental design. Horses were either administered hypertonic (2,400 mosm/kg of body weight, IV) or isotonic (300 mosm/kg, IV) saline solution. Each solution was administered at a dosage of 5 ml/kg (infusion rate, 80 ml/min). Samples for determination of PCV, plasma volume, blood volume, plasma osmolality, total amount of plasma protein and plasma concentrations of protein, Na, K, and Cl were collected at 0 hour (baseline, before fluid infusion) and 0.5 hour (at the end of fluid infusion), and subsequently, at 0.25- or 0.5-hour intervals for 4.5 hours. All horses were given the predetermined dose of fluids by 0.5 hour after beginning the saline infusion. Values of P less than or equal to 0.05 were considered significant. Administration of hypertonic saline solution was associated with decreased mean body weight by 4.5 hours, but weight change after isotonic saline administration was not significant. Other than body weight and plasma protein concentration, between-trial difference (treatment effect) was not observed for any measured variable or index. The F values indicated that increasing the number of horses would have not changed these results. A time effect was evident across both trials, so that mean (+/- SD) plasma volume increased (12.3 +/- 1.07%) and mean plasma protein concentration (-12.1 +/- 1.03%) and PCV (-11.9 + 0.67%) decreased proportionately and transiently in association with administration of either fluid at that volume. Other time effects included increased plasma osmolality and Na and Cl concentrations. Blood volume estimates and total amount of plasma protein remained unchanged. These data indicate that in conscious clinically normal horses, changes in plasma protein concentration reflect changes in plasma volume and that blood volume may be regulated by alterations in plasma volume and red cell mass. These data also indicate that changes in plasma volume and constituent concentrations may be similar in response to administration of either 0.9% (300 mosm/kg) or 7.2% (2,400 mosm/kg) NaCl solutions (5 ml/kg) and that clinically normal horses can rapidly regulate variable Na loads.