Twenty-four horses were randomly allocated to 3 groups. All horses underwent a ventral midline celiotomy, and the large colon was exteriorized and instrumented. Group-1 horses served as sham-operated controls, group-2 horses underwent 6 hours of colonic ischemia, and group-3 horses were subjected to 3 hours of ischemia and 3 hours of reperfusion. Baseline blood samples were collected, then low-flow colonic ischemia was induced in horses of groups 2 and 3 by reducing colonic arterial blood flow to 20% of baseline. All horses were monitored for 6 hours. Citrated systemic venous (SV) blood samples were collected from the main pulmonary artery, and colonic venous (CV) samples were collected from the colonic vein draining the ventral colon. Samples were collected at 0, and 2, 3, 3.25, 4, and 6 hours for determination of one-stage prothrombin time, activated partial thromboplastin time, antithrombin III activity, and fibrinogen concentration. Data were analyzed statistically, using two-way ANOVA for repeated measures, and post-hoc comparisons were made by use of Student Newman Keul's test. Statistical significance was set at P < 0.05. There were significant decreases in all hemostatic variables by 2 hours in SV and SV samples from horses of all 3 groups, but there were no differences among the 3 groups for any of these variables. These hemostatic alterations could have been secondary to a hypercoagulable state or to fluid therapy-induced hemodilution. Colonic ischemia-reperfusion was not the cause of these alterations because these alterations also were observed in the sham-operated control horses. Significant temporal alterations existed even after accounting for the hemodilution. The most plausible explanation for these alterations is that hemostatic activation was incited by the celiotomy and manipulation of the colon during exteriorization and instrumentation. Comparison of paired SV and CV samples for each hemostatic variable revealed significant differences for the absolute values of one-stage prothrombin time and fibrinogen concentration, but not for activated partial thromboplastin time or antithrombin III activity. This indicates that monitoring SV hemostatic variables does not necessarily provide an accurate assessment of hemostatic function in regional vascular beds. Large-colon ischemia with or without reperfusion did not alter hemostatic function.

Receptors for opsonins, such as complement component C3b (CR1) and immunoglobulins, Fc receptors, interact with adhesion glycoproteins in mediating immune functions. Defects in expression of the adhesion glycoproteins CD11/CD18 results in severely hampered in vitro and in vivo adherence-related functions of leukocytes. Little is known regarding the effect of leukocyte adhesion deficiency (LAD) on ligand binding and receptor expression. We investigated the binding and expression of CR1 and Fc receptors by bovine neutrophils isolated from dairy calves suffering from LAD, compared with clinically normal (hereafter referred to as normal) age-matched calves. Neutrophils were also assayed for endogenously bound IgG and IgM and for exogenous binding of C3b, IgG1, IgG2, IgM, and aggregated IgG (aIgG), using flow cytometry. Luminol-enhanced chemiluminescence (CL) production in response to IgG2 opsonized zymosan was studied, and specific inhibition of CL was used to determine the specificity of IgG2 binding. Activation of protein kinase C with phorbol myristate acetate was used to determine the effect of cellular activation on expression of CR1. A greater percentage of neutrophils from normal calves bound C3b than did neutrophils from LAD-affected calves. Receptor expression was similar. Activation with phorbol myristate acetate resulted in increased expression of CR1 on neutrophils from normal and LAD-affected calves, but expression was almost twofold greater on neutrophils from normal calves. There was no difference between LAD-affected and normal calves in percentage of neutrophils that bound endogenous IgG and IgM. A greater percentage of neutrophils from normal calves bound exogenous IgM than did neutrophils from LAD-affected calves. Receptor expression for aIgG was greater on neutrophils from LAD-affected calves than on those from normal calves. Luminol-enhanced CL of neutrophils in response to IgG2 opsonized zymosan was not different between LAD-affected and normal calves. Results indicate increased binding and expression of Fc receptors for aIgG and decreased binding and expression for C3b and IgM on neutrophils from calves with LAD. Leukocyte adhesion deficiency may be compounded by added defects in the expression and binding of receptors for opsonins, such as C3b and IgM.

Cardiopulmonary responses were evaluated in 12 dogs undergoing endoscopy (gastroscopy and enteroscopy). Constant endoscopic insufflation was used to distend the stomach and small intestine for 30 minutes in groups of small (< 10 kg n = 4), medium (10 to 20 kg n = 4), and large (> 20 kg n = 4) dogs. Cardiopulmonary measurements within groups prior to gastric distention (preendoscopy) were compared with postendoscopy measurements and with those made during endoscopy. After distending the stomach and small intestine, increased luminal pressure within the body of the stomach and in the descending duodenum (P < 0.05) and increased abdominal girth (P < 0.05) were observed, with the greatest changes in small dogs. Caudal vena cava pressures and mean arterial and pulmonary artery pressures increased (P < 0.05) during endoscopy. Cardiac index varied, with small dogs having greater cardiac index (P < 0.05) during endoscopy, compared with that in medium and large dogs. Minute volume remained unchanged during insufflation, despite a decrease in tidal volume (P < 0.05), because of an increase in respiratory rate (P < 0.05). Arterial blood gas analysis revealed a mild, mixed metabolic/respiratory acidosis in all groups. Although cardiopulmonary changes associated with gastrointestinal tract endoscopy were common, the changes were often small and of little clinical significance.

Eighteen dogs undergoing lateral thoracotomy at the left fifth intercostal space were randomly assigned to 1 of 3 postoperative analgesic treatment groups of 6 dogs each as follows: group A, morphine, 1.0 mg/kg of body weight, IM; group B, 0.5% bupivacaine, 1.5 mg/kg given interpleurally; and group C, morphine, 1.0 mg/kg given interpleurally. Heart rate, respiratory rate, arterial blood pressure, arterial blood gas tensions, alveolar-arterial oxygen differences, rectal temperature, pain score, and pulmonary mechanics were recorded hourly for the first 8 hours after surgery, and at postoperative hours 12, 24, and 48. These values were compared with preoperative (control) values for each dog. Serum morphine and cortisol concentrations were measured at 10, 20, and 30 minutes, hours 1 to 8, and 12 hours after treatment administration . All dogs had significant decreases in pHa, PaO2, and oxygen saturation of hemoglobin, and significant increases in PaCO2 and alveolar-arterial oxygen differences in the postoperative period, but these changes were less severe in group-B dogs. Decreases of 50% in lung compliance, and increases of 100 to 200% in work of breathing and of 185 to 383% in pulmonary resistance were observed in all dogs after surgery. Increases in work of breathing were lower, and returned to preoperative values earlier in group-B dogs. The inspiratory time-to-total respiratory time ratio was significantly higher in group-B dogs during postoperative hours 5 to 8, suggesting improved analgesia. Blood pressure was significantly lower in group-A dogs for the first postoperative hour. Significant decreases in rectal temperature were observed in all dogs after surgery, and hypothermia was prolonged in dogs of groups A and C. Significant differences in pain score were not observed between treatment groups. Cortisol concentration was high in all dogs after anesthesia and surgery, and was significantly increased in group-B dogs at hours 4 and 8. Significant differences in serum morphine concentration between groups A and C were only observed 10 minutes after treatment administration. In general, significant differences in physiologic variables between groups A and C were not observed. Results of the study indicate that anesthesia and thoracotomy are associated with significant alterations in pulmonary function and lung mechanics. Interpleurally administered bupivacaine appears to be associated with fewer blood gas alterations and earlier return to normal of certain pulmonary function values. Interpleural administration of morphine does not appear to provide any advantages, in terms of analgesia or pulmonary function, compared with its IM administration.

Cortical bone concentrations of enrofloxacin were determined over time in dogs after SC administration of the drug. Nineteen healthy adult dogs were anesthetized and were given 2.5 or 5.0 mg of enrofloxacin/kg of body weight, SC. Serial serum and bone samples were obtained for determination of enrofloxacin concentrations at intervals until 8 hours after drug administration. Cortical bone samples were procured by surgical disarticulation of successive second phalanges. Additional cortical bone samples were taken from long bones in 4 dogs. Mean +/- SD peak serum enrofloxacin concentration was 0.54 +/- 0.10 micrograms/ml for the 2.5-mg/kg dosage and 0.97 +/- 0.34 micrograms/ml for the 5.0-mg/kg dosage. Serum concentration was significantly higher than bone concentration for each dosage. Mean peak bone concentrations reached 29% of peak serum values: 0.15 +/- 0.09 micrograms/g and 0.29 +/- 0.09 micrograms/g for 2.5-mg/kg and 5.0-mg/kg dosages, respectively. Serum concentration for the 5.0-mg/kg dosage was significantly greater than that for the 2.5-mg/kg dosage for all times, whereas bone concentrations for the 5.0-mg/kg dosage were significantly higher at all times after 180 minutes. For the duration of the study, cortical bone concentrations of enrofloxacin at either dosage exceeded the minimum inhibitory concentration (MIC) for the Enterobacteriaceae, but reliably exceeded the MIC for Staphylococcus sp only at the 5.0-mg/kg dosage. At no time did cortical bone concentrations of enrofloxacin exceed the MIC for Pseudomonas aeruginosa at either dosage. To validate extrapolation of data from the second phalanx to long bones and from anesthetized to awake dogs, 16 healthy dogs being euthanatized in unrelated studies were given 2.5 or 5.0 mg of enrofloxacin/kg, sc. These dogs were not anesthetized but were euthanatized at 60, 120, or 240 minutes after drug administration, and multiple cortical bone samples were taken. Antibiotic concentrations in the second phalanx were not significantly different from those in long bones. Comparison of enrofloxacin concentrations in cortical bone of awake and anesthetized dogs suggested no differences between groups. We concluded that general anesthesia and use of the antibiotic concentrations in the second phalanx as representative of those in long bones did not affect results of this study.

Six healthy, adult horses, with normal (mean +/- SEM) baseline serum concentrations of total triiodothyronine (T3, 1.02 +/- 0.16 nmol/L), free T3 (FT3, 2.05 +/- 0.33 pmol/L), total thyroxine (T4, 19.87 +/- 1.74 nmol/L), free T4 (FT4, 11.55 +/- 0.70 pmol/L), total reverse T3 (rT3, 0.68 +/- 0.06 nmol/L), and cortisol (152.75 +/- 17.50 nmol/L), were judged to be euthyroid on the basis of response to a standardized thyroid-stimulating hormone response test. Serum concentrations of T3, FT3, T4, FT4, rT3, and cortisol were determined immediately before and every 24 hours during a 4-day period of food deprivation, when water was available ad libitum. Similar variables were measured 72 hours after refeeding. Decreases (to percentage of baseline, prefood deprivation value) in circulating T3 (42%), T4 (38%), FT3 (30%), and FT4 (24%) concentrations were maximal after 2, 4, 2, and 4 days of food deprivation, respectively (P < 0.05). Increases (compared with baseline, prefood deprivation value) in rT3 (31%) and cortisol (41%) concentrations were maximal after 1 and 2 days of food deprivation, respectively (P < 0.05). Refeeding resulted in increase in serum T4 and FT4, and decrease in rT3 and cortisol concentrations toward baseline values, after 72 hours (P < 0.05). Refeeding did not effect a return of T3 or FT3 concentration to baseline values after 72 hours (P < 0.05). Food deprivation appears to cause changes in serum concentrations of T3, FT3, T4, FT4, rT3, and cortisol in horses that are similar to those in human beings. This effect of food deprivation should be considered when results of serum thyroid hormone and cortisol assays are interpreted in the face of clinical disease. These results further emphasize the invalidity of making a clinical diagnosis of hypothyroidism on the basis of baseline, serum thyroid hormone concentrations in horses, especially if the horses have been anorectic or inappetent.

A repeated-measures study was conducted on 5 dogs to clinically, radiographically, and echocardiographically characterize the actions of the angiotensin-converting enzyme inhibitor, enalapril, before and after development of experimentally induced heart failure. Heart failure was artificially induced, using a surgically implanted programmable ventricular pacemaker, which stimulated the heart at a rate of 245 beats/min until a low-output cardiomyopathic a state developed. This condition was then stabilized by decreasing the pacing rate to 190 beats/min. Pacing-induced heart failure was successfully induced in a mean +/- SD 4.2 +/- 1.95 weeks. The condition closely resembled the clinical, radiographic, and echocardiographic features of naturally acquired idiopathic dilated cardiomyopathy in dogs. Enalapril was well tolerated by dogs, and clinical adverse reactions did not develop. Results of echocardiographic studies indicated that enalapril treatment during the control period resulted in a significant (P < 0.05) increase in velocity of circumferential fiber shortening and a significant (P < 0.05) decrease in left ventricular ejection time. Therapeutic responses to enalapril were evident after development of heart failure. These included reduced severity of clinical signs of disease, evidence of decreased radiographically determined cardiac size (2 of 5 dogs), radiographic evidence of a reduction in pulmonary edema and congestion (4 of 5 dogs), significant (P < 0.05) reductions in left atrial and ventricular chamber dimensions (left atrial dimension, diastolic left ventricular internal dimension as determined echocardiographically), and improvement in some echocardiographic indices of left ventricular performance (velocity of circumferential fiber shortening and left ventricular ejection time).

Icterus condemnations compose a substantial proportion (41%) of total condemnations of bob veal, the class of veal composed of calves < 3 weeks old and weighing up to 68 kg. At postmortem examination, bob veal condemned because of icterus have generalized yellow discoloration of tissues, which is commonly associated with large, yellow liver (fatty liver), and a paucity of other gross pathologic changes. To establish that the generalized yellow discoloration was attributable to high tissue bilirubin concentrations and to examine the underlying mechanism(s) that might be responsible, blood samples and tissue specimens were obtained from clinically normal and icteric bob veal calves at slaughter. For comparison, blood samples were collected from clinically normal, 1- to 5-day-old Holstein calves being raised on local dairy farms. Hematologic and serum biochemical analyses were obtained for the 3 groups of calves (normal local, normal slaughter, and icteric slaughter), and tissues of slaughter calves were examined for histologic evidence of inflammatory or degenerative changes. Mean +/- SD total bilirubin concentration and creatine kinase (CK) activity in icteric bob veal (3.3 +/- 0.8 mg/dl; 869 +/- 788 U/L), normal bob veal (1.4 +/- 0.7 mg/dl; 486 +/- 890 U/L), and normal local calves (0.5 +/- 0.2 mg/dl; 156 +/- 158 U/L) were significantly different. When data for both normal and icteric bob veal calf groups were combined for analysis, total bilirubin concentration regressed significantly on hepatic lipid scores (P = 0.00003) and CK activity (P = 0.00049). Colostrum consumption was determined by measuring serum total protein concentration and serum gamma-glutamyltransferase activity. Bob veal calves that had not consumed colostrum had significantly higher total bilirubin (P = 0.00005) and CK (P = 0.0008) values. It was concluded that normal and icteric bob veal calves have significant increase in total bilirubin concentration, and icterus of bob veal calves is secondary to unconjugated hyperbilirubinemia. Lack of colostrum consumption was strongly correlated with icterus in bob veal calves.

Pharmacokinetic variables of skeletal muscle creatine kinase (CK) activity after IV administration of a muscle extract; CK bioavailability after IM administration of the muscle extract; and effect of IM administration of saline solution, to appreciate the possible release of CK consecutive to muscle puncture, were determined in 6 cows. A general equation for the quantitative estimation of skeletal muscle damage also was derived. Administration of saline solution IM had no effect on plasma CK activity (ANOVA, P > 0.05) in any of the cows. After IV administration of the muscle extract (150 U/kg of body weight), mean volume of the central compartment, plasma half-life, and plasma clearance of CK were 0.027 +/- 0.007 L/kg, 520 +/- 109 minutes, and 6.43 +/- 2.29 ml/kg/h, respectively. After IM administration (150 U/kg), mean bioavailability of CK was 51 +/- 17% and maximal plasma CK activity (500 +/- 97 U/L) was observed at 454 +/- 131 minutes. The rate of CK activity entry into plasma was determined by use of deconvolution analysis. Two peaks were observed; the first appeared before the 30th minute after IM administration, and the second appeared at 3.3 +/- 1.1 hours. Amplitudes were 6.31 +/- 4.45 and 6.57 +/- 3.08 U/kg/h, for the first and the second peaks, respectively. The quantity of CK liberated from control muscle was 0.69 +/- 0.12 U/kg/h, corresponding to a normal daily catabolism of 5.8 +/- 1.0 mg of muscle/kg. From these results, the following equation can be proposed to determine the corresponding mean equivalent of destroyed muscle (Qmuscle, test article) after IM administration of a test article: Qmuscle, test article (g/kg) = 4.41 X 10(-6) AUC (U/h/L), with AUC being the CK plasma activity area under the curve.

Plasma concentration of immunoreactive atrial natriuretic peptide (ir-ANP) was investigated in 83 Cavalier King Charles Spaniels with variable severity of mitral regurgitation caused by chronic valvular disease (CVD). Severity of mitral incompetence was assessed by echocardiography. Significant differences in plasma concentrations of ir-ANP were not found between clinically normal dogs (New York Heart Association functional class O), dogs with only cardiac murmur (class I), and dogs with echocardiographic evidence of slight to moderate left atrial and ventricular dilatation (class II). Dogs with severe left atrial and ventricular dilatation and clinical signs of congestion (classes III and IV) were found to have significantly (P < 0.001) increased plasma concentration of ir-ANP. Overall, moderate degree of association was found between plasma concentration of ir-ANP and left atrial and left ventricular diameters (Pearson's r = 0.65, 0.60, respectively, P < 0.001), as well as heart rate (r = 0.47, P < 0.01). However, left atrial enlargement as found to have the predominant effect on plasma ir-ANP concentration. It is concluded that the plasma concentration of ir-ANP did not become markedly increased before decompensation of chronic mitral regurgitation associated with severe enlargement of the left atrium and ventricle in Cavalier King Charles Spaniels.