Search Results

You are looking at 1 - 10 of 14 items for

  • Author or Editor: Warren Beard x
  • Refine by Access: All Content x
Clear All Modify Search

Abstract

Objective—To determine the effect of a tongue-tie on upper airway mechanics in clinically normal horses exercising on a treadmill following sternothyrohyoid myectomy.

Animals—6 Standardbreds.

Procedure—Upper airway mechanics were measured with horses exercising on a treadmill at 5, 8, and 10 m/s 4 weeks after a sternothyrohyoid myectomy was performed. Pharyngeal and tracheal inspiratory and expiratory pressures were measured by use of transnasal pharyngeal and tracheal catheters connected to differential pressure transducers. Horses were fitted with a facemask and airflow was measured by use of a pneumotachograph. Horses underwent a standardized exercise protocol on a treadmill at 5, 8, and 10 m/s with and without a tongue-tie in a randomized cross-over design. Inspiratory and expiratory airflow, tracheal pressure, and pharyngeal pressure were measured, and inspiratory and expiratory resistances were calculated.

Results—We were unable to detect an effect of a tongue-tie on any of the respiratory variables measured.

Conclusions and Clinical Relevance—Results indicate that a tongue-tie does not alter upper airway mechanics following sternothyrohyoid myectomy in clinically normal horses during exercise. (Am J Vet Res 2001;62:779–782)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To determine the pharmacokinetics of morphine after IM administration in a clinical population of horses.

Design—Prospective clinical study.

Animals—77 horses.

Procedures—Morphine sulfate (0.1 mg/kg [0.045 mg/lb], IM) was administered to horses, and blood samples were obtained at predetermined time points. Plasma morphine concentrations were measured via liquid chromatography and mass spectrometry. In preliminary investigations, samples were obtained from 2 healthy horses at 12 time points (up to 12 hours after drug administration) and analyzed via 2-stage pharmacokinetic analysis. In the clinical phase, blood samples were obtained from 75 hospitalized horses at various times (total, 2 to 3 samples/horse) up to 9 hours after drug administration, and data were analyzed via a naïve pooled pharmacokinetic model.

Results—In the clinical phase, the apparent terminal half-life (t½) of morphine was approximately 1.5 hours, volume of distribution per bioavailability was approximately 4.5 L/kg, and clearance per bioavailability was approximately 35 mL/kg/min. Peak plasma concentration in naïve pooled analysis was 21.6 ng/mL and occurred approximately 4 minutes after administration. Morphine concentrations were below the limit of quantification ≤ 7 hours after administration in 74 horses. Adverse effects attributed to morphine administration were uncommon and considered mild.

Conclusions and Clinical Relevance—The short t½ of morphine in horses suggested frequent administration may be needed to maintain targeted plasma concentrations. Variations in plasma concentrations suggested optimal dosages may differ among horses. The drug was well tolerated at the described dose, but patients receiving morphine should be monitored carefully.

Full access
in Journal of the American Veterinary Medical Association

Abstract

Objective

To investigate the effect of a mask and pneumotachograph on ventilation, respiratory frequency, and tracheal and nasopharyngeal pressures in horses running on a treadmill.

Design

Six horses ran at 50, 75, and 100% of the speed that resulted in maximum oxygen consumption, with and without a mask and pneumotachograph. Tracheal and pharyngeal inspiratory and expiratory pressures, respiratory frequency, and arterial blood gases were measured.

Animals

Six Standardbred horses.

Procedure

Oxygen consumption was measured during an incremental exercise test to determine the speed that resulted in maximal oxygen consumption for each horse. Tracheal and pharyngeal pressures were measured, using transnasal tracheal and pharyngeal side-hole catheters connected to differential pressure transducers. Carotid arterial blood samples were collected and PaO2 , PaCO2 , and pH were measured with a blood gas analyzer.

Results

Peak tracheal and pharyngeal inspiratory pressures were significantly more negative, peak tracheal and pharyngeal expiratory pressures were significantly more positive and respiratory frequency was significantly lower (all P < 0.05) at all speeds when horses wore a mask The PaCO2 , was higher and arterial pH and PaO2 , were lower (P < 0.05) when horses wore a mask.

Conclusions

The mask and pneumotachograph altered upper airway pressures, respiratory frequency, and ventilation in horses running on a treadmill.(Am J Vet Res 1996; 57: 250-253)

Free access
in American Journal of Veterinary Research

Summary

Effects of low-flow ischemia and reperfusion of the large colon on systemic and colonic hemodynamic and metabolic variables were determined in horses. Twenty-four adult horses were randomly allocated to 3 groups: sham-operated (n = 6), 6 hours of ischemia (n = 9), and 3 hours of ischemia and 3 hours of reperfusion (n = 9). Low-flow ischemia was induced in groups 2 and 3 by reducing colonic arterial blood flow to 20% of baseline. Heart rate, arterial blood pressures, cardiac index, pulmonary artery pressure, right atrial pressure, and colonic blood flow were monitored. Arterial, mixed-venous, and colonic venous blood gas and oximetry analyses; PCV; and blood lactate and pyruvate and plasma total protein concentrations were measured. Data were recorded, and blood samples were collected at baseline and at 30-minute intervals for 6 hours; additionally, data were collected at 185, 190, and 195 minutes (corresponding to 5, 10, and 15 minutes of reperfusion in group-3 horses). There were no differences among groups at baseline or across time for any systemic hemodynamic or metabolic variable. Colonic blood flow did not change across time in group-1 horses. Colonic blood flow significantly (P < 0.05) decreased to 20% of baseline at induction of ischemia in horses of groups 2 and 3 and remained significantly decreased throughout the ischemic period in horses of groups 2 (6 hours) and 3 (3 hours). Colonic blood flow significantly (P < 0.05) increased above baseline by 5 minutes of reperfusion in group-3 horses. Colonic oxygen delivery and oxygen consumption, and colonic venous pH, Po2 percentage saturation of hemoglobin, and oxygen content were significantly (P < 0.05) decreased within 30 minutes after induction of ischemia in horses of groups 2 and 3; colonic venous Po2 colonic oxygen extraction ratio, and lactate and pyruvate concentrations were significantiy (P < 0.05) increased by 30 minutes of ischemia. These alterations continued throughout ischemia, but within 5 minutes of reperfusion in group-3 horses, these variables either returned to baseline (pH, Pco2 lactate, pyruvate), significantly (P < 0.05) increased above baseline (Po2 oxygen content, % saturation of hemoglobin), or significantly (P < 0.05) decreased below baseline (colonic oxygen extraction ratio). Colonic oxygen consumption remained decreased during reperfusion in group-3 horses. Colonic mucosal ischemia-reperfusion injury observed in this model of ischemia was associated with local colonic hemodynamic and metabolic alterations in the presence of systemic hemodynamic and metabolic stability. Reactive hyperemia was observed at restoration of colonic blood flow in group-3 horses and persisted during reperfusion. Colonic venous metabolic alterations were corrected at reperfusion, indicating adaptation of the colon to the return of blood flow and oxygen delivery with resultant decrease in anaerobic metabolism. The early alterations in these variables may simply represent a washout of metabolic by-products.

Free access
in American Journal of Veterinary Research

Summary

Pharyngeal or esophageal trauma was diagnosed in 9 horses after nasogastric intubation. Evidence of trauma (edema or ulceration) was detected in the pharynx of 3 horses and in the esophagus of 6 horses. Complications associated with nasogastric intubation were first observed in 5 horses while they were intubated and in 4 horses after extubation. Clinical signs of pharyngeal or esophageal trauma were similar, and included salivation, bruxism, coughing, and nasal discharge. Treatment, including extubation, enteral feeding through a small nasogastric tube, or esophagostomy distal to the affected site, was attempted in 6 horses. Three of 6 treated horses survived, but 4 of 5 horses with perforated esophagus were euthanatized.

Free access
in Journal of the American Veterinary Medical Association

Abstract

Objective—To determine survival rate and athletic ability after nonsurgical or surgical treatment of cleft palate in horses.

Design—Retrospective case series.

Animals—55 horses with cleft palate.

Procedures—13 of the 55 horses died or were euthanized without treatment and were not included in all analyses. Medical records were reviewed for signalment, history, method of diagnosis, soft or hard palate involvement, type of surgical procedure performed, postoperative complications, and survival to hospital discharge. Information on athletic ability was acquired from race records and follow-up conversations with owners, trainers, or referring veterinarians.

Results—The predominant reason for initial evaluation was milk or feed in the nostrils (60%). The diagnosis was confirmed by means of videoendoscopy of the upper portion of the airway in all cases. Most cases involved the soft palate only (92.7%). Twenty-six of the 55 (47.3%) horses underwent surgical repair, and 12 of these had dehiscence at the caudal edge of the soft palate. Among potential racehorses, 14 of 33 had surgery. Of these, 12 of 14 survived to discharge and 2 horses raced. Among potential racehorses, 10 of 33 were discharged without surgery and 2 of these raced. Among nonracehorses, 12 of 22 underwent surgery and 11 survived to discharge. All horses that were discharged and for which follow-up information was available survived to 2 years of age or older without ill thrift despite dehiscence at the caudal edge of the soft palate and continued mild nasal discharge.

Conclusions and Clinical Relevance—Horses with cleft palate had a higher survival rate than previously reported.

Full access
in Journal of the American Veterinary Medical Association

Summary

Medical records of 59 racehorses with noncomminuted midsagittal proximal phalanx fractures repaired by means of lag screw fixation between 1973 and 1991 were reviewed. Fractures were classified as short incomplete fractures (7), long incomplete fractures (32), complete fractures extending into the proximal interphalangeal joint (13), and complete fractures extending through the lateral cortex of the proximal phalanx (7). Time from fracture repair to first race following fracture repair, number of racing starts, and fastest race times before and after surgery were obtained from race records and compared among horses grouped by fracture type and between horses that returned to racing and those that did not race. Five horses with short incomplete fractures, 21 horses with long incomplete fractures, 6 horses with complete fractures extending into the proximal interphalangeal joint, and 5 horses with complete fractures extending to the lateral cortex returned to racing. A significantly lower percentage of horses returned to racing following repair of complete fractures extending into the proximal interphalangeal joint (46%), than following repair of short incomplete fractures (71%), long incomplete fractures (66%), or complete fractures extending to the lateral cortex (71%). Time from fracture to repair for horses that returned to racing (mean, 14.7 days; range, 1 to 60 days) was not significantly different from that for horses that did not race (mean, 5.8 days; range, 1 to 21 days). For all fracture groups, median number of races before injury was not significantly different from median number of races after repair, and median fastest race time before fracture was not significantly different from median fastest race time after fracture repair.

Free access
in Journal of the American Veterinary Medical Association

SUMMARY

Twenty-four horses were randomly allocated to 3 groups. Horses were anesthetized, subjected to a ventral midline celiotomy, and the large colon was exteriorized and instrumented. Group-1 horses served as sham-operated controls. Group-2 horses were subjected to 6 hours of low-flow colonic arterial ischemia, and group-3 horses were subjected to 3 hours of ischemia and 3 hours of reperfusion. Baseline (bl) samples were collected, then low-flow ischemia was induced by reducing ventral colonic arterial blood flow to 20% of bl. All horses were monitored for 6 hours after bl data were collected. blood samples were collected from the colonic vein and main pulmonary artery (systemic venous [sv]) for measurement of plasma endotoxin, 6-keto prostaglandin F (6-kPG), thromboxane B2 (txb 2), and prostaglandin E2 (pge 2) concentrations. Tumor necrosis factor and interleukin-6 activities were measured in colonic venous (cv) serum samples. Data were analyzed, using two-way anova, and post-hoc comparisons were made, using Dunnett's and Tu- key's tests. Statistical significance was set at P < 0.05. Endotoxin was not detected in CV or sv plasma at any time. There was no detectable tumor necrosis factor or interleukin-6 activity in CV samples at any time. There were no differences at bl among groups for CV or sv 6-kPG, pge 2, or txb 2 concentrations, nor were there any changes across time in group-1 horses. Colonic venous 6-kPG concentration increased during ischemia in horses of groups 2 and 3; CV 6-kPG concentration peaked at 3 hours in group-3 horses, then decreased during reperfusion, but remained increased through 6 hours in group-2 horses. Systemic venous 6-kPG concentration increased during reperfusion in group-3 horses, but there were no changes in group- 2 horses. Colonic venous pge 2 concentration increased during ischemia in horses of groups 2 and 3, and remained increased for the first hour of reperfusion in group-3 horses and for the 6-hour duration of ischemia in group-2 horses. There were no temporal alterations in sv pge 2 concentration. There was no difference in CV or sv ixb2 concentration among or within groups across time; however, there was a trend (P = 0.075) toward greater CV txb 2 concentration at 3.25 hours, compared with bl, in group-3 horses. Eicosanoid concentrations were significantly lower in sv, compared with CV plasma. Prostaglandin E2 and 6-kPG concentrations were approximately 3 to 8 and 5 to 10 times greater, respectively, in CV than in sv plasma. The increased concentrations of 6-kPG and pge 2 in CV plasma were likely attributable to their accumulation secondary to colonic ischemia. The increased values of these vasodilator eicosanoids may have a role in the reactive hyperemia observed during reperfusion. The increased 6-kPG concentration in sv plasma may represent spillover from the colonic vasculature, but more likely reflects systemic production.

Free access
in American Journal of Veterinary Research

SUMMARY

Thirty horses were randomly assigned to 1 of 5 groups. All horses were anesthetized and subjected to ventral midline celiotomy, then the large colon was exteriorized and instrumented. Colonic arterial blood flow was reduced to 20% of baseline (bl) and was maintained for 3 hours. Colonic blood flow was then restored, and the colon was reperfused for an additional 3 hours. One of 5 drug solutions was administered via the jugular vein 30 minutes prior to colonic reperfusion: group 1, 0.9% NaCl; group 2, dimethyl sulfoxide: 1 g/kg of body weight; group 3, allopurinol: 25 mg/kg; group 4, 21-aminosteroid U-74389G: 10 mg/kg; and group 5, manganese chloride (MnCl2): 10 mg/kg. Hemodynamic variables were monitored and recorded at 30-minutes intervals. Systemic arterial, systemic venous (sv), and colonic venous (cv) blood samples were collected for measurement of blood gas tensions, oximetry, lactate concentration, Pcv, and plasma total protein concentration. The eicosanoids, 6-keto prostaglandin F, prostaglandin E2 and thromboxane B2, were measured in cv blood, and endotoxin was measured in cv and sv blood. Full-thickness biopsy specimens were harvested from the left ventral colon for histologic evaluation and determination of wet weight-to-dry weight ratios (WW:DW). Data were analyzed, using two-way ANOVA for repeated measures, and statistical significance was set at P < 0.05. Heart rate, mean arterial pressure, and cardiac output increased with MnCl2 infusion; heart rate and cardiac output remained increased throughout the study, but mean arterial pressure returned to bl values within 30 minutes after completion of MnCI2 infusion. Other drug-induced changes were not significant. There were significant increases in mean pulmonary artery and mean right atrial pressures at 2 and 2.5 hours in horses of all groups, but other changes across time or differences among groups were not observed. Mean pulmonary artery pressure remained increased through 6 hours in all groups, but mean right atrial pressure had returned to bl values at 3 hours. Mean colonic arterial pressure was significantly decreased at 30 minutes of ischemia and remained decreased through 6 hours; however, by 3.25 hours it was significantly higher than the value at 3 hours of ischemia. Colonic arterial resistance decreased during ischemia and remained decreased throughout reperfusion in all groups; there were no differences among groups for colonic arterial resistance. Colonic venous Po2, oxygen content, and pH decreased, and Pco2 and lactate concentration increased during ischemia but returned to bl values during reperfusion. Compared with bl values, colonic oxygen extraction ratio was increased from 0.5 to 3 hours. By 15 minutes of reperfusion, colonic oxygen extraction ratio had decreased from the bl value in all groups and either remained decreased or returned to values not different from bl through 6 hours. Colonic venous 6-keto prostaglandin F and prostaglandin E2 concentrations increased during ischemia, but returned to bl on reperfusion; there were no changes in thrombox- ane2 concentration among or within groups. Endotoxin was not detected in cv or sv blood after ischemia or reperfusion. There were no differences among or within groups for these variables. Low-flow ischemia and reperfusion (i-r) of the large colon caused mucosal injury, as evidenced by increases in percentage of surface mucosal disruption, percentage depth of mucosal loss, mucosal hemorrhage, mucosal edema, mucosal interstitial-to-crypt ratio, mucosal neutrophil index, submucosal venular neutrophil numbers, and mucosal cellular debris index. There was a trend (P = 0.06) toward greater percentage depth of mucosal loss at 6 hours in horses treated with dimethyl sulfoxide, compared with the vehicle control solution. There were no differences in the remainder of the histologic variables among groups. Full-thickness and mucosal WW:DW increased with colonic I-R, but there were no differences among groups. There was a trend (P = 0.09) toward neutrophil accumulation, as measured by myeloperoxidase activity, in the lungs after colonic I-R, but there were no differences among groups. There was no change in lung WW:DW after colonic I-R. There were no beneficial effects of drugs directed against oxygen-derived free radical-mediated damage on colonic mucosal injury associated with low-flow I-R. Deleterious drug-induced hemodynamic effects were not observed in this study.

Free access
in American Journal of Veterinary Research

Summary

Histomorphologic/morphometric evaluation, leukocyte scintigraphy, and myeloperoxidase activity were used to determine whether neutrophils accumulate in the large colon of horses during low-flow ischemia and reperfusion. Twenty-four adult horses were assigned to 1 of 3 groups: group 1, sham-operated (n = 6); group 2, 6 hours of ischemia (n = 9); and group 3, 3 hours of ischemia and 3 hours of reperfusion (n = 9). Low-flow ischemia of the large colon was induced in horses of groups 2 and 3 by reducing colonic arterial blood flow to 20% of baseline. Radiolabeled (99mTc) autogenous neutrophils were injected at 175 minutes, which corresponded to 5 minutes prior to reperfusion in group-3 horses. Full-thickness biopsy specimens of the left ventral colon were collected at baseline and at 30-minute intervals for 6 hours; a portion of the biopsy specimen was placed in formalin for histologic examination, and the remainder was used to measure mucosal radioactivity and myeloperoxidase activity. There were no differences in baseline mucosal neutrophil index, mucosal neutrophil numbers, submucosal venular neutrophil numbers, mucosal radioactivity, or mucosal myeloperoxidase activity among groups, or over time in group-1 horses. Neutrophils accumulated in the colonic mucosa during ischemia and further increased at reperfusion, as indicated by neutrophil index (morphology) and mucosal neutrophil numbers (morphometry); mucosal neutrophil index was significantly (P < 0.05) greater in group-3 horses during reperfusion than at the corresponding periods of ischemia in group-2 horses. Neutrophil numbers were significantly (P < 0.05) increased in submucosal venules at 10 minutes of reperfusion in group-3 horses and were significantly (P < 0.05) greater in group-3 than in group-2 horses during the interval from 3 to 6 hours. Mucosal radioactivity significantly (P < 0.05) increased at reperfusion in group-3 horses; there was a trend (P = 0.076) toward greater mucosal radioactivity in group-3, compared with group-2 horses, throughout the 3- to 6-hour interval. There were no differences in mucosal myeloperoxidase activity among or within any of the 3 groups over time.

Neutrophils accumulated in the large colon of horses during low-flow ischemia and reperfusion. Neutrophil infiltration was detected by histologic examination and leukocyte scintigraphy, but not by measurement of myeloperoxidase activity. The accumulation of neutrophils during ischemia and the further neutrophil infiltration during reperfusion indicate that neutrophils may contribute to reperfusion injury of the large colon.

Free access
in American Journal of Veterinary Research