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Objective—To evaluate effects of butorphanol, acepromazine, and N-butylscopolammonium bromide (NBB) on visceral and somatic nociception and duodenal motility in conscious, healthy horses.

Animals—6 adult horses.

Procedures—Visceral nociception was evaluated by use of colorectal distention (CRD) and duodenal distention (DD) threshold. Somatic nociception was evaluated via thermal threshold (TT). Nose-to-ground height, heart rate, and respiratory rate were also measured. Each horse received each treatment in randomized order; investigators were not aware of treatments. Butorphanol was administered IV as a bolus (18 μg/kg) followed by constant rate infusion at 13 μg/kg/h for 2 hours, whereas acepromazine (0.04 mg/kg), NBB (0.3 mg/kg), and saline (0.9% NaCl) solution (2 mL) were administered IV as a bolus followed by constant rate infusion with saline solution (10 mL/h) for 2 hours. Variables were measured before and for 3 hours after treatment. Data were analyzed by use of a 3-factor ANOVA followed by a Bonferroni t test for multiple comparisons.

Results—Nose-to-ground height decreased after acepromazine. Respiratory rate decreased after acepromazine and increased after butorphanol. Heart rate increased briefly after NBB. Some horses had an increase in TT after butorphanol and acepromazine, but there was not a significant treatment effect over time. Drug effect on DD or motility was not evident. The CRD threshold increased significantly at 5, 65, 155, and 185 minutes after acepromazine and from 5 to 65 minutes after NBB.

Conclusions and Clinical Relevance—Each drug caused predictable changes in sedation and vital signs, but consistent anti-nociceptive effects were not evident.

Full access
in American Journal of Veterinary Research


Objective—To compare cardiac output (CO) measured by use of the partial carbon dioxide rebreathing method (NICO) or lithium dilution method (LiDCO) in anesthetized foals.

Sample Population—Data reported in 2 other studies for 18 neonatal foals that weighed 32 to 61 kg.

Procedures—Foals were anesthetized and instrumented to measure direct blood pressure, heart rate, arterial blood gases, end-tidal isoflurane and carbon dioxide concentrations, and CO. Various COs were achieved by administration of dobutamine, norepinephrine, vasopressin, phenylephrine, and isoflurane to allow comparisons between LiDCO and NICO methods. Measurements were obtained in duplicate or triplicate. We allowed 2 minutes between measurements for LiDCO and 3 minutes for NICO after achieving a stable hemodynamic plane for at least 10 to 15 minutes at each CO.

Results—217 comparisons were made. Correlation (r = 0.77) was good between the 2 methods for all determinations. Mean ± SD measurements of cardiac index for all comparisons with the LiDCO and NICO methods were 138 ± 62 mL/kg/min (range, 40 to 381 mL/kg/min) and 154 ± 55 mL/kg/min (range, 54 to 358 mL/kg/min), respectively. Mean difference (bias) between LiDCO and NICO measurements was −17.3 mL/kg/min with a precision (1.96 × SD) of 114 mL/kg/min (range, −131.3 to 96.7). Mean of the differences of LiDCO and NICO measurements was 4.37 + (0.87 × NICO value).

Conclusions and Clinical Relevance—The NICO method is a viable, noninvasive method for determination of CO in neonatal foals with normal respiratory function. It compares well with the more invasive LiDCO method.

Full access
in American Journal of Veterinary Research


Objective—To determine the effects of dobutamine, norepinephrine, and vasopressin on cardiovascular function and gastric mucosal perfusion in anesthetized foals during isoflurane-induced hypotension.

Animals—6 foals that were 1 to 5 days of age.

Procedures—6 foals received 3 vasoactive drugs with at least 24 hours between treatments. Treatments consisted of dobutamine (4 and 8 μg/kg/min), norepinephrine (0.3 and 1.0 μg/kg/min), and vasopressin (0.3 and 1.0 mU/kg/min) administered IV. Foals were maintained at a steady hypotensive state induced by a deep level of isoflurane anesthesia for 30 minutes, and baseline cardiorespiratory variables were recorded. Vasoactive drugs were administered at the low infusion rate for 15 minutes, and cardiorespiratory variables were recorded. Drugs were then administered at the high infusion rate for 15 minutes, and cardiorespiratory variables were recorded a third time. Gastric mucosal perfusion was measured by tonometry at the same time points.

Results—Dobutamine and norepinephrine administration improved cardiac index. Vascular resistance was increased by norepinephrine and vasopressin administration but decreased by dobutamine at the high infusion rate. Blood pressure was increased by all treatments but was significantly higher during the high infusion rate of norepinephrine. Oxygen delivery was significantly increased by norepinephrine and dobutamine administration; O2 consumption decreased with dobutamine. The O2 extraction ratio was decreased following norepinephrine and dobutamine treatments. The gastric to arterial CO2gap was significantly increased during administration of vasopressin at the high infusion rate.

Conclusion and Clinical Relevance—Norepinephrine and dobutamine are better alternatives than vasopressin for restoring cardiovascular function and maintaining splanchnic circulation during isofluraneinduced hypotension in neonatal foals.

Full access
in American Journal of Veterinary Research


Objective—To evaluate the efficacy of omeprazole paste, a commonly used antiulcer drug, on intragastric pH in clinically normal neonatal foals.

Animals—6 clinically normal foals between 5 and 14 days of age.

Procedure—Intragastric pH was recorded in each foal by use of a disposable antimony pH electrode with internal reference. Values for intragastric pH were recorded every 4 seconds by use of an ambulatory pH monitor. There were two 24-hour recordings of intragastric pH for each foal, with 24 hours between recordings. Foals were not administered any drugs during the first recording. Foals were administered omeprazole paste (4 mg/kg, PO) 1 hour after the start of the second recording. Mean pH was calculated for each hour of each 24-hour recording session. Hourly mean values were compared between the first and second 24-hour recordings.

Results—Complete data were obtained from 4 of 6 foals during the first 24-hour recording and 6 of 6 foals during the second 24-hour recording. Foals had significantly higher mean hourly intragastric pH for hours 2 to 22 following omeprazole administration, compared with corresponding hourly pH values in foals during the first recording.

Conclusions and Clinical Relevance—Omeprazole paste can effectively increase intragastric pH in clinically normal neonatal foals within 2 hours after oral administration of the first dose and can be administered to neonatal foals at the rate of 4 mg/kg, PO, every 24 hours. (Am J Vet Res 2004;65:1039–1041).

Full access
in American Journal of Veterinary Research


Objective—To characterize intragastric pH profiles in critically ill foals and determine whether administration of ranitidine altered pH profiles.

Design—Prospective observational study.

Animals—23 hospitalized neonatal foals ≤ 4 days of age.

Procedure—Intragastric pH was measured continuously for up to 24 hours by use of an indwelling electrode and continuous data recording system. In 21 foals, ranitidine was administered IV.

Results—10 foals had predominantly or exclusively alkaline profiles, 10 had profiles typical of those reported for healthy foals, with periods of acidity (hourly mean pH < 5.0 at least once), and 3 had atypical profiles with periods of acidity. All 10 foals that had intragastric pH profiles typical of healthy foals survived, whereas only 2 foals with alkaline profiles survived, and none of the foals with atypical profiles survived. The effects of ranitidine administration could not be assessed in 13 foals because of a high baseline intragastric pH. In 7 of the remaining 9, ranitidine administration resulted in an alkalinizing response, but this response was often of blunted duration. Ranitidine administration did not appear to alter the intragastric pH profile in the remaining 2 foals.

Conclusions and Clinical Relevance—Results suggested that hospitalized critically ill foals often have intragastric pH profiles different from those reported for healthy foals and may respond differently to ranitidine administration than do healthy foals. Many critically ill foals have continuously alkaline intragastric pH profiles, questioning the need for prophylactic administration of ranitidine in all critically ill foals. (J Am Vet Med Assoc 2001;218:907–911)

Full access
in Journal of the American Veterinary Medical Association
in Journal of the American Veterinary Medical Association


Objective—To identify factors associated with short-term survival in bacteremic neonatal foals, evaluate the racing performance of Thoroughbred survivors, and evaluate changes in causative organisms and their antimicrobial susceptibility.

Design—Retrospective case series.

Animals—423 bacteremic foals.

Procedures—Medical records of foals that were hospitalized in 1982 through 2007 were reviewed, and those with bacteremia were included in the study. Data retrieved included signalment, physical examination and clinicopathologic findings at admission, localized infections, concurrent illnesses, duration of hospitalization, and outcome (survival to discharge from the hospital vs nonsurvival). The number, identity, and antimicrobial susceptibility of organisms isolated from blood samples were also obtained. Racing records for surviving Thoroughbred foals and maternal siblings were examined.

Results—Of 423 bacteremic foals, 254 survived. Odds of survival were negatively associated with age at admission, septic arthritis, band neutrophil count, and serum creatinine concentration and positively associated with year of admission, diarrhea, rectal temperature, neutrophil count, and arterial blood pH. Overall, microbial culture of blood samples yielded 554 isolates; Escherichia coli was consistently isolated most frequently. Percentage of isolates susceptible to enrofloxacin, but no other antimicrobial, decreased over time. Surviving Thoroughbred foals did not differ from siblings with regard to percentage of starters, percentage of winners, or number of starts; however, surviving foals had significantly fewer wins and total earnings.

Conclusions and Clinical Relevance—During the study period, microbial resistance to antimicrobials commonly used to treat bacteremic foals did not develop. Surviving bacteremic Thoroughbred foals were as likely to start races as their siblings but earned less money.

Full access
in Journal of the American Veterinary Medical Association
in Journal of the American Veterinary Medical Association


To determine intragastric pH in newborn foals and to examine the effect of IV or oral administration of an H2-receptor antagonist on intragastric pH.


Prospective controlled study.


6 healthy mixed-breed neonatal foals.


Intragastric pH was measured, using an antimony electrode. Foals were monitored on days 2, 4, and 6 after birth, and each received 3 treatments. The pH was recorded for 4 hours before treatment and for 10 hours after ranitidine administration (2 mg/kg [0.91 mg/lb] of body weight, IV; 6.6 mg/kg [3 mg/lb PO) or 20 hours after corn syrup administration. Mean and median pH and percentage of time pH was ≥ 4 were calculated.


Mean intragastric pH significantly increased for 5 hours after IV administration of ranitidine, compared with baseline data. Percentage of time intragastric pH was ≥ 4 increased significantly for 4 hours after ranitidine administration, and median pH increased significantly for hours 2 to 4 after administration. Oral administration of ranitidine significantly increased mean and median pH for hours 2 to 8 after administration and percentage of time pH was ≥ 4 for hours 2 to 7 after administration.

Clinical Implications

Neonatal foals have highly acidic gastric fluid. Intravenous or oral administration of ranitidine significantly increased intragastric pH for 4 and 8 hours, respectively. Suckling affected intragastric pH and underscored the need for frequent feeding of neonatal foals. (J Am Vet Med Assoc 1998; 212:1407–1412)

Free access
in Journal of the American Veterinary Medical Association