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Effect of carprofen administration during banding or burdizzo castration of bulls on plasma cortisol, in vitro interferon- production, acute-phase proteins, feed intake, and growth¹

W. Y. Pang^*,, B. Earley^*,2, T. Sweeney^, and M. A. Crowe^,

^* Teagasc, Grange Research Centre, Dunsany, Co. Meath, Ireland; and Faculty of Veterinary Medicine and and Conway Institute, University College Dublin, Belfield, Dublin 4, Ireland

	Abstract

Top Abstract INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
The objective of this study was to determine the effect of carprofen (C) administration before banding or burdizzo castration of bulls on cortisol, in vitro interferon- (IFN-) production, acute-phase proteins, feed intake, and growth. Fifty Holstein Friesian bulls (5.5 mo old; 191 ± 3.7 kg) were blocked by weight and assigned randomly to 1 of 5 treatments (n = 10/treatment): 1) untreated control (2) banding castration at 0 min (Band); 3) Band following an i.v. injection of 1.4 mg/kg of BW of C at –20 min (Band+C); 4) Burdizzo castration at 0 min (Burd); or 5) Burd following 1.4 mg/kg of BW of C at –20 min (Burd+C). Castration acutely increased plasma cortisol concentrations compared with control; no significant differences occurred in peak and interval to peak cortisol responses between Band and Band+C or Burd and Burd+C groups. The administration of C in Band+C reduced (P < 0.05) the cortisol concentration between 6 and 12 h postcastration compared with Band animals. Overall, the integrated cortisol response was greater (P < 0.05) in the castrates than in control, whereas C treatments tended to reduce this response compared with Band (P = 0.08) and Burd (P = 0.07), respectively. Plasma fibrinogen was elevated in Band animals on d 14 and in Burd animals on d 3 and 14. Carprofen administration reduced Band- and Burd-induced fibrinogen production on d 14 and 3, respectively. Plasma haptoglobin was elevated in Band animals on d 3 and 35 compared with control, and C adminstration was effective in reducing the haptoglobin elevation on d 35 in Band+C compared with Band. There were no differences among treatments in in vitro IFN- production induced by concanavalin A and phytohemagglutinin on d 1 and 2. Overall from d –1 to 16, there were no DMI differences among treatments. From d –1 to 35, there were no ADG differences among treatments. In conclusion, banding and burdizzo castration increased plasma cortisol with no change in in vitro IFN- production. Carprofen (1.4 mg/kg of BW) tended to reduce the integrated cortisol response, and it reduced cortisol secretion in banded animals between 6 and 12 h postcastration. There was an increased acute-phase protein production following castration; this response was effectively moderated by the administration of C before castration.

Key Words: acute-phase protein • carprofen • castration • cattle • interferon- • stress

	INTRODUCTION

Top Abstract INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Castration has been shown to elicit physiological stress, inflammatory reactions (indicated by acute phase proteins), pain-associated behavior, suppression of immune function [indicated by in vitro interferon- (IFN-) production], and a reduction in performance (Molony et al., 1995; Fisher et al., 1996; 1997) to varying degrees. Techniques used to castrate male cattle include surgical removal of the testicles (Jennings, 1984), the application of rubber rings or tightened latex bands (referred to as banding; Fell et al., 1986; Chase et al., 1995), and use of a burdizzo instrument to crush the testicular cords (Robertson et al., 1994).

Attempts to alleviate the undesirable effects of castration with analgesic achieved mixed results (Faulkner et al., 1992; Fisher et al., 1996). Earley and Crowe (2002) and Ting et al. (2003a, b) showed that systemic analgesia with ketoprofen, a nonsteroidal anti-inflammatory drug (NSAID) with a half-life of 30 min, was more effective than local anesthesia or caudal epidural anesthesia in reducing inflammatory responses associated with burdizzo and surgical castration of bulls. Carprofen, (C; 6-chloro-alpha-methyl-9H-carbazole-2-acetic acid), also an NSAID, has an elimination half-life in the range of 44.5 to 64.6 h in cattle, which is longer than those of other NSAID used as veterinary drugs and hence could have a more moderating effect over a longer period.

The objective of this study was to evaluate the effect of the antiinflammatory drug C on plasma cortisol, in vitro IFN- production from cultured blood leukocytes, acute-phase proteins, feed intake, and growth following the castration of bull calves. The hypothesis was that C would suppress the rise in plasma cortisol and prevent immune suppression (in terms of in vitro IFN- production) without altering blood hematology following banding or burdizzo castration.

	MATERIALS AND METHODS

Top Abstract INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Treatments
Fifty Holstein Friesian bulls (5.5 mo old; 191 ± 3.7 kg) were blocked by weight and randomly assigned to 1 of 5 treatments (n = 10/treatment): 1) untreated control (2) banding castration at 0 min (Band); 3) Band following an i.v. injection of 1.4 mg/kg of BW of C at –20 min (Band+C); 4) Burdizzo castration at 0 min (Burd); or 5) Burd following 1.4 mg/kg of BW of C at –20 min (Burd+C). All procedures were conducted under experimental license from the Irish Department of Health in accordance with the Cruelty to Animals Act, 1876, and the European Communities (Amendment of Cruelty to Animals Act, 1876) Regulations, 1994.

Animal Housing and Management
Bulls were housed in individual tie-stalls beginning on d 14 (day of treatment = d 0) to acclimate them to handling, restraint, and their novel housing environment. Animals had ad libitum access to water and grass silage (in vitro DM digestibility = 866 g/kg) supplemented with 1.5 kg of a barley-soybean concentrate (CP = 103.5 g of DM/kg) per animal daily. Individual silage intakes were recorded daily from d –14 to 16 (from d 17, the animals were turned out to grass) to determine DMI. Animals were weighed on d –14 before assignment to treatment, and on d –1, 7, 14, 21, 28, and 35 to determine ADG.

Experimental Procedures
The Band and Band+C animals were castrated (time = 0 min) with latex bands applied to the neck of the scrotum using the Callicrate Smart Bander (St. Francis, KS) following instrument guidelines. Burdizzo castration (time = 0 min) was performed in the Burd and Burd+C bulls following the procedure of Fisher et al. (1996). As part of the castration procedure, gentle manual restraint of the bulls was used. Carprofen was administered in Band+C and Burd+C bulls 20 min before castration at the rate of 1.4 mg of C/kg of BW (Rimadyl solution [50 mg/mL of C]; Pfizer Animal Health, Dublin, Ireland) via an indwelling jugular catheter followed by 2 mL of 0.9% sterile saline to flush the catheter. Catheterization was performed on d –1 following the procedure of Ting et al. (2003b). Precise dose rates for C were determined based on the BW of each animal obtained on d –1 of the study. Animals not receiving C in Band, Burd, and control groups were given an equivalent volume of sterile 0.9% saline solution via the jugular catheter. Animals in the control group were sham-handled for a period equivalent to the time required to perform the castration procedure in the remaining treatment groups.

On d 0, jugular venous blood samples (heparinized plasma) were collected from each bull at –2, –1.5, –1, –0.5, –0.25, 0, 0.25, 0.5, 0.75, 1, 1.5, 2, 2.5, 3, 3.5, 4, 4.5, 5, 5.5, 6, 6.5, 7, 7.5, 8, 10, 12, 24, and 72 h relative to the time of castration for subsequent cortisol assay. Heparinized blood samples for stimulated leukocyte production of IFN- and EDTA blood samples for routine hematology were collected before treatment on d 0 and on d 1 and 3. Further blood samples for hematology (see below) were collected on d 7, 14, 21, 28, and 35. Samples collected after d 1 were always taken between 0800 and 0900 GMT. Plasma samples were separated by centrifugation at 1,600 x g at 8°C for 15 min and subsequently stored at –20°C until assayed. Rectal temperatures (RT) of each bull were monitored with a digital electronic thermometer (Jørgen Kruuse A/S model VT-801 BWC; Marslev, Denmark) on d –1, –2 h before castration, 12 h after treatment, and on d 1, 2, 3, 7, 14, 21, 28, and 35.

Plasma Cortisol
Plasma cortisol concentrations were determined using a commercially available RIA kit (Corti-cote; ICN Pharmaceuticals, Orangeburg, NY) adapted and validated for bovine plasma (Fisher et al., 1996). The intraassay CV (n = 6) for samples containing 4.9, 17.3, and 51.7 ng/mL of cortisol were 15.3, 10.3, and 7.5%, respectively, and the interassay CV (n = 10) for the same samples were 10.9, 8.6, and 5.9%. For each calf, the peak post-treatment cortisol concentration was recorded, and the area under the curve (AUC) for cortisol vs. time (ng·mL^–1·h) was calculated for the pretreatment period from –2 h to 0 h, and for above the pretreatment baseline from 0 to 2 h, 0 to 4 h, 2 to 6 h, 6 to 12 h, and 0 to 12 h using the linear trapezoidal rule (Friend et al., 1977).

In Vitro IFN- Production
The stimulated lymphocyte production of IFN- was determined from harvested supernatant following a whole-blood culture (Wood et al., 1990). Duplicate 1.48-mL aliquots of heparinized blood were cultured in sterile 24-well flat culture plates (Sarstedt Ltd., Drinagh, Wexford, Ireland) with 20 µL of PBS (GibcoBRL, Life Technologies Ltd., Paisley, Scotland) containing either 1 mg/mL of phytohemagglutinin (PHA, product No. L-9132, Sigma-Aldrich, Inc., St. Louis, MO) or 1 mg/mL of concanavalin A (ConA; Sigma-Aldrich, Inc., product No. C 5275) or no additive for 24 h at 37°C in an atmosphere of 5% CO₂ in air. Aseptic techniques were practiced during this procedure under laminar flow conditions. The culture plates were then centrifuged at 1,600 x g at 4°C for 20 min; the supernatant was harvested and frozen at –20°C until it was assayed for IFN- production using an ELISA procedure (Rothel et al., 1990; catalogue No. 03000201, Bovigam, CSL Biosciences, Victoria, Australia). The in vitro PHA- and ConA-stimulated IFN- production was calculated by subtracting the absorbance at 450 nm of wells that received PBS alone from the absorbance of wells that received either PHA or ConA.

Acute-Phase Proteins
Plasma haptoglobin concentrations were measured using an assay kit (Tridelta Development Ltd., Wicklow, Ireland) on an automated analyzer (spACE; Alfa Wassermann, Inc., West Caldwell, NJ) according to the manufacturer’s procedure. The intraassay CV (n = 10) for samples containing 0.23 g/L and 0.97 g/L was 1.36% and 0.09%, respectively, and the interassay CV (n = 10) for the same samples was 11% and 6.9%, respectively. Plasma fibrinogen concentrations were measured according to the method described by Becker et al. (1984) on an automated analyzer (spACE). The intraassay CV (n = 3) for samples containing 266.4 mg/dL and 679.8 mg/dL was 4 and 4.2%, respectively, and the interassay CV (n = 13) for the same samples was 9.4 and 13%, respectively.

Routine Hematology
Red blood cell (RBC) number, white blood cell (WBC) number, differential WBC (percentage granulocyte, percentage monocyte, and percentage lymphocyte), packed cell volume, hemoglobin concentration, mean corpuscular volume, and platelet numbers were determined for unclotted (EDTA-treated) whole-blood samples with an automated cell counter (Celltac MEK-6108K; Nihon-Kohdon, Tokyo, Japan) within 1 to 2 h of blood sampling. Thin blood smears were also prepared on glass slides and stained using the hematology 3-step stain for differential WBC counts (Accralab, Biochemical Sciences; Fisher Scientific Company, Middletown, VA).

Statistical Analyses
All statistical analyses were performed using SAS V8.2 (SAS Inst. Inc., Cary, NC). Data that departed from the assumptions of normality and/or homogeneity of variance were subjected to appropriate transformations before ANOVA. Appropriate transformation was performed to get normality for the data if the raw data were not normally distributed [tested using the SAS procedure of "Proc univariate data = (variable data names) normal plot;"]. Data relating to the peak cortisol and interval to peak cortisol were analyzed by ANOVA using a randomized complete-block design for the main effect of treatment at each individual time point (Steel and Torrie, 1960). The hematological variables (RBC number, log₁₀ of WBC number, angular transformed {x = (180/) x arcsin [(p/100)], where p is a percentage [0 < p < 100; = 3.1416]} differential WBC subpopulations, packed cell volume, hemoglobin concentration, mean corpuscular volume, and platelet number), plasma haptoglobin, plasma fibrinogen, AUC for cortisol, log₁₀(x+1) of IFN- production, rectal temperature, ADG, and DMI data were similarly analyzed by ANOVA with the pretreatment values included as covariates. Following an F-test, Fisher’s least significant difference test was applied to determine statistical differences between treatments (Steel and Torrie, 1960). A probability of P < 0.05 was chosen as the level of significance for the statistical tests.

	RESULTS

Top Abstract INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Plasma Cortisol
Plasma cortisol response (i.e., AUC) from –2 to 0 h was similar (P = 0.52) among treatments. From 0 to 2 h following castration, cortisol AUC in the castrated animals increased acutely (Table 1) and was greater (P < 0.001) than in control; additionally, Band animals had greater (P = 0.001) AUC compared with Burd animals. The administration of C during the same period failed to prevent the elevation of cortisol in both the Band+C (P = 0.15) and Burd+C (P = 0.51) animals. From 0 to 4 h following castration, Band (P < 0.001) and Burd (P = 0.01) animals had greater AUC than control animals; in addition, Band animals had greater (P = 0.001) AUC compared with Burd animals. The administration of C during the same time period failed to prevent the elevation of cortisol in both the Band+C (P = 0.16) and Burd+C (P = 0.27) animals. From 2 to 6 h postcastration, Band animals had greater (P < 0.05) AUC than control animals. The administration of C in Band+C had no effect, though their AUC values were not different from control. From 6 to 12 h after castration, Band and Burd animals had greater (P < 0.05) cortisol response compared with control animals, and the administration of C to Band animals reduced the AUC at the same time period in comparison with Band animals. Peak cortisol concentrations were greater (P < 0.05) in all castration treatments than in control, and C administration had no effect on this parameter (Figure 1). The intervals to peak cortisol concentrations in Band-castrated animals were greater than (P < 0.001) in Burd-castrated animals. Overall, the integrated cortisol response (i.e., AUC) from 0 to 12 h was greater (P < 0.05) in all castrated animals except Burd+C animals compared with control animals. The provision of C tended to reduce the integrated cortisol response in Band+C (P = 0.08) and Burd+C (P = 0.07) animals compared with Band and Burd animals, respectively (Table 1). On d 1, the mean cortisol concentration of Band and Burd animals was still greater (P = 0.03; P = 0.01; respectively) than control. Carprofen was not effective in reducing cortisol concentration during this same period, though Band+C and Burd+C groups were not different from control (Figure 1). On d 3, mean cortisol concentration of Burd animals was greater (P = 0.001) than control, while Burd+C animals had lower (P < 0.05) cortisol concentration compared with Burd animals.

View larger version (28K): [in this window] [in a new window]   Figure 1. The effect of no treatment (Con), banding castration (Band), banding castration following carprofen (C) administration (Band+C), Burdizzo castration (Burd), or Burdizzo castration following C administration (Burd+C) on mean ± SE plasma cortisol concentrations in 5.5-mo-old bulls. The integrated plasma cortisol responses (area under the curve) were greater (P < 0.05) among castrated animals, except for Burd+C animals, compared with control animals. Peak cortisol concentrations were greater (P < 0.05) among castration treatments compared with control.

Interferon-
There were no differences (P > 0.05) among treatments in IFN- production in response to either ConA from leukocytes cultured in whole-blood samples collected on d 0 before castration and on d 2, or in the response to PHA on d 0, 1, and 2 (Figure 2). On d 1, Burd animals had lower (P < 0.05) IFN- production in response to ConA compared with Band.

View larger version (38K): [in this window] [in a new window]   Figure 2. The effect of no treatment (Control), banding castration (Band), banding castration following carprofen (C) administration (Band+C), Burdizzo castration (Burd), or Burdizzo castration following C administration (Burd+C) on mean ± SE concanavalin- (ConA) and phytohemagglutinin- (PHA) induced interferon- production in 5.5-mo-old bulls. No differences were found except on d 1, on which Burd animals had lower (P < 0.05) interferon- production in response to ConA compared with Band.

On d 1, Burd+C animals had lower (P < 0.05) RBC numbers compared with Burd. On d 21, Burd+C animals had greater (P < 0.05) granulocyte percentage (Gr%) and lower Ly% compared with Burd. On d 28, Burd had higher (P < 0.05) platelet numbers than Burd+C.

The Band+C animals had lower (P < 0.05) Gr% and greater Ly% compared with Band on d 2 and 7. On d 7, Band animals had a greater (P < 0.05) percentage of monocytes compared with Band+C. On d 7 and 14, Band animals had lower (P < 0.05) platelet numbers compared with Band+C.

Average Feed Intake and Daily Gain
There was no difference (P = 0.18) in DMI among treatment groups from d-14 to 1 before treatment. There were no differences (P = 0.70 for d 0 to 6; P = 0.26 for d 7 to 16) in DMI among treatments before d 16, the day before the animals were put to grass (data not shown). There were no differences (P = 0.70, 0.36, 0.45, 0.14, and 0.53) for weeks 1, 2, 3, 4, and 5, respectively, in ADG among treatments (data not shown). Overall, from d –1 to 35, the mean ADG was lower (P < 0.05) in Band (0.41 ± 0.13 kg) compared with Burd (0.79 ± 0.13 kg) animals.

Rectal Temperature
Rectal temperature was similar (P > 0.84) among treatment groups on d –1 and –2 h before treatment (Table 3). At 12 h following treatment, Burd animals had greater (P < 0.05) RT compared with control. At d 1 postcastration, Band and Burd animals had higher (P < 0.05) RT than control. At d 2 following castration, all castrated animals had higher (P < 0.05) RT compared with control. There were no RT differences (P > 0.05) among treatments on d 3, 7, 14, 21, 28, and 35 (data not shown).

	DISCUSSION

Top Abstract INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

Carprofen tended to reduce the integrated cortisol AUC (0 to 12 h) but had no effect on peak plasma cortisol and the interval to peak cortisol in castrated animals. It was proposed that the carriage of protein-bound C into the inflamed area might be very significant and might result in a reservoir effect. Carprofen was effective in reducing the cortisol response induced by Band and Burd castration though only in a later period (6 to 12 h postcastration, and d 3, respectively). The findings are not supportive of our hypothesis regarding the attenuation of the cortisol response associated with castration.

The lack of effect of C (0.5 mg/kg of BW subcutaneously) on discomfort scores in newborn lambs castrated or tail docked with rubber rings was reported by Price and Nolan (2001), and they proposed this might be due to the low dose administered or that C might have been absorbed so slowly that therapeutic plasma concentrations were not achieved at the time of ring application. Previous studies in sheep (Dolan and Nolan, 1999) have suggested that NSAID might not be useful in management or in preventing ischemic pain. In contrast, it was reported that the provision of ketoprofen, also an NSAID, at 3 mg/kg of BW i.v. effectively reduced the integrated cortisol response to burdizzo castration (Ting et al., 2003b) and surgical castration (Earley and Crowe, 2002; Ting et al., 2003a). However, there was no advantage in treating either with 2 split doses of ketoprofen (1.5 mg/kg of BW per dose) or a repeated ketoprofen dose 24 h after 2 doses of 1.5 mg/kg of BW (Ting et al., 2003a). So, the efficacy of C might not be positively related to its long plasma half-life.

The mechanism of action of C in cattle is unknown but it is unlikely to involve inhibition of either cyclooxygenase (COX-1) or 12-lipoxygenase (Lees et al., 1996). Beretta et al. (2005) reported that in horses C is a selective inhibitor of cyclooxygenase subtype 2 (COX-2, which is induced in inflammatory conditions) rather than COX-1. Therefore, C will not affect the homeostatic functions of the prostanoids preferentially synthesised by COX-1 and will not induce gastrointestinal bleeding associated with COX-1 inhibition. Schatzmann et al. (1990) demonstrated an analgesic action of 0.7 mg/kg of i.v. C in horses for approximately 24 h, and concluded that total plasma C concentrations in excess of 1.5 µg/mL were required to provide an analgesic effect. Given that C has such a long half-life in cattle, improved analgesia might be obtained by injection at an earlier time than 20 min before castration, as used in this study, or by increased doses.

In this study, Band and Burd caused less acute-phase protein production than those reported in surgical castrations; hence this suggests that these 2 nonsurgical castration methods cause less inflammation compared with surgical methods. Plasma haptoglobin was elevated in Band animals on d 3 and 35 compared with control. Carprofen administration was effective in reducing the haptoglobin elevation in Band+C in comparison with Band. Following castration on d 3, fibrinogen concentration was elevated in Burd animals, and C administration was effective in suppressing this elevation in Burd+C animals. On d 14, Band and Burd animals had elevated fibrinogen compared with control animals. The C treatment was effective in reducing this fibrinogen response in the Band+C but not the Burd+C group. In contrast, Ting et al. (2003b) reported that the burdizzo castration-induced increase in plasma haptoglobin and fibrinogen on d 1 and 3 were consistent with previous reports findings in surgical castrations (Faulkner et al., 1992; Fisher et al., 1997; Earley and Crowe, 2002).

Haptoglobin production can be related to the magnitude of an inflammatory stimulus (Conner and Eckersall, 1988). The greater haptoglobin concentrations in Band compared with Burd animals on d 35 would suggest that Band causes longer inflammatory responses compared with Burd castration. The effect of C administration in reducing fibrinogen and haptoglobin would indicate C treatment is effective in reducing the magnitude of castration-induced inflammatory responses.

Immunological assessment is a useful indicator of cattle welfare (Amadori et al., 1997), and the establishment of protective immunity depends critically on IFN- (Arad et al., 1995). Interferon- is a cytokine produced by activated T lymphocytes and natural killer cells and helps to regulate immune responses to antigens (Clough and Roth, 1998). In the current study, there were no detectable differences in either ConA- or PHA-induced IFN- production among the castration treatments compared with control on d 0, 1, and 3. This would indicate that the responsiveness of the lymphocytes of the Band- and Burd-castrated animals was not compromised. By contrast, ConA-induced IFN- production in the Burdizzo-castrated animals was lower compared with control animals on d 1 (Ting et al., 2003b).

In general, there was no difference found in neutrophil:lymphocyte and other hematological parameters among treatments, which would indicate that the health of the animals was not compromised. Similarly, Ting et al. (2003b) found no difference in WBC numbers in burdizzo-castrated calves. In the current study, Band and Burd castrations did not significantly affect WBC numbers except on d 7; Band animals had greater WBC than Burd and control animals. Similarly, Macaulay (1989) reported greater total WBC for surgically or burdizzo-castrated calves than for sham-operated calves. On d 1 and 28, Band+C animals had greater WBC numbers than control. However, the administration of C in Burdizzo-castrated calves did not affect WBC counts.

On d 2, Band+C animals had lower Gr% compared with Band and Burd+C, and on d 7 Band animals had higher Gr% compared with Band+C, Burd, and control; there was no difference between Band+C and control. This would suggest that C administration could reduce Gr% in Band-castrated calves. However, on d 14, Burd+C animals had higher Gr% compared with control, and on d 21, Burd+C animals had higher Gr% compared with Burd. This would suggest that C was not effective in reducing Gr% in Burd calves.

Overall, from d 0 to 16, there was no difference in DMI or ADG among castrated groups compared with the control group. By contrast, Ting et al. (2003b) reported burdizzo castration resulted in reduced animal growth rate but no feed intake differences. The ADG was lower in Band compared with Burd animals, which is in agreement with the findings that Burdizzo castration appeared to produce the least pain compared with surgical and banding castrations (Robertson et al., 1994).

In conclusion, Banding and Burdizzo castrations acutely increased the secretion of cortisol with no suppression of ConA- and PHA-induced IFN- production from leukocytes in whole-blood cultures and no reduction in animal feed intakes and growth rates. Whereas C tended to reduce the overall cortisol response but had no effect on the initial peak response to castration, the elevation in acute-phase protein production caused by castration was effectively moderated by the administration of C. The results of the current study indicate that systemic analgesia using C failed to suppress the initial cortisol rise (from 0 to 6 h) but reduced acute phase protein production following castration. More studies are required to further explore the relationship between the administration of C and the timing of its analgesic effects relative to when castration is performed.

	Footnotes

 
¹ This study was supported by a Teagasc Walsh Fellowship to W. Y. Pang. The authors thank G. Claffey (Faculty of Veterinary Medicine, University College Dublin) for excellent technical help and assistance during the study. The authors also acknowledge the help from postgraduates and the excellent technical support and dedication of J. A. Farrell, J. Larkin, M. Murray, M. Nolan and D. Prendiville at Teagasc Grange. Many thanks are due to the farm staff at Teagasc Grange for care and management of the animals.

² Corresponding author: bearley{at}grange.teagasc.ie

Received for publication June 20, 2005. Accepted for publication September 20, 2005.

	LITERATURE CITED

Top Abstract INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 


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