Kirkwood RN. Pharmacological intervention in swine reproduction. Swine Health Prod.1999;7(1):29-35.
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If gilts are known to be cyclic, the options to control estrus are breed-and-abort or feeding allyl trenbolone (Regumate(R)). For breed and abort, terminate pregnancy 25-30 days postbreeding with two injections of prostaglandin F2[alpha] (PGF2[alpha]), 6-8 hours apart. Gilts should return to estrus within 4-6 days with normal fertility. When feeding allyl trenbolone, you must ensure individual feeding so that gilts receive at least 15 mg (Regumate(R)) per day. There is probably no problem with overdosing, but underdosing (<13 mg per day) may cause cystic follicles. If gilts are known to be prepubertal, gonadotropin (PG600(R)) works well. If inducing estrus with gonadotropin, breed at the induced estrus but expect some possible depression in reproductive performance. If the gilts' cyclic status is unknown, gonadotropin can be used but there may be risks. If gilts are having silent heats, cystic follicles may form and the gilts will become infertile--treat for 14-18 days with allyl trenbolone followed by gonadotropin at withdrawal. Gonadotropin also works well after weaning of the first litter.Injection can be administered on the day of, or the day after, weaning. For farrowing induction, determine gestation length on each farm and do not inject PGF2[alpha] more than 2 days before due date. Inject a half-dose of PGF2[alpha] intravulvally at the beginning and end of the day (split-dose). Do not use oxytocin unless at least one pig has been born or continual supervision is practiced.
Keywords: swine, reproduction, pharmacology
Received: July 24, 1998
Accepted: October 8, 1998
This production tool provides practical guidelines for pharmacological intervention in swine reproduction and cites references to illustrate potential outcomes. The areas of reproduction to be addressed are the induction and control of estrus, interventions at breeding, and the control of farrowing. As an introductory statement, I wish to emphasize my belief that, where possible, the most rational strategy is one of no intervention. However, modern swine production practices are often dictated by economic forces that require some degree of strategic control. The swine practitioner's role is to know when and how best to intervene in order to gain the optimum return for the intervention dollar.
Exogenous hormones are an invaluable tool for the swine practitioner but if used inappropriately may result in production problems. When a reproduction problem is encountered, first look for and try to correct underlying causes before resorting to hormone administration. For the strategies described in this text, it is assumed that management problems either were not identifiable or were not correctable.
It is essential to thoroughly understand the estrous cycle before considering intervention. In simple terms, the 21-day porcine estrous cycle is composed of an approximately 16-day luteal phase and a 5-day follicular phase (Figure 1). During the luteal phase, the ovaries (corpora lutea) produce progesterone, which limits follicular development to the medium-sized follicle stage and so prevents the onset of estrus. At about 12-14 days of the luteal phase, uterine production of prostaglandin F2[alpha] (PGF2[alpha]) causes regression of corpora lutea and so terminates progesterone production. Removing the progesterone block allows resumption of appropriate secretory patterns of the pituitary gonadotropins, luteinizing hormone (LH), and follicle stimulating hormone (FSH) which, in turn, allows ovarian follicular development to be completed with the production of estrogen, ultimately resulting in behavioral estrus. In weaned sows, the wean-to-estrus interval is equivalent to the follicular phase of the estrous cycle. Approximately coincident with the onset of estrus, there is a surge release of LH, which causes a cascade of events within the follicle, including a switch from estrogen to progesterone production and also the production of intrafollicular PGF2[alpha], culminating with ovulation.
If gilts are known to be cyclic, the options for controlling estrus are limited to breed-and-abort and the feeding of allyl trenbolone. A prolonged luteal phase (pseudopregnancy) with induced luteolysis can also be induced, but this process is still largely experimental. Note that, unlike cattle, a single injection of PGF2[alpha] in pigs will not induce luteolysis before day 12 of the estrous cycle and so is of limited value. However, if required, one can reduce the length of the estrous cycle by 2-5 days by injecting PGF2[alpha] every 24 or 36 hours between days 6 and 10 of the cycle.1
For breed-and-abort, a successfully established pregnancy results in the endogenous production of progesterone, which will block estrus until pregnancy is terminated. In theory, pregnancy can be terminated at any time prior to term and the gilt should return to estrus 5-6 days later (but this may take as long as 10 days). However, uterine involution must occur after pregnancy. Although a gilt may return to estrus, if uterine involution is incomplete it may limit subsequent litter size by adversely affecting embryo/fetal survival. Also, terminating pregnancy after 25-30 days may raise ethical and aesthetic issues. If undertaken, terminate pregnancy 25-30 days postbreeding with a split dose of PGF2[alpha] (i.e., a half dose intravulvally a.m. and then again p.m.). Gilts should return to estrus in 4-6 days with normal fertility.2,3
Feeding allyl trenbolone (Regumate(R)) is an effective way to control estrus.4 Allyl trenbolone is an orally active progestagen; i.e., it mimics the biological activity of progesterone. While being fed, allyl trenbolone does not prevent normal luteolysis, but will continue to block the onset of estrus after luteolysis occurs. Ideally, gilts should be individually fed so that they consume at least 15 mg per day. While there is probably no problem with overdosing (except economic), underdosing allyl trenbolone (<13 mg per day) may cause cystic follicles.5,6 Anecdotal evidence suggests variable responses to allyl trenbolone in the field-- some producers report having good success while others do not. In all likelihood, producers who observe a poor response to allyl trenbolone treatment are not using it correctly. As stated above, a minimum intake of 15 mg per day by every treated gilt is essential. Since allyl trenbolone needs to be fed only from luteolysis, if cycle dates are known you can minimize allyl trenbolone feeding by only providing it from day 14 of the estrous cycle until 5 days before gilts are scheduled to be bred. Expect 90%-95% of gilts to achieve estrus on days 4-8 after the last feeding.7
In the start-up phase of large commercial units, it is important to produce pigs as soon as possible to maximize cash flow. In practice, this often means breeding gilts at their pubertal estrus in order to meet weekly breeding targets, even though research results suggest that this will reduce first litter sizes. If gilts are known to be prepubertal, treating with gonadotropin (e.g., PG600(R)) following the manufacturer's recommendations is quite effective for inducing estrus and ovulation. The exogenous gonadotropins act in the same manner as endogenous gonadotropins during the follicular phase of the estrous cycle (Figure 1). However, up to 30% of treated gilts do not show behavioral estrus (but will probably ovulate).8,9 Also up to 30% of those that demonstrate behavioral estrus will fail to cycle normally (i.e., will have an irregular return).9 Therefore, if inducing with gonadotropin, I recommend breeding at the induced estrus, but expect possible depression in farrowing rate and/or litter size.
This recommendation was recently tested by the Alberta Pork Research Centre.9 A 1200-sow startup herd reported a problem of delayed puberty, causing a failure to achieve breeding targets. The gilts in the replacement pool appeared well developed (>100 kg) at the site visit, and boar exposure was being managed appropriately (i.e., mature boars and direct contact). Because so many gilts were failing to achieve estrus, the clinical diagnosis was a failure to reach puberty rather than the occurrence of silent heats. Therefore, an intervention strategy employing gonadotropin was implemented. During a 19-day period, gilts in alternate pens received gonadotropin (PG600(R)) intramuscularly (IM), with remaining gilts serving as controls. Daily boar exposure continued for all gilts. At detection of estrus, gilts that received gonadotropin were assigned to be bred or allowed to cycle, depending on gilt breeding requirements. Control gilts were always bred at their first observed estrus. All breedings were by artificial insemination (AI) at the detection of estrus and 24 hours later.
Of the gonadotropin-treated gilts, 78% displayed estrus within 7 days (Table 1). Of the 171 gilts included in the study, 133 were bred and 99 conceived. Of the 34 nonconceiving gilts, 23 had regular returns and 11 had irregular returns. Of 38 nonbred gilts, 24 had a regular return-to-estrus and 14 had irregular returns. During this period, fewer control gilts were bred (84 of 224; P<.0001) but their conception rate was higher (P<.01) than for gonadotropin-treated gilts. The entry-to-service interval was similar for bred gonadotropin-treated and control gilts, but age at first service was lower (P<.02) for gonadotropin-treated gilts compared to controls (Table 1). Subsequent litter size was not affected by gonadotropin treatment (Table 1).
These data demonstrate that gonadotropin may provide an effective way to achieve breeding targets. However, when gilts are bred at the induced estrus, a significant depression in farrowing rate can be expected. Using the calculation:
proportion of gilts bred x farrowing rate x litter size,
as a crude measure of gilt productivity, piglet production from PG600(R)-treated gilts was:
0.78 x 0.744 x 9.4 = 5.46 pigs,
while from controls production was:
0.375 x 0.886 x 9.7 = 3.22 pigs.
This indicates that the ability to achieve breeding targets using gonadotropin outweighs a possible depression in fertility.
If the gilts' cyclic status is unknown, gonadotropin can be used successfully,10 but there may be risks. If gilts are having silent heats and are actually cyclic, cystic follicles may form after gonadotropin treatment (Foxcroft GR, personal communication, 1997). However, in contrast, in studies in which gonadotropins have been administered with the intention of inducing accessory corpora lutea at various days during the estrous cycle, the occurrence of cystic follicles was not mentioned and so, presumably, were not evident.11,12 Therefore, it is possible that cyclic gilts that have cystic follicles after gonadotropin treatment may have already been cystic at the time of gonadotropin injection. Further, it is possible that gilts that have silent heats respond to gonadotropic stimulation differently than gilts with normal cycles. The safe way with these gilts is to provide 14-18 days of allyl trenbolone, followed by gonadotropin at withdrawal. Doing this will greatly reduce/eliminate luteal phase gilts. The risk here is that you waste the cost of gonadotropin if they are cyclic or the cost of allyl trenbolone if they are not. Using PGF2[alpha] is of no value because <15% of gilts can be expected to be at the 12- to 15-day point of their cycle.
A common scenario is a small proportion of incoming gilts (5%-15%) failing to show estrus within a reasonable period after entry (e.g., 28 days). It has been suggested that these gilts are either having a silent estrus or are prepubertal but relatively infertile.4 In either case, an argument can be made that they should be culled. However, if there is pressure to keep them, and using allyl trenbolone (as outlined in the previous paragraph) is not possible, then a "last chance" injection of gonadotropin can be administered and they can be bred at the induced estrus. Any gilt failing to exhibit estrus by 7 days should be culled. If a well-developed gilt fails to show a natural estrus and then subsequently fails to respond to gonadotropic stimulation, she is not a reasonable candidate for becoming a productive and profitable sow. Any bred gilt that fails to conceive to the service should also, arguably, be culled as infertile.
Gonadotropins are most frequently used in sows at the weaning of the first litter, when longer and more variable wean-to-estrus intervals are often encountered. Several studies have examined this area and all agree that gonadotropin treatment results in a shorter and more synchronous onset of the postweaning estrus (Table 2).13-16 The day of injection (i.e., at weaning or the next day) has no effect on the response obtained.17 Although gonadotropin is an excellent tool for inducing a synchronous postweaning estrus, you should examine the herd records before using it to determine whether it would be cost effective or even necessary.
Gonadotropins are also used to induce estrus in weaned sows that experience prolonged wean-to-estrus intervals. There is little experimental evidence supporting the use of gonadotropins for this purpose. However, is has been shown that injecting sows not in estrus by 7 days after weaning with gonadotropin did not improve their reproductive performance (Table 3).18 These sows were probably infertile and gonadotropin treatment did not resolve this infertility.
A possible pharmacological intervention at breeding is the injection of oxytocin (5 IU intravulvally) at the time of AI. To perform an intravulval injection, we use a 20-g 0.5-inch needle and inject externally at the vulval-cutaneous junction. Research data have indicated that oxytocin treatment improved both farrowing rate and subsequent litter size (Table 4), especially for inexperienced technicians.19
In my clinical experience, I have observed a 5% increase in farrowing rate in two large start-up herds that received this intervention. However, these were not controlled studies. The use of oxytocin has been associated with adverse behavioral sow reactions (mild to extreme agitation) in 10%-15% of sows, reflecting the potency of this hormone and the likelihood of pain associated with its use. In contrast, the Alberta farms reported no adverse reactions. However, if adverse sow reactions are encountered, a low dose (25%-50%) of PGF2[alpha] intra-vulvally should be substituted for the oxytocin, which should provide the same benefit.20 The mechanism controlling this effect is not understood. However, since oxytocin will induce endogenous PGF2[alpha] production (and vice versa), it is likely that both hormones will advance the onset of ovulation and so will result in a better synchronization between insemination and ovulation.
Before implementing an induction program, first confirm a viable reason for doing so:
If farrowing is to be induced, do not use book values for gestation length; rather, determine gestation length on the individual farm and do not induce more than 2 days before the due date. Further, gestation must be periodically monitored, particularly in units with a high staff turnover. Calculate the gestation length from first breeding; depending on whether the sow is initially bred at the onset of estrus (and different personnel may differ in their subjective assessment of when estrus starts) or somewhat later, the breeding may vary by more than 24 hours relative to ovulation, resulting in an apparent change in mean duration of and/or increased variation in gestation length.
The ability to predictably induce farrowing will facilitate improved supervision and so reduce neonatal piglet mortality.21 The administration of PGF2[alpha] or its analogues has long been known to be effective for inducing parturition in sows,22 but a considerable range in the interval between treatment and parturition can still be expected. Indeed, fewer than 65% of induced sows are likely to farrow during normal working hours and so be candidates for farrowing supervision.21,23
Various additional treatments have been applied in attempts to improve the promptness of parturition after PGF2[alpha]. The injection of oxytocin approximately 24 hours after the injection of PGF2[alpha] has been shown to reduce the variation in the time to onset of parturition.24 However, while oxytocin causes a more rapid and synchronous onset of parturition, it often disrupts the process of piglet delivery, necessitating manual assistance.25-27 Injecting estradiol before or at the time of PGF2[alpha] administration inconsistently affects the onset or duration of parturition.28-30 The injection of carazolol, a [beta]-andrenergic blocking agent, was shown in sows to result in a prompt onset of labor and an acceleration of the parturition process.31,32 The mechanism whereby carazolol influenced farrowing has been suggested to involve the binding of myometrial [beta]-andrenergic receptors, thereby inhibiting the tocolytic effect of endogenous epinephrine released in response to the pain of parturition.32 Carazolol is not available in North America, so the Alberta Pork Research Centre is currently examining the potential benefits of other analgesics for the parturient process in sows.
It is now established that the intravulval injection of PGF2[alpha] at half the manufacturer's recommended dose is as effective as an IM injection at the full recommended dose for inducting parturition in sows.23,33 The reason for the efficacy of the lower PGF2[alpha] dose administered intra-vulvally possibly involves a higher local ovarian PGF2[alpha] concentration, since the venous drainage of the reproductive tract is greatly interconnected.34 Therefore, an intravulval injection would likely result in a relatively high PGF2[alpha] concentration in the uterine vein and thus, by countercurrent cycling, also in the ovarian artery. The Alberta Pork Research Centre is currently examining this hypothesis.
The forgoing discussion clearly indicates the efficacy of PGF2[alpha] for inducing parturition in sows. However, the relative lack of predictability should also be addressed. It is known from work in sheep that terminal luteolysis requires a pulsatile release of PGF2[alpha]. Further, it has been shown that a poor response to PGF2[alpha] is at least partially due to a failure to induce terminal luteolysis in some sows.30 Assuming a similar requirement for pulsatile PGF2[alpha] release in swine, a single PGF2[alpha] injection may occasionally fail to initiate this pulsatile endogenous PGF2[alpha] release. Therefore, if the luteolytic signal was reinforced, enhanced predictability should ensue.
Exogenous oxytocin has been shown to cause an endogenous release of PGF2[alpha] in sows in early gestation.35,36 Further, a recent study has shown that 6 hours after an initial PGF2[alpha] injection, a second PGF2[alpha] injection or an injection of oxytocin markedly improved the predictability of parturition (Table 5).37
In the first study, oxytocin did not precipitate more farrowings during the first 24 hours, and so the effect was not comparable to the known effect on uterine contraction and piglet delivery of oxytocin given 20-24 hours after PGF2[alpha] (i.e., stimulation of onset of piglet delivery). In a subsequent study, injection of oxytocin 6 hours after PGF2[alpha] injection reduced the incidence of late-responding sows but also increased the number farrowing on the day of induction.38 This indicates that the physiological response to oxytocin will depend on the proximity to natural onset of farrowing and, if natural farrowing is imminent, the uterine contraction/piglet delivery response may predominate. From these data, it would appear that the luteolytic signal (i.e., pulsatile PGF2[alpha] release) can be reinforced by either more PGF2[alpha] or more oxytocin. However, given the variable response to oxytocin, the split-dose PGF2[alpha] should be recommended.
Included in this section are protocols that show promise but are still under investigation. They should not be attempted until more information is available.
An alternative approach for estrus control and synchronization is to induce a prolonged luteal phase, and then induce luteolysis as required. To this end, ovulation and subsequent formation of corpora lutea will cause the production of progesterone, which will block estrus. If a prolonged luteal phase can be established, this progesterone production will be maintained until terminated by either a natural or induced luteolysis. A prolonged luteal phase can be established by the serial administration of estradiol between days 11 and 19 of the estrous cycle.39 However, this is labor intensive and estradiol is not cleared for use in pigs. Another way to induce a prolonged luteal phase may be administering a single dose of human chorionic gonadotropin (hCG) on day 12 of the estrous cycle.40 The mechanism involved is to induce follicular development and the endogenous production of estradiol.40 Because this is a cleared product that is simple to use and inexpensive compared to other protocols, this approach is attractive.
The Alberta Pork Research Centre has recently examined applying hCG in this manner.41 Forty-four PIC Camborough prepubertal gilts (86 kg [190 lb] bodyweight) were assigned either to receive
Boar exposure for estrus detection was implemented from day 15 until the end of the study and blood samples were obtained at 20 and 30 days for progesterone determination. Control gilts were allowed to cycle with no further intervention. Gilts receiving hCG and not showing estrus by day 30 received 175 cloprostenol (IM) to initiate luteolysis. Gilts returning between 17 and 24 days were considered to have had a cycle of normal duration. Gilts were slaughtered 5-10 days after their second estrus and their ovaries were recovered to determine ovulation rate.
Of the 20 control gilts, 16 had normal cycles, one had a short cycle (16 days), and three had long cycles (mean 30 days). Of the 24 hCG-treated gilts, one had a normal cycle, one had a short cycle (14 days), 15 had long cycles (mean 33 days), and seven were not detected in estrus and were considered to be the result of either estrus detection failure or failure of luteolysis. Of the 15 gilts exhibiting long cycles, two were detected as estrous on day 30 (day of PGF2[alpha] injection), five were estrous on day 31, and one was estrous on day 32. Since the objective of the PGF2[alpha] was to induce luteolysis and initiate the follicular phase, these extremely rapid responses suggest that natural luteolysis had already occurred. Therefore, while these data support the hypothesis that hCG administered at day 12 of the estrous cycle will effectively prolong the luteal phase, an extension of the estrous cycle beyond 28-30 days was not always realized. This contrasts with earlier data suggesting that a luteal phase of up to 60 days is possible when 1000 IU hCG was injected.40 The earlier work further noted that the interestrus interval was dependent on the dose of hCG and it is possible that with modern pigs and/or the product employed, the 1000 IU dose we used was too low. We are currently examining this protocol further.
Numbers of corpora lutea tended to be higher (P=.14) in treated gilts (13.6+/-0.7 for controls and 15.2+/-0.7 for hCG-treated). This suggests that inducing a prolonged luteal phase may provide a benefit similar to skip-a-heat. However, the impact on subsequent fertility and fecundity requires further research. Therefore, this protocol should not be attempted until further information is available.
Another exogenous hormone that may provide benefit at the time of breeding is GnRH (Table 6).42 At breeding at their second estrus, gilts received either
Breedings were by a single AI at the detection of estrus with a minimum dose of 3 x 109 spermatozoa. GnRH injection increased both farrowing rate and litter size. The mechanism(s) involved in these effects are not clear but earlier work with GnRH-treated primiparous sows noted an increase in both circulating progesterone and numbers of embryos.43
1. Gadsby J, Graffinger M, Almond GW. Induction of short cycles in pigs with prostaglandin F analogs. Proc 14th IPVS Cong. Bologna; 1996; 565.
2. Podany J, Vanicek J, Stejskal J, Jelenek L. Induction of abortion with prostaglandin F2[alpha] in gilts and their subsequent fertility. Theriogenology. 1982; 17:393-400.
3. Pressing AL, Dial GD, Stroud CM, et al. Prostaglandin-induced abortion in swine: Endocrine changes and influence on subsequent reproductive activity. Am J Vet Res. 1987; 48:45-50.
4. Foxcroft GR, Aherne FX, Kirkwood RN. Natural and hormonal synchronization of puberty, estrus and farrowing. Proc V Intl Symp Swine Reprod and AI. Mexico; 1998.
5. Davis DL, Knight JW, Killian DB, Day BN. Control of estrus in gilts with a progestogen. J Anim Sci. 1979; 49:1506-1509.
6. Kraeling RR, Dziuk PJ, Pursel VG, Rampacek GB, Webel SK. Synchronization of estrus in swine with allyl trenbolone (RU-2267). J Anim Sci. 1981; 52:831-835.
7. Martinat-Botte F, Bariteau F, Badouard B, Terqui M. Control of pig reproduction in a breeding programme. J Reprod Fertil (suppl). 1985; 33:211-228.
8. Tilton SL, Bates RO, Prather RS. Evalution of response to hormonal therapy in prepubertal gilts of different genetic lines. J Anim Sci. 1995; 73:3062-3068.
9. Kirkwood RN, Monaghan PG, Misutka SC. Use of PG600(R) to facilitate achievement of breeding targets. Proc 15th IPVS Cong. Birmingham; 1998; 3:404.
10. Rogozarski DZ, Tesic MM, Mirilovic MD, Novakovic RJ. The usage of hormonal medicines as stimulators of fertile oestrus with older gilts. Proc 14th IPVS Cong. Bologna 1996; 589.
11. Guthrie HD, Polge C. Control of oestrus and fertility in gilts with accessory corpora lutea by prostaglandin analogues, ICI 79,939 and ICI 80,996. J Reprod Fertil. 1976; 48:427-430.
12. Guthrie HD. Fertility after estrous cycle control using gonadotropin and prostaglandin F2[alpha] treatment in sows. J Anim Sci.1979; 49:158-162
13. Hurtgen JP, Leman AD. Use of PMSG in the prevention of seasonal post weaning anestrus in sows. Theriogenology. 1979; 12:207-214.
14. Lancaster RT, Foxcroft GR, Boland MP, et al. Fertility of sows injected with exogenous oestradiol and/or gonadotrophins to control post-weaning oestrus. Anim Reprod Sci. 1985; 8:365-373.
15. Kirkwood RN, Soede NM, Dyck GW, Thacker PA. The effect of immunoneutralization of PMSG at a gonadotropin-induced oestrus on the duration of ovulation and reproductive performance of sows. Anim Sci. 1995; 61:321-324.
16. Kirkwood RN, Aherne FX, Foxcroft GR. Effect of gonadotropin at weaning on reproductive performance of primiparous sows. Swine Health and Production. 1998; 6:51-55.
17. Kirkwood RN, Giebelhaus RJ. Day of injection does not affect the response of weaned sows to PG600(R). Swine Health Prod. 1998; 6:171-173.
18. Tubbs RC, Cox NM, Dyer K. Effect of PG600(R) on farrowing rate, litter size, and wean-to-service interval in sows with delayed (>7 days) wean-to-estrus interval. Proc 14th IPVS Cong. Bologna 1996; 579.
19. Flowers WL. Influence of oxytocin as a prebreeding stimulation for sows. J Anim Sci (suppl 1). 1996; 74: 236.
20. Pena FJ, Dominguez JC, Alegre B, Pelaez J. Effect of vulvomucosal injection of PGF2[alpha] at insemination on subsequent fertility and litter size in pigs under field conditions. Anim Reprod Sci. 1998; 52:63-69.
21. Holyoake PK, Dial GD, Trigg, T, King VL. Reducing pig mortality through supervision during the perinatal period. J Anim Sci. 1995; 73:3543-3551.
22. Ash RW, Heap RB. The induction and synchronization of parturition in sows treated with ICI 79.936, an analogue of prostaglandin F2[alpha]. J Agric Sci. (Cambridge) 1973; 81:365-368.
23. Kirkwood RN, Thacker PA, Aherne FX, Goonewardene LA. The effect of dose and route of administration of prostaglandin F2[alpha] on the parturient response of sows. Swine Health Prod. 1995; 4:123-126.
24. Holtz W, Hartmann FJ, Welp C. Induction of parturition in swine with prostaglandin analogues and oxytocin. Theriogenology. 1983; 19:583-592.
25. Dial GD, Almond GW, Hilley HD, et al. Oxytocin precipitation of prostaglandin-induced farrowing in swine: Determination of the optimal dose of oxytocin and optimal interval between prostaglandin F2[alpha] and oxytocin. Am J Vet Res. 1987; 48:966-970.
26. Welp C, ochle W, Holtz W. Induction of parturition in swine with a prostaglandin analog and oxytocin: a trial involving dose of oxytocin and parity. Theriogenology. 1984; 22:509-520.
27. Kirkwood RN, Thacker PA. Effect of propanolol on the onset and duration of parturition in sows. Can Vet J. 1995; 36:238-239.
28. Eckerle BT, Edgerton LA, Jacobs AL, Newton GR. Estrogen-induced delay of farrowing in swine. Theriogenology. 1992; 37:1205-1212.
29. Kirkwood RN, Thacker PA. Effects of prepartum oestradiol injection on parturition in sows and piglet survival. Anim Sci. 1995; 60:481-483.
30. Kirkwood RN, Aherne FX. The relationship between estrogen pretreatment and routeof administration of cloprostenol on progesterone concentrations and farrowing in sows. Swine Health Prod. 1998; 6:219-221.
31. Bostedt H, Rudloff PR. Prophylactic administration of the beta-blocker carazolol to influence the duration of parturition in sows. Theriogenology. 1983; 20:191-196.
32. Holtz W, Schmidt-Baulain R, Meyer H, Welp C. Control of prostaglandin-induced parturition in sows by injection of the beta-adrenergic blocking agent carazolol or carazolol and oxytocin. J Anim Sci. 1990; 68:3967-3971.
33. Friendship RM, Templeton CL, Deckert AE. An evaluation of vulvomucosal injections of prostaglandins for induction of parturition in swine. Can Vet J. 1990; 31:433-436.
34. Oxenreider SL, McClure RC, Day BN. Arteries and veins of the internal genitalia of female swine. J Reprod Fert. 1965; 9:19-27.
35. Carnahan KG, Prince BC, Mirando MA. Exogenous oxytocin stimulates uterine secretion of prostaglandin F2[alpha] in cyclic and early pregnant swine. Biol. Reprod.1996; 55:838-843.
36. Edgerton LA, Kaminski MA, Silvia WJ. Changes in uterine secretion of prostaglandin F2[alpha] in response to oxytocin during the estrous cycle, early pregnancy, and estrogen-induced pseudopregnancy in swine. Biol Reprod. 1996; 55:657-662.
37. Kirkwood RN, Aherne FX. Increasing the predictability of cloprostenol-induced farrowing in sows. Swine Health Prod. 1998; 6:57-59.
38. Kirkwood RN. Influence of a new PGF/oxytocin protocol on the timing of farrowing and serum progesterone. Proc 15th IPVS Cong. Birmingham 1998; 3:92.
39. Guthrie HD. Estrous synchronization and fertility in gilts treated with estradiol-benzoate and prostaglandin F2[alpha]. Theriogenology. 1975; 4:69-75.
40. Guthrie HD, Bolt DJ. Changes in plasma estrogen, luteinizing hormone, follicle stimulating hormaone and 13, 14-dihydro-15-keto-prostaglandin F2[alpha] during blockade of luteolysis in pigs after human chorionic gonadotropin treatment. J Anim Sci. 1983; 57:993-1000.
41. Kirkwood RN, Thacker PA. Use of hCG to induce a prolonged luteal phase in gilts. Proc 15th IPVS Cong. Birmingham 1998; 3:87.
42. Kirkwood RN. (Unpublished data).
43. Kirkwood RN, Lythgoe ES, Aherne FX. Effect of lactation feed intake and gonadotrophin-releasing hormone on the reproductive performance of sows. Can J Anim Sci. 1987; 65:752-755.
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