The present study was undertaken to determine the relationship between dose of porcine growth hormone (pGH) and growth performance of pigs. Porcine GH was administered daily for 35 d [buffer-injected control = (C); 10 micrograms/kg body weight (BW) = (L); 30 micrograms/kg BW = (M); 70 micrograms/kg BW = (H)] to barrows (initial wt = 50 kg). Growth rate was significantly increased by pGH (14% for H dose vs C). Feed efficiency was increased in a dose-related manner (L = 7%, M = 10%, H = 17%) by pGH. There was a concurrent change in carcass composition of pGH-treated pigs. The H dose of pGH decreased the percentage of carcass lipid by 25% (P less than .05). Muscle mass was significantly increased in H vs C pigs (31 vs 26 kg). Serum insulin-like growth factor 1 (IGF-1) concentration increased in a manner that was linearly related to the pGH dose (r = .87). No antibodies to pGH were detected in any of the pigs. In summary, these results extend our earlier findings that pGH increases growth performance markedly. Based on the present findings it appears that the maximally effective dose of pGH is greater than 70 micrograms.kg BW-1.d-1 since several indices of the growth-promoting and metabolic effects of pGH (% carcass protein, % carcass lipid and feed efficiency) had not plateaued.

Highly purified porcine growth hormone (pGH; USDA-B1) was administered by im injection (22 micrograms X kg body weight-1 X d-1) to rapidly growing Yorkshire barrows for 30 d. Growth hormone significantly increased growth rate (10%), feed efficiency (4%), cartilage growth and muscle mass. However, pGH did not affect carcass adipose tissue mass. Intramuscular lipid content of the longissimus was increased 50% by pGH administration. Plasma pGH concentration was elevated (7- to 11-fold) for 3 to 5 h post-injection. Chronic administration of pGH depressed pituitary GH content and concentration approximately 45%. No GH antibodies were detected in the plasma of GH-treated swine. Plasma somatomedin-C concentration was increased 55% by GH treatment 3 h post-injection. Plasma glucose and insulin concentrations were both significantly increased in GH-treated swine, suggesting that the animals had developed a state of insulin resistance. Plasma-free fatty acid concentration tended to be higher in GH-treated animals. Treatment of swine with pGH significantly decreased plasma blood urea nitrogen. Assessment of animal health during the trial and postmortem indicated that pGH administration did not have any adverse effects. In summary, treatment of young, rapidly growing swine with pGH stimulated growth performance without affecting animal health or inducing the production of GH antibodies.

The current study was undertaken to determine the effects of human growth hormone-releasing factor [hpGRF-(1-44)-NH2] on growth performance in pigs and whether this response was comparable to exogenous porcine growth hormone (pGH) treatment. Preliminary studies were conducted to determine if GRF increased plasma GH concentration after iv and im injection and the nature of the dose response. Growth hormone-releasing factor stimulated the release of pGH in a dose-dependent fashion, although the individual responses varied widely among pigs. The results from the im study were used to determine the dose of GRF to use for a 30-d growth trial. Thirty-six Yorkshire-Duroc barrows (initial wt 50 kg) were randomly allotted to one of three experimental groups (C = control, GRF and pGH). Pigs were treated daily with 30 micrograms of GRF/kg body weight by im injection in the neck. Pigs treated with pGH were also given 30 micrograms/kg body weight by im injection. Growth rate was increased 10% by pGH vs C pigs (P less than .05). Growth rate was not affected by GRF; however, hot and chilled carcass weights were increased 5% vs C pigs (P less than .05). On an absolute basis, adipose tissue mass was unaffected by pGH or GRF. Carcass lipid (percent of soft-tissue mass) was decreased 13% by GRF (P less than .05) and 18% by pGH (P less than .05). Muscle mass was significantly increased by pGH but not by GRF. There was a trend for feed efficiency to be improved by GRF; however, this was not different from control pigs. In contrast, pGH increased feed efficiency 19% vs control pigs (P less than .05). Chronic administration of GRF increased anterior pituitary weight but did not affect pituitary GH content or concentration. When blood was taken 3 h post-injection, both GRF- and pGH-treated pigs had lower blood-urea nitrogen concentrations. Serum glucose was significantly elevated by both GRF and pGH treatment. This was associated with an elevation in serum insulin. These results indicate that increasing the GH concentration in blood by either exogenous GH or GRF enhances growth performance. The effects of pGH were more marked than for GRF. Further studies are needed to determine the optimal dose of GRF to administer in growth trials and the appropriate pattern of GRF administration in order to determine whether GRF will enhance pig growth performance to the extent that exogenous pGH does.

Hypoxia in a neonate caused by intermittent positive pressure ventilation 405 of the latter to the administration of experimental drugs designed to lower pulmonary vascular resistance. There may also be a temptation to increase the peak inspiratory pressures in such a situation. In the case described, any of the above measures might have had dire consequences.We have seen hypoxia relieved by stopping IPPV on previous occasions, but have been unable to document the event. We have also seen patients with bronchopulmonary dysplasia whose early neonatal course was similar to that described above.The indications for IPPV were obscure and this case serves as a reminder that IPPV should not be undertaken without good reason. It also emphasises the importance of proper assessment of a patient after transfer from another hospital.

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