Vaginal birth versus elective caesarean section: effects on gastric function in the neonate.
Plasma gastrin concentration increases in late gestation and reaches a peak at birth or shortly after birth in many species ('neonatal hypergastrinaemia'). We investigated the hypothesis that gastrin and gastric acid secretion in the neonate is influenced by the final rise in plasma cortisol associated with spontaneous (vaginal) birth. Caesarean-delivered (CD, n = 28) or vaginally delivered (VD, n = 24) premature or full-term piglets (97-115 days gestation) were killed immediately after birth (using pentobarbitone). Compared with newborn CD pigs, the newborn VD pigs had significantly higher (P < 0.05) concentrations of cortisol (669 +/- 60 versus 223 +/- 2 nM) and gastrin (57 +/- 4 versus 33 +/- 1 pM) in plasma, and significantly lower gastric fluid pH (3.3 +/- 0.2 versus 4.7 +/- 0.3), amidated (bioactive) gastrin in the antrum (550 +/- 77 versus 1220 +/- 29 pmol g-1) and glycine-extended (precursor) gastrin in the antrum (81 +/- 10 versus 143 +/- 5 pmol g-1). There were significant linear correlations between log plasma cortisol values and plasma gastrin (r = 0.40, P < 0.05) or gastric fluid pH (r = -0.51, P < 0.05) in newborn pigs. The effects of cortisol in the immediate postnatal period were investigated in forty-one CD pigs born at 111-112 days gestation and treated with saline, metyrapone (an inhibitor of cortisol synthesis) or adrenocorticotrophic hormone (ACTH) from 0 to 7 days after birth. At 7 days, plasma gastrin in ACTH-treated pigs (elevated plasma cortisol) was significantly lower than in saline-treated pigs, but not different from that in metyrapone-treated pigs (low plasma cortisol). No treatment effects were observed postnatally for antral gastrin and fundic cobalamin-binding protein concentrations. These results suggest that in the intrapartum period the high circulating cortisol levels stimulate the normal rise in gastrin and acid secretion associated with spontaneous vaginal delivery in the piglet, whereas postnatally, cortisol is unlikely to play an important role in the subsequent development of gastrin and acid secretion.
Sangild
P T
PT
Department of Clinical Studies, Veterinary and Agricultural University, Copenhagen, Denmark.
Hilsted
L
L
Nexø
E
E
Fowden
A L
AL
Silver
M
M
D000311:Adrenal Glands / Q000033:anatomy & histology; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D002585:Cesarean Section / Q000009:adverse effects*; D005260:Female; D005744:Gastric Acid / Q000378:metabolism; D005755:Gastrins / Q000097:blood / Q000378:metabolism; D006854:Hydrocortisone / Q000097:blood / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D007743:Labor, Obstetric / Q000502:physiology*; D008797:Metyrapone / Q000494:pharmacology; D009929:Organ Size; D011247:Pregnancy; D011706:Pyloric Antrum / Q000378:metabolism; D013270:Stomach / Q000502:physiology*; D013552:Swine; D014155:Transcobalamins / Q000378:metabolism
D005755:Gastrins; D014155:Transcobalamins; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone; D008797:Metyrapone