Grajwer L A, Sperling M A, Sack J, Fisher D A
Pediatr Res. 1977 Jul;11(7):833-6. doi: 10.1203/00006450-197707000-00011.
Studies were conducted in newborn lambs to gain insight into the significance and mechanism(s) responsible for the rapid rise in plasma immunoreactive glucagon (IRG) which occurs in human and other newborn species immediately after delivery. Three sets of experiments were conducted: group A, control studies (n = 5) in which delivery into room air was followed 1 hr later by cutting of the umbilical cord and periodic blood sampling for a further hour; group B, studies (n = 5) in which somatostatin (SRIF), a known inhibitor of IRG and insulin (IRI) secretion, was infused int othe fetus for 10 min before, and for 1 hr after delivery and immediate cord cutting; group C, studies (n = 5) in which an identical dose regimen of SRIF was infused into fasting newborn lambs aged 24-72 hr. The doses of SRIF used were several fold higher than those proven to suppres pancreatic hormones secretion in other species. In the control studies, plasma IRG levels remained stable until the cord was cut, after which event levels rose 5-6-fold (59 +/- 15 pg/ml to 305 +/- 98 pg/ml, P less than 0.05). Simultaneously, plasma free fatty acid (FFA) concentrations rose significantly (280 +/- 80 to 780 +/- 100 muEq/liter, P less than 0.05) and IRI remained unchanged. Plasma glucose concentrations, however, in contrast to observations in other species, did not fall, and therefore, hypoglycemia was not the stimulus for the glucagon surge. SRIF infusion at birth (group B) did not prevent the rise in IRG. Again blood glucose values did not fall, but in contrast to the control studies plasma IRI levels rose and the rise in FFA did not occur. Later SRIF infusion (group C) resulted a prompt and sustained suppression of IRG and IRI and a significant fall in blood glucose. These results suggest that an adrenergic mechanism rather than curtailment of nutrients is the major stimulus to the neonatal surge in IRG.
为深入了解人类和其他新生物种出生后立即出现的血浆免疫反应性胰高血糖素(IRG)迅速升高的意义及机制,对新生羔羊进行了研究。进行了三组实验:A组为对照研究(n = 5),将羔羊娩出至室内空气中,1小时后切断脐带,并在接下来的1小时内定期采血;B组研究(n = 5),在分娩前10分钟及分娩并立即切断脐带后1小时,向胎儿输注生长抑素(SRIF),生长抑素是已知的IRG和胰岛素(IRI)分泌抑制剂;C组研究(n = 5),向24 - 72小时龄的空腹新生羔羊输注相同剂量方案的SRIF。所用SRIF的剂量比已证明能抑制其他物种胰腺激素分泌的剂量高几倍。在对照研究中,血浆IRG水平在脐带切断前保持稳定,脐带切断后,IRG水平升高了5 - 6倍(从59±15 pg/ml升至305±98 pg/ml,P < 0.05)。同时,血浆游离脂肪酸(FFA)浓度显著升高(从280±80升至780±100 μEq/升,P < 0.05),而IRI保持不变。然而,与其他物种的观察结果相反,血浆葡萄糖浓度并未下降,因此,低血糖不是胰高血糖素激增的刺激因素。出生时输注SRIF(B组)并未阻止IRG升高。同样,血糖值并未下降,但与对照研究相反,血浆IRI水平升高且FFA未升高。后期输注SRIF(C组)导致IRG和IRI迅速且持续受到抑制,血糖显著下降。这些结果表明,肾上腺素能机制而非营养物质减少是新生儿IRG激增的主要刺激因素。