Yuan S Z, Blennow M, Runold M, Lagercrantz H
Department of Woman and Child Health, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden.
Biol Neonate. 1997;72(4):255-64. doi: 10.1159/000244491.
The aim of this study was to test the effects of glucose on the gasping ability and survival in a rat pup model during acute anoxia. Newborn rat pups of both 1 and 8 days of age were given glucose (30 and 60 mg/animal) or saline intraperitoneally and subsequently subjected to anoxia (100% N2). Glucose supplement induced hyperglycemia. Respiration was recorded by barometric plethysmography. The rat pups responded to acute anoxia with a robust sequence of respiratory pattern: hyperpnea, primary apnea, hypoxic gasping and secondary apnea. During anoxia the 1-day-old rats gasped much longer than the 8-day-old rats (23.4 +/- 1.0 vs. 6.1 +/- 0.5 min, p < 0.001). No difference was found in gasping duration between the saline control and the glucose-supplemented 1-day-old rat pups. The 8-day-old supplemented rats gasped much longer (9.3 +/- 0.5 min) than the control rats (6.1 +/- 0.5 min, p < 0.01). The animals autoresuscitated when they received oxygen (100%) during the gasping period. When oxygen was given after the gasping period, the survival rate was 33.3% in control and 0% in supplemented 1-day-old rats, and 100% in control and 50% in glucose-supplemented 8-day-old rats (p < 0.02). Further controlled experiments for a fixed period of anoxia to 13.5 min resulted in survival rates of 50.0% for controls and 28.6% for supplemented animals, respectively. The overall survival rate was then 85.2% in control and 52.9% in supplemented 8-day-old rats (p < 0.05). Lactate concentration in blood rapidly increased in the first 6 min of anoxia and thereafter gradually increased to 22.1 mmol/l around the last gasp in the 1-day-old rats. Hyperglycemia did not cause further accumulation of lactate despite a transient elevation over the control rats at 6 min of anoxia. In the 8-day-old supplemented animals the lactate level was only modestly increased, probably due to the prolonged gasping period. In conclusion, we found that gasping performance was well preserved in the 8-day-old glucose-supplemented rats, whereas the autoresuscitation mechanism after the last gasp might be altered due to hyperglycemia. In addition, the accumulation of lactate in the blood did not affect the gasping performance and the mechanisms of autoresuscitation.
本研究的目的是在急性缺氧期间,测试葡萄糖对幼鼠模型的喘息能力和存活率的影响。对1日龄和8日龄的新生幼鼠腹腔注射葡萄糖(30和60mg/只动物)或生理盐水,随后使其处于缺氧状态(100%氮气)。补充葡萄糖会导致高血糖。通过气压体积描记法记录呼吸情况。幼鼠对急性缺氧的反应表现为一系列强烈的呼吸模式:呼吸急促、原发性呼吸暂停、低氧喘息和继发性呼吸暂停。在缺氧期间,1日龄大鼠的喘息时间比8日龄大鼠长得多(23.4±1.0分钟对6.1±0.5分钟,p<0.001)。生理盐水对照组和补充葡萄糖的1日龄幼鼠在喘息持续时间上没有差异。补充葡萄糖的8日龄大鼠喘息时间比对照组大鼠长得多(9.3±0.5分钟对6.1±0.5分钟,p<0.01)。动物在喘息期接受氧气(100%)时会自动复苏。在喘息期之后给予氧气时,1日龄对照组大鼠的存活率为33.3%,补充葡萄糖组为0%;8日龄对照组大鼠的存活率为100%,补充葡萄糖组为50%(p<0.02)。对缺氧固定时间为13.5分钟的进一步对照实验结果显示,对照组的存活率为50.0%,补充组动物的存活率为28.6%。8日龄对照组大鼠的总体存活率为85.2%,补充组为52.9%(p<0.05)。在缺氧的前6分钟,血液中的乳酸浓度迅速升高,在1日龄大鼠最后一次喘息时,乳酸浓度逐渐升高至22.1mmol/L左右。尽管在缺氧6分钟时,高血糖导致乳酸水平比对照组短暂升高,但并未导致乳酸进一步积累。在8日龄补充葡萄糖的动物中,乳酸水平仅适度升高,可能是由于喘息期延长所致。总之,我们发现补充葡萄糖后存活的8日龄大鼠的喘息能力得到了很好的保留,而最后一次喘息后的自动复苏机制可能因高血糖而改变。此外,血液中乳酸的积累并不影响喘息能力和自动复苏机制。