Dyess D L, Christenberry D P, Peeples G L, Collins J N, Ardell J L, Roberts W S, Tacchi E J, Powell R W
Department of Surgery, University of South Alabama College of Medicine, Mobile, USA.
J Invest Surg. 1998 Nov-Dec;11(6):381-92. doi: 10.3109/08941939809032215.
This study was designed to determine the effects of severe hypoxemia on newborn piglet visceral blood flow. While the hemodynamic effects of a severe hypoxemic insult are well characterized in newborn animals, its impact on organ perfusion in premature infants is not well characterized. Cannulas were placed in the femoral vessels and left atrium of term (1-14 days old) and prematurely delivered (cesarean section at 90% of term gestation) piglets. After stabilization, some animals were subjected to 1 h of ventilator-controlled hypoxia (yielding PaO2 approximately = 30-40 torr) followed by 30 min of reoxygenation; the remaining animals served as unchallenged controls. Radiolabeled microspheres were injected in all animals at times 0 min (baseline), 5 and 60 min (hypoxia), and 90 min (reoxygenation). Blood flows (mL/min/g tissue) to organs were determined using reference organ techniques. Control animals displayed no alterations in any of the variables monitored. Throughout the experimental period, organ blood flows were almost uniformly lower (p<.05, ANOVA) in premature versus term animals. The trend toward increased cerebral and cardiac blood flows during hypoxia observed in the premature piglets was similar to that of term animals, but of lower magnitude. In term piglets, hypoxia produced an immediate and significant (*p<.05) decline in small-intestinal blood flow followed by autoregulatory escape (2.02+/-0.17 mL/min/g at time 0, 1.56+/-0.15 mL/min/g at 5 min hypoxia, 1.88+/-0.18 mL/min/g at 60 min hypoxia, 2.26+/-0.19 mL/min/g at 30 min reoxygenation), an effect not readily observed in the premature piglets (0.48+/-0.10 mL/min/g at time 0, 0.44+/-0.07 mL/min/g at 5 min hypoxia, 0.46+/-0.10 mL/min/g at 60 min hypoxia, 0.42+/-0.08 mL/min/g at 30 min reoxygenation). However, mucosal blood flows measured in these younger animals declined throughout the experimental period to almost 50% of baseline, compared to a complete restoration to baseline blood flow observed following reoxygenation of term piglets. Intestinal blood flow in premature infants is small when compared to term animals, and alterations in small intestinal blood mucosal flow induced by hypoxia appear less well tolerated by the premature animals. Taken together, this may in part account for the increased risk of developing intestinal ischemic diseases in premature infants who are even temporarily exposed to a severe hypoxic challenge.
本研究旨在确定严重低氧血症对新生仔猪内脏血流的影响。虽然严重低氧血症损伤对新生动物的血流动力学影响已得到充分描述,但其对早产儿器官灌注的影响尚不明确。将插管置于足月(1 - 14日龄)和早产(妊娠90%时剖宫产)仔猪的股血管和左心房。稳定后,部分动物接受1小时的呼吸机控制的低氧(使动脉血氧分压约为30 - 40托),随后再给氧30分钟;其余动物作为未受刺激的对照。在0分钟(基线)、5分钟和60分钟(低氧)以及90分钟(再给氧)时向所有动物注射放射性微球。使用参考器官技术测定各器官的血流(毫升/分钟/克组织)。对照动物所监测的任何变量均无改变。在整个实验期间,与足月动物相比,早产动物的器官血流几乎均较低(方差分析,p<0.05)。早产仔猪在低氧期间脑血流和心脏血流增加的趋势与足月动物相似,但幅度较小。在足月仔猪中,低氧导致小肠血流立即且显著下降(*p<0.05),随后出现自动调节逃逸(0分钟时为2.02±0.17毫升/分钟/克,低氧5分钟时为1.56±0.15毫升/分钟/克,低氧60分钟时为1.88±0.18毫升/分钟/克,再给氧30分钟时为2.26±0.19毫升/分钟/克),而在早产仔猪中未观察到这种效应(0分钟时为0.48±0.10毫升/分钟/克,低氧5分钟时为0.44±0.07毫升/分钟/克,低氧60分钟时为0.46±0.10毫升/分钟/克,再给氧30分钟时为0.42±0.08毫升/分钟/克)。然而,这些较年幼动物的黏膜血流在整个实验期间下降至几乎为基线的50%,而足月仔猪再给氧后观察到血流完全恢复至基线。与足月动物相比,早产儿的肠血流较小,并且低氧诱导的小肠黏膜血流改变似乎较早产动物更难以耐受。综上所述,这可能部分解释了即使只是暂时暴露于严重低氧挑战的早产儿发生肠道缺血性疾病风险增加的原因。