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慢性低氧血症期间产后肠道功能的改变。

Alterations in postnatal intestinal function during chronic hypoxemia.

作者信息

Bernstein D, Bell J G, Kwong L, Castillo R O

机构信息

Division of Cardiology, Stanford University, California 94305.

出版信息

Pediatr Res. 1992 Mar;31(3):234-8. doi: 10.1203/00006450-199203000-00008.

DOI:10.1203/00006450-199203000-00008
PMID:1561008
Abstract

Growth failure is a major complication of chronic hypoxemia, as seen in infants and children with cyanotic congenital heart disease. To determine whether chronic hypoxemia during infancy affects the gastrointestinal tract, we examined small intestinal growth and digestive enzyme activities in chronically hypoxemic newborn lambs and in age-matched controls. Chronic hypoxemia was produced by placing an inflatable occluder around the main pulmonary artery and performing a balloon atrial septostomy. Aortic oxygen saturation was reduced to 60-74% for 2 wk, after which the small intestine was removed for analysis. During chronic hypoxemia, somatic growth rate was decreased to 60% of control (hypoxemic, 135 +/- 20 versus control, 216 +/- 26 g/d, p less than 0.02). No differences in caloric intake were found (hypoxemic, 129 +/- 4 versus control, 128 +/- 4 kcal/kg/d). Chronic hypoxemia did not alter small intestinal growth, as measured by jejuno-ileal weight, jejuno-ileal length, mucosal weight, or mucosal protein or DNA contents. However, sp act of lactase, the principal disaccharidase of the infant lamb intestine, were significantly decreased (hypoxemic, 0.08 +/- 0.01 versus control, 0.146 +/- 0.03 units of enzyme activity/mg DNA, p less than 0.05), as were the total small intestinal contents of lactase (hypoxemic, 61.7 +/- 7.0 versus control, 120.6 +/- 21.7 units of enzyme activity, p less than 0.01). There also were decreases in specific and total activities of other digestive enzymes such as maltase, amino-oligopeptidase, and alkaline phosphatase in hypoxemic intestine that did not achieve statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

生长发育迟缓是慢性低氧血症的主要并发症,如在患有青紫型先天性心脏病的婴幼儿中所见。为了确定婴儿期的慢性低氧血症是否会影响胃肠道,我们检测了慢性低氧血症新生羔羊和年龄匹配的对照羔羊的小肠生长情况及消化酶活性。通过在主肺动脉周围放置可充气封堵器并进行球囊房间隔造口术来制造慢性低氧血症。将主动脉血氧饱和度降低至60% - 74%,持续2周,之后取出小肠进行分析。在慢性低氧血症期间,躯体生长速率降至对照组的60%(低氧血症组,135±20克/天,对照组,216±26克/天,p<0.02)。未发现热量摄入有差异(低氧血症组,129±4千卡/千克/天,对照组,128±4千卡/千克/天)。通过空肠 - 回肠重量、空肠 - 回肠长度、黏膜重量或黏膜蛋白及DNA含量测量,慢性低氧血症并未改变小肠生长。然而,羔羊小肠主要双糖酶乳糖酶的比活性显著降低(低氧血症组,0.08±0.01,对照组,0.146±0.03酶活性单位/毫克DNA,p<0.05),乳糖酶的小肠总含量也降低(低氧血症组,61.7±7.0,对照组,120.6±21.7酶活性单位,p<0.01)。低氧血症小肠中其他消化酶如麦芽糖酶、氨基 - 寡肽酶和碱性磷酸酶的比活性和总活性也有所降低,但未达到统计学显著性。(摘要截选至250字)

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