Serum cytosolic β-glucosidase activity in a rat model of necrotizing enterocolitis

被引:25
作者
Dimmitt, RA
Glew, R
Colby, C
Brindle, M
Skarsgard, E
Moss, RL
机构
[1] Univ Alabama Birmingham, Dept Pediat, Div Neonatol, Birmingham, AL 35233 USA
[2] Univ New Mexico, Dept Biochem, Albuquerque, NM 87131 USA
[3] Stanford Univ, Dept Pediat, Palo Alto, CA 94304 USA
[4] Stanford Univ, Dept Surg, Palo Alto, CA 94304 USA
[5] Yale Univ, Dept Surg, New Haven, CT 06520 USA
关键词
D O I
10.1203/01.PDR.0000081310.47579.49
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
The diagnosis of necrotizing enterocolitis (NEC) is made from a combination of clinical and radiographic findings. There are no useful screening biochemical markers of intestinal injury. The serum concentration of cytosolic beta-glucosidase (CBG), an enzyme found primarily in enterocytes, is markedly elevated in animal models of ischemia and bowel obstruction. We hypothesized that in a rat model of NEC, serum CBG activity would significantly increase before microscopic evidence of severe intestinal injury. Cohorts of 2-wk-old Sprague-Dawley rats (n = 10/cohort) were anesthetized and underwent laparotomy with occlusion of the superior mesenteric artery (SMA). Platelet-activating factor (200 mug/animal) was injected in the proximal duodenum. Serum and intestinal samples were obtained at time 0 (control) and 30, 60, and 90 min of ischemia (I) and after 90 min of I followed by 60 min of reperfusion (I/R). Histopathologic injury was categorized as either no or minimal injury or mural necrosis by two masked investigators and CBG activity was measured by ELISA. Data were analyzed with Fisher's exact test and ANOVA. Only the I/R group had significantly greater mural necrosis compared with the control group (90% versus 0%, respectively, p < 0.001). In contrast, CBG activity was significantly elevated after only 90 min of I and after I/R (15.1 +/- 5.6 and 16.4 +/- 4.3 units/mL, respectively, p < 0.05). We conclude that serum CBG is elevated before transmural intestinal injury in this model and may have utility as an early marker of ischemia in patients at risk for NEC.
引用
收藏
页码:462 / 465
页数:4
相关论文
共 20 条
[1]   INTESTINAL ALKALINE-PHOSPHATASE AND BASE DEFICIT IN MESENTERIC OCCLUSION [J].
BARNETT, SM ;
DAVIDSON, ED ;
BRADLEY, EL .
JOURNAL OF SURGICAL RESEARCH, 1976, 20 (03) :243-246
[2]   NEONATAL NECROTIZING ENTEROCOLITIS - THERAPEUTIC DECISIONS BASED UPON CLINICAL STAGING [J].
BELL, MJ ;
TERNBERG, JL ;
FEIGIN, RD ;
KEATING, JP ;
MARSHALL, R ;
BARTON, L ;
BROTHERTON, T .
ANNALS OF SURGERY, 1978, 187 (01) :1-7
[3]   Impact of necrotizing enterocolitis on length of stay and hospital charges in very low birth weight infants [J].
Bisquera, JA ;
Cooper, TR ;
Berseth, CL .
PEDIATRICS, 2002, 109 (03) :423-428
[4]  
BOLEY SJ, 1977, SURGERY, V82, P848
[5]  
CALMAN C, 1958, SURGERY, V44, P43
[6]   NECROTIZING ENTEROCOLITIS - A REVIEW OF PATHOGENETIC MECHANISMS AND IMPLICATIONS FOR PREVENTION [J].
CAPLAN, MS ;
MACKENDRICK, W .
PEDIATRIC PATHOLOGY, 1993, 13 (03) :357-369
[7]  
CHANG CWT, 1991, ENZYME, V45, P145
[8]   Circulating thrombopoietin levels in neonates with infection [J].
Colarizi, P ;
Fiorucci, P ;
Caradonna, A ;
Ficuccilli, F ;
Mancuso, M ;
Papoff, P .
ACTA PAEDIATRICA, 1999, 88 (03) :332-337
[9]  
De Toma G, 1983, Ital J Surg Sci, V13, P269
[10]   Circulating pro- and counterinflammatory cytokine levels and severity in necrotizing enterocolitis [J].
Edelson, MB ;
Bagwell, CE ;
Rozycki, HJ .
PEDIATRICS, 1999, 103 (04) :766-771