Permeability and surface area of the blood-nerve barrier in galactose intoxication.

Permeability and surface area of the blood-nerve barrier in galactose intoxication.
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半乳糖中毒时血神经屏障的渗透性和表面积。

DOI:
10.1016/0006-8993(93)90434-o
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发表时间:
1993
期刊:
影响因子:
2.9
通讯作者:
Kalichman,MW
Kalichman,MW
中科院分区:
医学3区
文献类型:
--
作者:
Mizisin,AP;Kalichman,MW

文献摘要

相似文献

通过使用体内注射方法测量坐骨神经中[14 C]甘露醇的血液-神经界面的渗透性-表面积(PSA)乘积,在对照和半乳糖喂养大鼠中研究了小分子量非电解质的血液-神经运动。PSA产品后,9至11个月的喂养对照大鼠的饮食含有0%的半乳糖和半乳糖中毒大鼠的饮食含有40%的半乳糖。半乳糖组神经含水量和神经干/湿重比均显著增加(P < 0.05)。与对照组相比,当参考神经干重(13.59 ± 2.90 × 10− 5 ml/s/g干重)时,半乳糖喂养动物的PSA产物增加了51%(P< 0.01)。相对于8.99 ± 1.59 × 10− 5 ml/s/g干重;平均值±标准差;半乳糖组与对照组相比)或30%(P< 0.001),当参考神经长度时(± 0.43 × 10− 5 ml/s/mm vs.1.87 ± 0.48 × 10− 5 ml/s/mm),但当参考神经湿重时则不然。有人建议,在半乳糖中毒,神经内体积的变化反映了神经水含量的增加,PSA产品最好归一化干重或长度,这是不受体积变化。标准化为干重,血神经屏障表面积(即血管和神经束膜)通过形态测量方法测定,在半乳糖中毒组中增加了34%。尽管这种增加与观察到的PSA产物增加一致,但大部分表面积增加发生在神经束膜中,据信其在亲水性非电解质的血神经转移中的作用远小于神经内膜血管。而用形态计量学方法计算的神经内膜血管紧密连接面积在半乳糖喂养的大鼠中增加了53%(P< 0.005)。这种增加可能是由于内皮细胞增殖,足以解释PSA产物增加。
The blood-nerve movement of a small molecular weight non-electrolyte was studied in control and galactose-fed rats by measuring the permeability-surface area (PSA) product of the blood-nerve interface to [14C]mannitol in sciatic nerve using an in vivo injection method. PSA products were measured after 9 to 11 months of feeding control rats a diet containing 0% galactose and galactose-intoxicated rats a diet containing 40% galactose. Nerves of the galactose-fed group were hydrated as reflected by a significant increase in nerve water content and wet weight to dry weight ratio (bothP< 0.05). Compared to controls, PSA products were increased by 51% (P< 0.01) in galactose-fed animals when referenced to nerve dry weight (13.59 ± 2.90 × 10−5ml/s/g dry wt. versus 8.99 ± 1.59 × 10−5ml/s/g dry wt.; mean ±S.D.; galactose vs. controls, respectively) or by 30% (P< 0.001) when referenced to nerve length (± 0.43 × 10−5ml/s/mm vs.1.87 ± 0.48 × 10−5ml/s/mm) but not when referenced to nerve wet weight. It is suggested that in galactose intoxication, where endoneurial volume changes reflect increases in nerve water content, PSA products are best normalized to dry weight or length, which are not affected by volume changes. Normalized to dry weight, the blood-nerve barrier surface area (i.e. vessels and perineurium) was determined by morphometric methods to be increased by 34% in the galactose-intoxicated group. Although this increase is consistent with the observed increase in PSA product, most of the increased surface area occurs in the perineurium, which is believed to have much less of a role than endoneurial vessels in blood-nerve transfer of hydrophilic non-electrolytes. However, endoneurial vessel tight junctional ‘area’ was calculated with morphometric methods to be increased by 53% in galactose-fed rats (P< 0.005). This increase,presumably due to endothelial cell proliferation, is sufficient to explain the increased PSA product.