Corrigendum to: alpha-fluoromethylhistidine depletes histamine from secreting but not from non-secreting rat stomach ECL cells
Corrigendum to: alpha-fluoromethylhistidine depletes histamine from secreting but not from non-secreting rat stomach ECL cells
复制标题
更正：α-氟甲基组氨酸会消耗组胺的分泌，但不会消耗非分泌性大鼠胃 ECL 细胞的组胺
DOI：
10.1016/s0014-2999(00)00386-1
复制
发表时间：
2000
影响因子：
5
通讯作者：
Håkanson
中科院分区：
文献类型：
--
作者：
Norlén;Lindstrom;Zhao;Kitano;Chen;Andersson;Håkanson
大鼠胃氧合黏膜组胺主要存在于肥大细胞（10%）和ECL细胞（90%）。与肥大细胞不同，ECL细胞在胃泌素的控制下工作。α-氟甲基组氨酸，一种不可逆的组胺形成酶，组胺脱羧酶的抑制剂，会消耗ecl细胞，但不会消耗肥大细胞的组胺。本报告显示组氨酸脱羧酶抑制ecl细胞组胺的有效性取决于组胺分泌的速率。大鼠连续皮下输注α-氟甲基组氨酸24 h，最大有效剂量（≥3 mg/kg/h）可抑制组氨酸脱羧酶，使粘膜氧合组胺降低80-90%。在禁食的大鼠中，减少了50%。α-氟甲基组氨酸能显著降低饲粮大鼠ECL细胞组胺免疫反应细胞数量（免疫细胞化学）和ECL细胞分泌囊泡数量（电镜），但对禁食大鼠无显著影响。氧合性粘膜组胺的半衰期（以组氨酸脱羧酶抑制测定）在喂养大鼠为2.6 h，在禁食大鼠为19.4 h。α-氟甲基组氨酸能显著降低饲喂大鼠对胃泌素反应的组胺分泌量（胃粘膜下微透析监测），而空腹大鼠则无此作用。经洗脱从大鼠胃中分离ECL细胞（纯度80%）。在不同浓度的胃泌素存在下，用α-氟甲基组氨酸或不加α-氟甲基组氨酸培养后测定其组胺含量。在含有10 nM胃泌素的培养基中，ECL细胞对α-氟甲基组氨酸（0.1 nM）的最有效浓度有反应，组胺含量降低80%。在没有胃泌素的情况下，ECL细胞对α-氟甲基组氨酸有反应，组胺减少45%；可释放组胺池未受影响。综上所述，组氨酸脱羧酶抑制和高分泌率组胺结合会迅速耗尽ecl细胞组胺池，而组氨酸脱羧酶抑制和低分泌率对组胺池的影响要小得多。
Histamine in the oxyntic mucosa of the rat stomach occurs in mast cells (10%) and ECL cells (90%). Unlike the mast cells, the ECL cells operate under the control of gastrin. α-Fluoromethylhistidine, an irreversible inhibitor of the histamine-forming enzyme, histidine decarboxylase depletes ECL-cell but not mast-cell histamine. This report shows that the effectiveness by which histidine decarboxylase inhibition depletes ECL-cell histamine depends on the rate of histamine secretion. Rats received α-fluoromethylhistidine by continuous subcutaneous infusion for 24 h. Maximally effective doses (≥3 mg/kg/h) inhibited histidine decarboxylase and reduced oxyntic mucosal histamine in fed rats by 80–90%. In fasted rats, the reduction was 50%. α-Fluoromethylhistidine greatly reduced the number of histamine-immunoreactive ECL cells (immunocytochemistry) and of secretory vesicles in the ECL cells (electron microscopy) in fed but not in fasted rats. The half-life of oxyntic mucosal histamine (determined upon histidine decarboxylase inhibition) was 2.6 h in fed rats and 19.4 h in fasted rats. The amount of histamine secreted in response to gastrin (monitored by gastric submucosal microdialysis) was greatly reduced by α-fluoromethylhistidine in fed rats but not in fasted rats. ECL cells were isolated from rat stomach by elutriation (80% purity). Their histamine content was determined after culture, with or without α-fluoromethylhistidine, in the presence of varying concentrations of gastrin. In a medium containing 10 nM gastrin, ECL cells responded to a maximally effective concentration of α-fluoromethylhistidine (0.1 nM) with 80% reduction in histamine content. In the absence of gastrin, ECL cells responded to α-fluoromethylhistidine with 45% reduction of histamine; the releasable histamine pool was unaffected. In conclusion, the combination of histidine decarboxylase inhibition and a high rate of histamine secretion will promptly exhaust the ECL-cell histamine pool, while histidine decarboxylase inhibition and a low secretion rate will affect the histamine pool much less.