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首页> 外文期刊>Cell and Tissue Research >Ischemia mobilizes histamine but not pancreastatin from ECL cells of rat stomach: evidence for a cytosolic histamine compartment
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Ischemia mobilizes histamine but not pancreastatin from ECL cells of rat stomach: evidence for a cytosolic histamine compartment

机译：缺血可从大鼠胃的ECL细胞中动员组胺，但不动员胰抑素：胞质组胺区室的证据

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摘要

Histamine in the rat stomach resides in enterochromaffin-like (ECL) cells and mast cells. The ECL cells are peptide-hormone-producing endocrine cells known to release histamine and chromogranin-A-derived peptides (such as pancreastatin) in response to gastrin. Ischemia (induced by clamping of the celiac artery or by gastric submucosal microinfusion of the vasoconstrictor endothelin) mobilizes large amounts of ECL-cell histamine in a burst-like manner. This report examines the ECL-cell response to ischemia and compares it with that induced by gastrin in rats. Arterial clamping (30 min) and gastric submucosal microinfusion (3 h) of endothelin, vasopressin, or adrenaline caused ischemia, manifested as a raised lactate/pyruvate ratio and mucosal damage. Whereas microinfusion of gastrin released both histamine and pancreastatin, ischemia mobilized histamine only. The mucosal concentrations of histamine and pancreastatin, the number and immunostaining intensity of the ECL cells, and the ultrastructure of the ECL cells were unchanged following ischemia. The long-term effects of ischemia and reperfusion (60–90 min) on gastric mucosa were examined in rats treated with the proton pump inhibitor omeprazole for 4 days. The activity of the ECL cells was suppressed (reflected in low histamine-forming capacity) but returned to normal within 1 week, illustrating the ability of the ECL cells to recover. We suggest that ischemia mobilizes cytosolic ECL-cell histamine without affecting the storage of histamine (and pancreastatin) in the secretory organelles and without causing lasting ECL-cell impairment.
机译：大鼠胃中的组胺存在于肠嗜铬样（ECL）细胞和肥大细胞中。 ECL细胞是产生肽激素的内分泌细胞，已知会响应胃泌素释放组胺和嗜铬粒蛋白-A衍生的肽（例如胰酶抑素）。缺血（由腹腔动脉夹闭或胃粘膜下微血管收缩血管内皮素的注入引起）以爆发状方式动员大量ECL细胞组胺。该报告检查了ECL细胞对缺血的反应，并将其与大鼠胃泌素诱导的反应进行了比较。内皮素，加压素或肾上腺素的动脉夹紧（30分钟）和胃黏膜下微输注（3小时）引起局部缺血，表现为乳酸/丙酮酸比升高和黏膜损伤。胃泌素的微量输注释放组胺和胰腺抑素，而缺血仅动员组胺。缺血后，ECL细胞的粘膜浓度，组胺和胰抑素浓度，细胞数目和免疫染色强度以及ECL细胞的超微结构均未改变。在质子泵抑制剂奥美拉唑治疗4天的大鼠中，观察了缺血和再灌注（60-90分钟）对胃粘膜的长期影响。 ECL细胞的活性受到抑制（反映为低的组胺形成能力），但在1周内恢复正常，这说明ECL细胞具有恢复的能力。我们建议缺血可动员细胞质ECL细胞组胺，而不会影响分泌细胞器中组胺（和胰抑素）的储存，也不会造成持久的ECL细胞损伤。

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  • 来源
    《Cell and Tissue Research》 |2008年第3期|405-415|共11页
  • 作者

    Maria Bernsand; Chun-Mei Zhao; Rolf H?kanson; Bj?rn Stenstr?m; Duan Chen; Per Norlén;

  • 作者单位

    Unit of Cellular and Molecular Pharmacology Department of Experimental Medical Sciences BMC F13 Lund University Lund Sweden;

    Department of Cancer Research and Molecular Medicine Norwegian University of Science and Technology Trondheim Norway;

    Unit of Cellular and Molecular Pharmacology Department of Experimental Medical Sciences BMC F13 Lund University Lund Sweden;

    Department of Cancer Research and Molecular Medicine Norwegian University of Science and Technology Trondheim Norway;

    Department of Cancer Research and Molecular Medicine Norwegian University of Science and Technology Trondheim Norway;

    Unit of Clinical and Experimental Pharmacology Department of Laboratory Medicine University Hospital 22185 Lund Sweden;

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  • 关键词

    Enterochromaffin-like cells; Stomach; Microdialysis; Ischemia; Rat (Sprague Dawley; Wistar);

    机译：肠嗜铬样细胞;胃;微透析;局部缺血;大鼠（Sprague Dawley;Wistar）;

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