Localization of central prostaglandin E2 antisecretory effects.
Localization of central prostaglandin E2 antisecretory effects.
复制标题
中枢前列腺素 E2 抗分泌作用的定位。
DOI：
10.1016/0016-5085(91)90198-t
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发表时间：
1991
期刊：
影响因子：
29.4
通讯作者：
Kauffman,G
中科院分区：
文献类型：
--
作者：
Barocelli,E;Impicciatore,M;Seaton,J;Conter,R;Kauffman,G
脑室内前列腺素E2（PGE2）抑制刺激胃酸分泌;然而，作用的中心部位尚不清楚。特异性PGE 2结合位点定位于下丘脑腹内侧核和中央杏仁核（A）。已显示核内的突触在中枢神经降压素诱导的抗分泌作用中起作用。这些研究验证了下丘脑腹内侧核、中央杏仁核和核丘微量注射PGE2抑制刺激胃酸分泌的假设。海马体是大脑的控制区域。在实验前两天，将金属套管立体定位在双侧大脑的特定区域中，并在戊巴比妥麻醉下将金属胃套管手术植入雄性250-g Sprague-Dawley大鼠中。在实验当天，大鼠禁食14小时，在给予五肽胃泌素（40 μ g/kg SC）之前10分钟通过中央套管给予生理盐水或PGE_2（0.1 - 1.0 μ g，0.2 μ L/侧）。每隔30分钟测量一次胃分泌，并以酸排出量（微摩尔/小时）表示。对照动物的酸排出量（平均值± SE）为161 ± 14 μ mol/h。下丘脑腹内侧核给予前列腺素E2 0.10、0.50和1.0 μ g/侧（a）可使酸排出量有规律地减少至53 ± 11、36 ± 10和27 ± 11 μ mol/h，NACB可使酸排出量减少至157 ± 36、60 ± 12和38 ± 12 μ mol/h;和（c）进入A分别将酸输出减少至144 ± 31、141 ± 26和90 ± 19 * μ mol/h（通过Neuman-Keuls检验，* P <0.05）。海马内给予前列腺素E2（0.50 μ g/侧）对酸排出量（134 ± 28 μ mol/h）无显著影响。虽然中央PGE2管理与体温过高，这发生在较低的剂量比所需的抑制酸分泌。将前列腺素E2注射到已知具有PGE2受体的特定脑区，中央杏仁核和下丘脑腹内侧核，以及注射到核内丘脑，可抑制刺激的胃酸分泌。这些观察结果表明，PGE 2可能在胃酸分泌的中枢控制中具有生理作用。
Intracerebroventricular prostaglandin E2(PGE2) inhibits stimulated gastric acid secretion; however, the central site of action is unknown. Specific PGE2binding sites have been localized to the ventromedial hypothalamic nucleus and central amygdala (A). The nuclear accumbens has been shown to play a role in central neurotensin-induced antisecretory effects. These studies tested the hypothesis that microinjections of PGE2into the ventromedial hypothalamic nucleus, central amygdala, and nuclear accumbens inhibit stimulated gastric acid secretion. The hippocampus served as a cerebral control region. Two days before the experiments, metal cannulas were stereotaxically positioned bilaterally into specific areas of the brain, and metal gastric cannulas were operatively implanted, under nembutal anesthesia, in male 250-g Sprague-Dawley rats. On the experimental day, the rats, fasted for 14 hours, were given saline or PGE2(0.1–1.0 μg in 0.2 μL/side) through the central cannulas 10 minutes before administering pentagastrin (40 μg/kg SC). Gastric secretion was measured at 30-minute intervals and expressed as acid output, micromoles per hour. Acid output (mean ± SE) in control animals was 161 ± 14 μmol/h. Prostaglandin E2administration at doses of 0.10, 0.50, and 1.0 μg/side (a) into ventromedial hypothalamic nucleus reduced acid output to 53 ± 11,*36 ± 10,*and 27 ± 11*μmol/h regularly; (b) into NACB reduced acid output to 157 ± 36, 60 ± 12,*and 38 ± 12*μmol/h; and (c) into A reduced acid output to 144 ± 31, 141 ± 26, and 90 ± 19*μmol/h, respectively (*P < 0.05 by Neuman-Keuls test). Prostaglandin E2(0.50 μg/side) administration into hippocampus had no significant effect on acid output (134 ± 28 μmol/h). Although central PGE2administration was associated with hyperthermia, this occurred at lower doses than those required to inhibit acid secretion. Prostaglandin E2administration into specific brain areas known to have PGE2receptors, the central amygdala and ventromedial hypothalamic nucleus, and into nuclear accumbens inhibits stimulated gastric acid secretion. These observations suggest that PGE2may have a physiological role in the central control of gastric acid secretion.