METABOLITES OF ARACHIDONIC-ACID FORMED BY HUMAN GASTROINTESTINAL TISSUES AND THEIR ACTIONS ON THE MUSCLE LAYERS

METABOLITES OF ARACHIDONIC-ACID FORMED BY HUMAN GASTROINTESTINAL TISSUES AND THEIR ACTIONS ON THE MUSCLE LAYERS
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DOI:
10.1111/j.1476-5381.1981.tb09989.x
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发表时间:
1981-01-01
影响因子:
7.3
通讯作者:
STAMFORD, IF
STAMFORD, IF
中科院分区:
医学2区
文献类型:
--
作者:
BENNETT, A;HENSBY, CN;STAMFORD, IF

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1气相色谱-质谱分析表明,在人胃、回肠末端或乙状结肠匀浆的肌肉或粘膜提取物中均存在花生四烯酸(AA)、6‐酮‐前列腺素f1 α和血栓素B2(TxB2)。前列腺素D2(PGD2)、pge2或pgf2 α多见于粘膜提取物。AA的12 -羟基衍生物(12 - HETE)在结肠的所有提取物中都被检测到,但仅在其他一些组织中被检测到。大多数测试的前列腺素收缩纵肌,效力顺序为U - 46619 (PGH2的环氧甲烷类似物)>PGE2>PGF2α>PGD2;pgi2通常引起松弛,而其分解产物或txb2的作用较弱且变化不大,或者pgf2 α收缩圆形肌肉,而pgi2和pge2通常引起松弛。pgd2,6 -酮- PGF1α, 6,15 -二酮- PGF1α或txb2通常很少或没有作用。pgi2拮抗剂对某些兴奋性前列腺素的收缩,对乙酰胆碱的收缩没有很大影响。对于两个肌肉层,沿胃肠道对前列腺素的敏感性有梯度。敏感性为胃bbb、回肠远端bbb、乙状结肠6。结果与胃肠道生理学和病理生理学有关。
1Gas chromatography‐mass spectrometry demonstrated the presence of arachidonic acid (AA), 6‐keto‐prostaglandin F1αand thromboxane B2(TxB2) in all extracts of homogenized muscle or mucosa from human stomach, terminal ileum or sigmoid colon. Prostaglandin D2(PGD2), PGE2or PGF2αwere usually found more often in the mucosal extracts. The 12‐hydroxy‐derivative of AA (12‐HETE) was detected in all extracts of the colon but in only some of the other tissues2Most prostanoids tested contracted the longitudinal muscle, the order of potency being U‐46619 (an epoxymethano analogue of PGH2)>PGE2>PGF2α>PGD2; PGI2usually caused relaxation, whereas its breakdown products or TxB2had weak and variable effects3U‐46619 or, less potently, PGF2αcontracted the circular muscle, whereas PGI2and usually PGE2caused relaxation. PGD2, 6‐keto‐PGF1α, 6, 15‐diketo‐PGF1αor TxB2usually had little or no effect4PGI2antagonized contractions to some excitatory prostanoids, without greatly affecting contractions to acetylcholine5For both muscle layers there was a gradient in sensitivity to prostanoids along the gastrointestinal tract. The sensitivities were stomach>distal ileum>sigmoid colon6The results are discussed in relation to gastrointestinal physiology and pathophysiology.