VASCULAR BED-DEPENDENT ROLES OF THE PEPTIDE CGRP AND NITRIC-OXIDE IN ACID-EVOKED HYPEREMIA OF THE RAT STOMACH
VASCULAR BED-DEPENDENT ROLES OF THE PEPTIDE CGRP AND NITRIC-OXIDE IN ACID-EVOKED HYPEREMIA OF THE RAT STOMACH
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DOI：
10.1113/jphysiol.1994.sp020385
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发表时间：
1994-11-01
影响因子：
5.5
通讯作者：
HEINEMANN, A
中科院分区：
文献类型：
--
作者：
HOLZER, P;WACHTER, C;HEINEMANN, A
1.已知通过破坏的胃粘膜屏障的酸反向扩散通过神经机制增加胃粘膜血流量。本研究探讨了如何酸诱发的变化。胃微循环与供应胃的主要动脉之一胃左动脉的血流变化进行比较，以及胃左动脉中的扩张介质是否与胃粘膜中的相同.实验在乌拉坦麻醉的大鼠上进行。采用超声渡越时移技术测定胃左动脉血流量，采用氢气清除法测定胃粘膜血流量.用0.15 M的15%乙醇灌胃诱发胃酸反扩散。盐酸使胃左动脉的血流量增加了4.7倍，明显大于胃粘膜血流量增加的2.9倍。血压和心率无明显变化。阿托品和P物质受体拮抗剂RP-67580.5未改变胃左动脉中酸诱发的充血。降钙素基因相关肽（CGRP）拮抗剂CGRP（8-37）对胃血流量无影响，但可阻断CGRP的扩张作用，抑制胃粘膜酸诱发充血的程度大于胃左动脉充血.通过N-ω-硝基-L-精氨酸甲酯（L-NAME）阻断一氧化氮合成引起胃左动脉和胃粘膜微血管收缩。L-NAME可阻断胃粘膜酸诱发的血管舒张反应，但对胃左动脉的舒张反应无明显抑制作用.数据表明，胃酸反扩散引起的胃充血反应是由粘膜微血管和壁外动脉扩张引起的。然而，两种血管床的扩张器机制不同。CGRP和一氧化氮是胃粘膜中重要的血管扩张介质，但在胃左动脉中的相关性较小。
1. Acid back-diffusion through a disrupted gastric mucosal barrier is known to increase gastric mucosal blood flow via a neural mechanism. The present study examined how the acid-evoked change in the. gastric microcirculation compares with blood flow changes in the left gastric artery, one of the major arteries supplying the stomach, and whether the dilator mediators in the left gastric artery are identical to those in the gastric mucosa.2. The experiments were performed on rats anaesthetized with urethane. Blood flow in the left gastric artery was measured by the ultrasonic transit time shift technique, and blood flow in the gastric mucosa was assessed by the hydrogen gas clearance method.3. Gastric acid back-diffusion evoked by perfusion of the stomach with 15% ethanol in 0.15 M. HCl increased blood flow in the left gastric artery by a factor of 4.7, which was significantly larger than the 2.9-fold increase in blood flow through the gastric mucosa. Blood pressure and heart rate were not altered appreciably.4. The acid-evoked hyperaemia in the left gastric artery was left unaltered by atropine and the substance P receptor antagonist RP-67580.5. The calcitonin gene-related peptide (CGRP) antagonist CGRP(8-37) had no effect on gastric blood flow but prevented the dilator action of CGRP and inhibited the acid-evoked hyperaemia in the gastric mucosa to a larger degree than the hyperaemia in the left gastric artery.6. Blockade of nitric oxide synthesis by N-omega-nitro-L-arginine methyl ester (L-NAME) caused constriction of the left gastric artery and the gastric mucosal microvessels. The acid-evoked vasodilatation in the gastric mucosa was blocked by L-NAME, whereas the dilator response in the left gastric artery was not significantly depressed.7. The data show that the gastric hyperaemic response to acid back-diffusion results from dilatation of mucosal microvessels and extramural arteries. The dilator mechanisms, however, differ between the two vascular beds. CGRP and nitric oxide are important vasodilator mediators in the gastric mucosa but are of less relevance in the left gastric artery.