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猫胃黏膜在2M氯化钠损伤后的修复及碳酸氢根离子释放:全身酸碱状态的作用

Gastric mucosal repair and release of HCO3- after damage by 2 M NaCl in cat: role of systemic acid base status.

作者信息

Guttu K, Grong K, Svanes K, Grønbech J E

机构信息

Department of Surgery, University of Bergen, Norway.

出版信息

Am J Physiol. 1994 Oct;267(4 Pt 1):G536-45. doi: 10.1152/ajpgi.1994.267.4.G536.

Abstract

To study the influence of acid base balance on gastric mucosal repair, NH4Cl or NaHCO3 was given intravenously to anesthetized cats after mucosal damage induced by intraluminal 2 M NaCl. Saline at pH 5 or 1 was perfused via an oral tube through the stomach lumen and evacuated via a pyloric tube to a chamber with pH and PCO2 electrodes. Luminal bicarbonate (HCO3-) was markedly increased early after damage in both acidotic and alkalotic animals. In alkalotic animals mucosal blood flow increased about twofold in response to mucosal damage, whereas the early hyperemic response was either completely attenuated or blunted in acidotic animals. HCO3- release was correlated to availability of HCO3- by blood in alkalotic animals with luminal pH 5. Alkalotic animals showed improved repair compared with acidotic animals, and mucosal restitution was correlated to availability of HCO3- by blood. We conclude that luminal leakage of HCO3- or plasma after mucosal damage depends on availability by blood and consumption of HCO3- within the mucosa and that blood borne HCO3- has a major influence on gastric mucosal repair.

摘要

为研究酸碱平衡对胃黏膜修复的影响,在通过腔内注入2M氯化钠诱导黏膜损伤后,对麻醉的猫静脉注射氯化铵或碳酸氢钠。pH值为5或1的生理盐水通过口腔插管经胃腔灌注,并通过幽门插管排至装有pH和PCO₂电极的腔室。在酸中毒和碱中毒动物中,损伤后早期管腔碳酸氢根(HCO₃⁻)均显著增加。在碱中毒动物中,黏膜损伤后黏膜血流量增加约两倍,而在酸中毒动物中,早期充血反应要么完全减弱,要么受到抑制。在管腔pH值为5的碱中毒动物中,HCO₃⁻释放与血液中HCO₃⁻的可用性相关。与酸中毒动物相比,碱中毒动物的修复情况更好,且黏膜恢复与血液中HCO₃⁻的可用性相关。我们得出结论,黏膜损伤后HCO₃⁻或血浆的管腔渗漏取决于血液中的可用性以及黏膜内HCO₃⁻的消耗,并且血液中的HCO₃⁻对胃黏膜修复有重大影响。

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