Verhaeren E H, Geeraerts V C, Lemli J
J Pharm Pharmacol. 1987 Jan;39(1):39-44. doi: 10.1111/j.2042-7158.1987.tb07159.x.
Rhein (1,8-dihydroxy-3-carboxyanthraquinone), in a concentration of 6 X 10(-4)M, inhibits water absorption from the colon and causes a net transfer of fluid and electrolyte into the intestinal lumen. Morphine (4 X 10(-4)M) counteracted the water and electrolyte secretion. Prior perfusion with morphine protected the large intestine from the laxative effect of a rhein perfusion. Differences in absorption rate of 99mTc-EDTA, a poorly absorbable marker, were found, as morphine caused nearly all radioactive compound to be retained in the colon, while rhein significantly facilitated the transfer of marker from colon through mucosal barrier to blood. The route followed by the 99mTc-EDTA complex was not the same as that followed by water, suggesting that 99mTc-EDTA travels by a paracellular route. Morphine counteracted the inhibition of Na+ absorption caused by rhein and antagonized the massive loss of K+ incurred by the presence of rhein in the colon. Cl- absorption is reversed to secretion in the presence of rhein while normal values were restored by morphine. Neither the HCO-3 content nor the pH were affected by either drug. Active absorption of glucose was completely blocked in the presence of rhein; the block could be antagonized by morphine.
大黄酸（1,8 - 二羟基 - 3 - 羧基蒽醌），浓度为6×10⁻⁴M时，可抑制结肠对水的吸收，并导致液体和电解质向肠腔内净转移。吗啡（4×10⁻⁴M）可抵消水和电解质的分泌。预先用吗啡灌注可保护大肠免受大黄酸灌注的泻下作用。发现难吸收标记物⁹⁹ᵐTc - EDTA的吸收率存在差异，因为吗啡使几乎所有放射性化合物保留在结肠中，而大黄酸则显著促进标记物从结肠通过黏膜屏障向血液的转移。⁹⁹ᵐTc - EDTA复合物所走的途径与水不同，这表明⁹⁹ᵐTc - EDTA通过细胞旁途径运输。吗啡抵消了大黄酸引起的Na⁺吸收抑制，并拮抗了大黄酸在结肠中导致的大量K⁺流失。在大黄酸存在下，Cl⁻的吸收转变为分泌，而吗啡可使其恢复到正常水平。两种药物均未影响HCO₃⁻含量和pH值。在大黄酸存在下，葡萄糖的主动吸收完全受阻；这种阻断可被吗啡拮抗。
