Powell D W, Tapper E J, Morris S M
Gastroenterology. 1979 Jun;76(6):1429-37.
Because aspirin and the heavy metal salts of related anions have effects on intestinal ion transport and on diarrheal states, we have studied the effect of aspirin (ASA) on the in vitro rabbit ileum in an attempt to understand its mechanism of action. Ten millimolar of aspirin increased the conductance of rabbit ileum by 10--50% but did not change the permselectivity of the shunt path as determined by measurement of diffusion potentials. In Cl-free and HCO3-free solutions, aspirin reduced both Na absorption and the short-circuit current (Isc), which suggests an effect on electrogenic Na transport. Such an effect was not unexpected, since aspirin interferes with ATP production. However, in Ringer solution, aspirin in concentrations as little as 1 mM in the serosal solution reduced the Isc as before but also stimulated Na and Cl absorption and reduced JRnet (? HCO3 secretion) to zero. Aspirin had no effect on Na transport in the absence of Cl and no effect on Cl transport in the absence of Na, which suggests that aspirin stimulated a coupled transport process. Although these effects of ASA resemble those of alpha-adrenergic agents, ASA's effect was not blocked by alpha-adrenergic blockers such as phentolamine or phenoxybenzamine. The exact mechanism of ASA-stimulated NaCl absorption remains to be determined.
由于阿司匹林及相关阴离子的重金属盐对肠道离子转运和腹泻状态有影响,我们研究了阿司匹林(ASA)对体外兔回肠的作用,以试图了解其作用机制。10毫摩尔的阿司匹林使兔回肠的电导增加了10%至50%,但通过扩散电位测量确定,并未改变旁路的通透选择性。在无氯和无碳酸氢根的溶液中,阿司匹林降低了钠的吸收和短路电流(Isc),这表明其对电生性钠转运有影响。这种影响并不意外,因为阿司匹林会干扰ATP的产生。然而,在林格氏液中,浆膜溶液中低至1毫摩尔浓度的阿司匹林像之前一样降低了Isc,但也刺激了钠和氯的吸收,并使净JR(?碳酸氢根分泌)降至零。在无氯时阿司匹林对钠转运无影响,在无钠时对氯转运也无影响,这表明阿司匹林刺激了一种偶联转运过程。尽管ASA的这些作用类似于α-肾上腺素能药物的作用,但ASA的作用并未被酚妥拉明或酚苄明等α-肾上腺素能阻滞剂阻断。ASA刺激氯化钠吸收的确切机制仍有待确定。