Proceedings of The Physiological Society
University of Cambridge (2008) Proc Physiol Soc 11, C87
The interaction of stretch, intraluminal pressure and E.coli heat stable (STa) enterotoxin on jejunal fluid absorption in the anaesthetised rat
M. L. Lucas1, P. J. Tainsh1, S. McColl1, H. L. Kenward1, P. C. Watson1, L. C. Gilligan1, V. Graham1, Y. B. Nelson1
1. IBLS, N&BS, Glasgow, United Kingdom.
A perfused intestinal loop preparation was used to measure luminal uptake of fluid in vivo by means of fluid volume recovery from the jejunum of the anaesthetised rat (70 mg/Kg i.p. sagatal). All procedures were carried out in conformity with current UK legislation. Data is given as the mean plus the standard error with the number of experiments in brackets. Significance was tested by 't'-test. Distension of the jejunum with a polythene loop in the lumen reduced fluid absorption (p<0.001) from 116 ± 18 (7) ul/cm/hr to 40 ± 5 (10) ul/cm/hr. Heat stable (STa)toxin from E.coli reduced fluid absorption further to 14 ± 13 (6) ul/cm/hr in the stretched intestine, not significantly different from zero fluid absorption. Distension by 30 cm hydrostatic pressure reduced fluid absorption (p<0.01) to 52 ± 10 (6) ul/cm/hr. Combination with STa reduced fluid absorption to 29 ± 10(5). Lack of net secretion implies that distension does not initiate a secretory event but prevents absorption. The lack of super-imposition of STa and distension effects implies a common absorption mechanism inhibited by both. Low rates of fluid absorption by coil distension were not restored by serosal application of lidocaine, i.v. hexamethonium or luminal perfusion of atropine. In contrast, luminal atropine did restore fluid absorption in jejunum distended by hydrostatic pressure,from 52 ± 10(6)ul/cm/hr to 103 ± 15(5)ul/cm/hr, not significantly different from the undistended jejunal value. The neural component to the inhibition of absorption is likely to be mediated through an axon reflex within a cholinergic neuron. In contrast, neither i.v. hexamethonium, serosal lidocaine nor luminal atropine restored fluid absorption after exposure to STa, making unlikely a local neural component to the action of STa. Luminal carbachol (1mM) reduced net fluid absorption to 31.9 ± 7.6 (6) ul/cm/hr that was significantly lower than control values and comparable to absorption rates after exposure to STa. Isotonic choline chloride perfused in combination with STa suppressed sodium ion dependent fluid absorption. Additionally perfusing with 1 mM carbachol gave no further decrease in fluid absorption, indicating that no secretion process was detected that could worsen inhibited absorption. This indicated that a cholinergically mediated secretory process was unlikely to be present in the proximal jejunum. The reduction in fluid absorption after STa exposure and after pressure distension is likely to be the result of a final convergence of both pathways on sodium: hydrogen ion exchange with the pressure distension mediated by the internal release of acetylcholine through an initiation of the intestino-intestinal stretch reflex.
Where applicable, experiments conform with Society ethical requirements