Changes in transepithelial water and electrolyte transport as causative or contributing factors of the diarrhoea and constipation found associated with changes in thyroid physiology were studied. Albino Wistar rats were pharmacologically made either hypothyroid or hyperthyroid. After sacrifice, the small intestine was mounted in Ussing chambers in order to measure in vitro ion net fluxes under short-circuit conditions. Hypothyroid animals showed an increase in intestinal transit time, Cl- absorption (mainly due to an increment in its mucosal to serosal component) and residual ion flux (which is believed to represent HCO3- secretion) when compared with euthyroid animals. The hyperthyroid animals showed a decrease in Cl- mucosal to serosal transport. Furthermore, a significant correlation was found between serum L-thyroxine (T4) levels and both net Cl- transport (r = -0.74, P < 0.00001) and residual ion flux (r = -0.55, P < 0.005). These results indicate that the effect of T4 is firstly to inhibit Cl-/HCO3- anion exchange thereby influencing transepithelial flux transport and secondly to affect intestinal motility. Such inhibition was not found when T4 was acutely added to rat ileum, suggesting that the effect on electrolyte transport probably requires protein synthesis. In conclusion, the phenomenon observed in vitro could explain the clinical manifestations of constipation and diarrhoea in hypo- and hyper-thyroidism respectively.
's Ilosp, London. studies wcre undertaken to assess the value of including base in ORS in (i) an animal model of intestinal secretion and (ii) children with acutc gastroenteritis. After exposure to cholera toxin, rat small intestine was perfused in situ with ORS containing base or identical OR5 in which base was replaced by chloride.
Altered states of thyroidism are associated to alterations in stool patterns. The aim of our study was to see whether T4 has a role in intestinal handling of electrolyte and water transport. In the first set of experiments, adult rats were dlvided into 3 groups (G-1,2,3) and either untreated (G-l), treated with Tapazolec Tq (G-2) or with Tapazole alone IG-3) for 4 wks. Transepithelial brdirectlonal fluxes of Na and C1 were measured land net calculated) across ileal mucosa mounted In Ussing chambers. Serum T4 in G-1 15.0+1.3pg/dl; mean+SD) and G-2 15.252.2) did not differ but both differed from G-3 12.75.5; p<0.001). Net ileal C1 flux (absorption "+"; secretion "-"1 did not differ between G-1 I-1.2~2.4 p~q/cm~hr) and G-2 (-.2+1;6) but both differed from G-3 (+3.1+1.3; p<0.001). T4 correlated with C1 net transport lr=.61;p<0.025), and the latter with n net lassumed to be HC03 net flux) lr=.65;p<0.005). In the 2nd set of experiments, rats were given orally T4 for 4 wks. They were then divlded in 3 groups, according to serum Tq levels: G-4, T4 ranging 6.0-7.5 pg/dl lcontrols), G-5, T4 7.6-9.5 and G-6, Tq >9.6. G-5 rats showed, when compared to G-4, marked shift toward secretion in JClnet IG-5: C1= -4.521.2 vs G-4: C1= +2.36+.92, ~(0.01. Again, serum T4 correlated (r= -.52,p<0.05) with C1 net transport. On the contrary, G-6 rats differed from G-5 In that they paradoxically showed higher rates of absorption far both Na and C1. We conclude that serum T4 affects intestinal net transport of C1 by shifting it toward secretion, while it affects in the opposite manner the net transport of JR. These effects, no longer seen at the highest T4 serum levels, are consistent with a direct effect of T4 on the C1/HC03 exchange mechanism, and may explain the alterations in stool patterns seen in dysthyroid states. THE EFFECTS OF VITAMIN E DEFICIENCY ON SMALLInstitute of Child Health, London, England The gastrointestinal mucosa is vulnerable to damage by lipid peroxidation. Vitamin E (El is a powerful membrane bound antioxidant present in high concentration in enterocytes. We have studied the effects of E deficiency on mucosal function. 20 day old male Wistar rats were placed on a diet either deficient in E or one to which E (103qfkg) had been added. Brush border membrane vesicles of small intestine were prepared by a CafCprecipitation method and glucose and sodium uptake measured. N~+ K + A T P~S~, CAMP and cGMP were determined in mucosal homogenates. Na+ stimulated glucose uptake was rapid with an 'overshoot' in both groups but after 9 months of E deficiency maximal glucose uptake was signifi~antly impaired (757'116 vs 1152'324 pmollhrlmg protein; meantlSD; n.5; pc0.05).H+ stimulated Na+ uptake was similarly reduced (380'148 vs 743'181, p<0.02).In the absence of a Na+ or H+ gradient, uptake of glucose and NaC was not affected by E deficiency. No significant differences in Na+K+ATPase activity or cyclic nucleotide concentrations were observed. These data show that intestinal transport is disturbed in E deficiency and suggest that thi...
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