The Arteriolar Vasodilatation Model of Vibrio cholerae Induced Diarrhoeal Disease

Abstract

Secretory diarrhoeal disease caused by enterotoxins produced by pathogenic bacteria is characterised by severe fluid loss into the intestine. A prevalent explanation for such high rates of loss, such as occur in episodes of cholera, is that intestinal epithelial cells (enterocytes) actively secrete chloride ion into the lumen. Fluid is drawn into the lumen because of the osmotic pressure difference that is created across the mucosa. Widely proposed as the cause of many forms of secretory diarrhoea, the enterocyte based paradigm displaced an earlier model of secretion i.e. fluid filtration caused by increased capillary hydrostatic pressure, possibly coupled with increased hydraulic conductivity. This would be aggravated by any concurrent inhibition of fluid absorption if it occurred. In the earlier and alternative paradigm, pathophysiological reductions in smooth muscle tone elevate capillary pressure, thereby increasing the hydrostatic pressure gradient that forces fluid from the capillary into the interstitial space and thence into the lumen. In this review, the present and historical evidence for the vasodilatation view of secretory diarrhoeal