Compensatory hypertrophy of the residual small intestine after partial enterectomy. A neurohumoral feedback?

Experiments were designed to test, using 76 pigs, 1) whether a humoral factor inducing compensatory hypertrophy is released after partial enterectomy or not, and 2) whether visceral sensitivity conducted to the central nervous system by the route of the vagus plays a role in the compensatory hypertrophy or not. Vascular parabiosis was established between pigs paired for an identical blood group and histocompatibility. A continuous blood cross circulation was maintained for 410 h either between two normal pigs or between a normal and a jejunectomized (30 per cent) pig. Their growth and food intake, and the tissue weight of their small intestine were checked. Both the jejunectomized pigs and their unoperated partners showed a significant hypertrophy of the small intestine, whether residual or intact, as compared to intact pigs cross circulated between them. The hypertrophy observed in the unoperated partners of the jejunectomized pigs was not the result of any hyperphagia. There was thus a true humoral mediation of the compensatory hypertrophy. Vagal deafferentation, i.e. a selective surgical suppression of the vagal afferent (sensory) pathways originating below the diaphragm, was performed in jejunectomized pigs. Their performances and small intestine morphology (whole tissue weight and dry weight of the mucosa) were compared to those measured in jejunectomized but vagally intact pigs. The dry weight of the mucosa of the residual small intestine in resected pigs was restored (after 28 days) at a value similar to that measured for the intact small intestine in controls. Opposite to that, the dry weight of the mucosa of the residual intestine of resected + deafferented pigs was significantly lower, due to the absence of any compensatory hypertrophy. This difference did not result from any change in the food intake level. Therefore it was concluded that vagal afferences from the digestive tract are necessary in eliciting the compensatory hypertrophy. From these results and some recent bibliographical data, it is tentatively concluded that compensatory hypertrophy of the residual small intestine after partial enterectomy might be mediated through a neuro-humoral feedback whose afferent way would be the vagal sensory pathway, and efferent way would be a hormonal one monitored by the hypothalamo-hypophyseal axis.