Vascular control in the colon and rectum

Blood flow and its intramural distribution in the large and small intestines 'at rest' appear to be quite similar, but there are some obvious differences in the regulation of the circulation in these two viscera. Autoregulation of blood flow is well developed in most regions of the gut, with the exception of the colon in which total blood flow varies greatly with arterial blood pressure. However, the colonic autoregulatory capacity can be improved by increasing the metabolic demand of the tissue, e.g. by intra-luminal placement of nutrients. Metabolic and myogenic factors seem to be mutually responsible for autoregulatory behaviour in the large intestine. Functional vasodilatation occurs in the large intestine in response to increased metabolism, a reaction which can be evoked for instance by intra-luminal placement of volatile fatty acids. Mechanical stimulation of the mucosa in the proximal colon also elicits a local hyperaemic response which is postulated to be mediated via an intrinsic nervous reflex possibly releasing 5-HT. In the distal colon and the rectum mechanical stimulation evokes a more wide-spread hyperaemia which is reported to be the result of a pelvo -pelvic reflex with vasoactive intestinal polypeptide (VIP) as a possible mediator. Activation of the sympatho-adrenal system causes constriction of the large intestinal resistance and capacitance vessels. Reflex increase in sympathetic activity, as in exercise or haemorrhage, causes a redistribution of flow and a mobilization of blood from the large intestine to other tissues, thereby, in stress situations, promoting the circulation in more vital organs such as the heart and brain. The most distal part of the large intestine, in particular the rectum, seems to have a unique extrinsic vasodilator control via the parasympathetic pelvic nerves. Activation of these nerves elicits a very pronounced and well maintained vasodilator response in the rectum but only a transient one in the distal colon. This neural vasodilator response is little affected by muscarinic blockade and, hence, largely non-cholinergic in nature. VIP is released from the colon and rectum during pelvic nerve stimulation, the rectal output being especially large and well correlated in time to the concomitant vasodilatation. The rectal vessels are very sensitive to VIP, and intra-arterial infusion of this peptide causes a vascular response which closely resembles that of pelvic nerve stimulation. Such evidence indicates that VIP might be the neurotransmitter responsible for the non-cholinergic vasodilatation in the most distal part of the large intestine.