Autonomic nervous system mediated effects of food intake. Interaction between gastrointestinal and cardiovascular systems.

Abstract

The studies presented in this thesis focused on the autonomic nervous system mediated interactions between the gastrointestinal and cardiovascular systems in response to food intake and on potential consequences of failure of these interactions. The effects of food intake on cardiovascular parameters, including muscle sympathetic nerve activity, were studied in healthy young and healthy elderly individuals, in patients who were admitted to the geriatric ward and in patients with irritable bowel syndrome. Furthermore, we studied whether there was a temporal relationship between food intake and the occurrence of acute focal brain ischemia in patients with a compromised cerebral blood flow. During and after food intake, the oxygen demand of the gastrointestinal system increases, causing an increased blood flow towards the digestive organs. In order to maintain a stable systemic blood pressure during this redistribution of blood, a number of mechanisms mediated by the autonomic nervous system are activated. When these mechanisms fail, blood pressure falls. We found a prevalence of postprandial hypotension of 40% in healthy elderly and 91% in patients who were admitted to the geriatric ward. To differentiate the effects of the volume of a meal from those of the nutrient content, pressure controlled balloon distension of the stomach, and intraduodenal nutrient infusion were used, respectively. Our results showed that an important reflex that increases sympathetic activity and blood pressure in response to distension of the stomach and was described previously by our group, the so-called gastrovascular reflex, attenuates with aging. The role of this reflex might be to compensate for the shift in blood flow toward the splanchnic system during eating. The importance of this gastrovascular reflex was demonstrated by administering glucose into the duodenum without distending the stomach. This prevented activation of the gastrovascular reflex and we found that by doing this, blood pressure indeed decreased after glucose administration in the duodenum. This fall in blood pressure was greater in healthy elderly than in healthy young individuals. Thus, we found two reasons that might explain why aging is accompanied by an increased prevalence of blood pressure falls after eating. The blood pressure fall in postprandial hypotension is usually mild, but we hypothesized that mild hypotension in combination with a compromised cerebral blood flow due to stenosis or occlusion of the carotid arteries, might lead to focal brain ischemia. As a first step, we investigated whether there is a temporal relationship between food or alcohol intake and the occurrence of focal brain ischemia in those patients. The results could not support the existence of such a relationship, suggesting that this mechanism does not play a major role. Another group of patients who also suffer from symptoms in response to food intake that might be mediated by the autonomic nervous system are those with irritable bowel syndrome. We found no difference in muscle sympathetic nervous activity increase after food intake between healthy young subjects and patients with irritable bowel syndrome, but there were consistent differences in measures of the parasympathetic system, suggestive of a reduced parasympathetic reactivity.