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

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

Postprandial hypotension in clinical geriatric patients and healthy elderly: prevalence related to patient selection and diagnostic criteria.

Contains fulltext : 89682.pdf (publisher's version ) (Open Access)The aims of this study were to find out whether Postprandial hypotension (PPH) occurs more frequently in patients admitted to a geriatric ward than in healthy elderly individuals, what the optimal interval between blood pressure measurements is in order to diagnose PPH and how often it is associated with symptoms.The result of this study indicates that PPH is present in a high number of frail elderly, but also in a few healthy older persons. Measuring blood pressure at least every 10 minutes for 60 minutes after breakfast will adequately diagnose PPH, defined as >20 mmHg systolic fall, in most patients. However with definition of PPH as >30 mmHg systolic fall, measuring blood pressure every 10 minutes will miss PPH in one of three patients. With the latter definition of PPH the presence of postprandial complaints is not associated with the existence of PPH

Symptomatic Carotid Plaques Demonstrate Less Leaky Plaque Microvasculature Compared With the Contralateral Side: A Dynamic Contrast-Enhanced Magnetic Resonance Imaging Study

Contains fulltext : 207086.pdf (publisher's version ) (Open Access)Background Rupture of a vulnerable carotid atherosclerotic plaque is an important underlying cause of ischemic stroke. Increased leaky plaque microvasculature may contribute to plaque vulnerability. These immature microvessels may facilitate entrance of inflammatory cells into the plaque. The objective of the present study is to investigate whether there is a difference in plaque microvasculature (the volume transfer coefficient K(trans)) between the ipsilateral symptomatic and contralateral asymptomatic carotid plaque using noninvasive dynamic contrast-enhanced magnetic resonance imaging. Methods and Results Eighty-eight patients with recent transient ischemic attack or ischemic stroke and ipsilateral >2 mm carotid plaque underwent 3 T magnetic resonance imaging to identify plaque components and to determine characteristics of plaque microvasculature. The volume transfer coefficient K(trans), indicative for microvascular density, flow, and permeability, was calculated for the ipsilateral and asymptomatic plaque, using a pharmacokinetic model (Patlak). Presence of a lipid-rich necrotic core, intraplaque hemorrhage, and a thin and/or ruptured fibrous cap was assessed on multisequence magnetic resonance imaging . We found significantly lower K(trans) in the symptomatic carotid plaque compared with the asymptomatic side (0.057+/-0.002 min(-1) versus 0.062+/-0.002 min(-1); P=0.033). There was an increased number of slices with intraplaque hemorrhage (0.9+/-1.6 versus 0.3+/-0.8, P=0.002) and lipid-rich necrotic core (1.4+/-1.9 versus 0.8+/-1.4, P=0.016) and a higher prevalence of plaques with a thin and/or ruptured fibrous cap (32% versus 17%, P=0.023) at the symptomatic side. Conclusions K(trans) was significantly lower in symptomatic carotid plaques, indicative for a decrease of plaque microvasculature in symptomatic plaques. This could be related to a larger amount of necrotic tissue in symptomatic plaques. Clinical Trial Registration URL : http://www.clinicaltrials.gov.uk . Unique identifier: NCT 01208025