Nutrient stimulation of mesenteric blood flow - implications for older critically ill patients.

Nutrient ingestion induces a substantial increase in mesenteric blood flow. In older persons (aged ≥ 65 years), particularly those with chronic medical conditions, the cardiovascular compensatory response may be inadequate to maintain systemic blood pressure during mesenteric blood pooling, leading to postprandial hypotension. In older ambulatory persons, postprandial hypotension is an important pathophysiological condition associated with an increased propensity for syncope, falls, coronary vascular events, stroke and death. In older critically ill patients, the administration of enteral nutrition acutely increases mesenteric blood flow, but whether this pathophysiological response is protective, or precipitates mesenteric ischaemia, is unknown. There are an increasing number of older patients surviving admission to intensive care units, who are likely to be at increased risk of postprandial hypotension, both during, and after, their stay in hospital. In this review, we describe the prevalence, impact and mechanisms of postprandial hypotension in older people and provide an overview of the impact of postprandial hypotension on feeding prescriptions in older critically ill patients. Finally, we provide evidence that postprandial hypotension is likely to be an unrecognised problem in older survivors of critical illness and discuss potential options for management.

Fetal and neonatal iron deficiency but not copper deficiency increases vascular complexity in the developing rat brain.

OBJECTIVES: Anemia caused by nutritional deficiencies, such as iron and copper deficiencies, is a global health problem. Iron and copper deficiencies have their most profound effect on the developing fetus/infant, leading to brain development deficits and poor cognitive outcomes. Tissue iron depletion or chronic anemia can induce cellular hypoxic signaling. In mice, chronic hypoxia induces a compensatory increase in brain blood vessel outgrowth. We hypothesized that developmental anemia, due to iron or copper deficiencies, induces angiogenesis/vasculogenesis in the neonatal brain. METHODS: To test our hypothesis, three independent experiments were performed where pregnant rats were fed iron- or copper-deficient diets from gestational day 2 through mid-lactation. Effects on the neonatal brain vasculature were determined using quantitative real-time polymerase chain reaction to assess mRNA levels of angiogenesis/vasculogenesis-associated genes and GLUT1 immunohistochemistry to assess brain blood vessel density and complexity. RESULTS: Iron deficiency, but not copper deficiency, increased mRNA expression of brain endothelial cell- and angiogenesis/vasculogenesis-associated genes (i.e. Glut1, Vwf, Vegfa, Ang2, Cxcl12, and Flk1) in the neonatal brain, suggesting increased cerebrovascular density. Iron deficiency also increased hippocampal and cerebral cortical blood vessel branching by 62 and 78%, respectively. DISCUSSION: This study demonstrates increased blood vessel complexity in the neonatal iron-deficient brain, which is likely due to elevated angiogenic/vasculogenic signaling. At least initially, this is probably an adaptive response to maintain metabolic substrate homeostasis in the developing iron-deficient brain. However, this may also contribute to long-term neurodevelopmental deficits.