Assessment of Gastric Mucosal Perfusion by Laser-Doppler Flowmetry

Abstract

Prolonged and/or severe intestinal mucosal hypoperfusion may lead to ischemic insult of splanchnic organs which have been hypothesized to play a role in the pathogenesis of the multiple organ dysfunction syndrome (MODS) [1, 2], a frequent complication of low flow states including hypovolemia, cardiogenic and septic shock. The normal neuro-hormonal response to low flow states includes earlier musculocutaneous and splanchnic vasoconstrictions mediated by both sympathetic and renin-angiotensin systems [3, 4]. During sympathetic stimulation, a vascular phenomenon known as “autoregulatory escape” has been described in the gastric [5] and intestinal circulations [6], i.e. after sympathetic stimulation, initial decrease in gastrointestinal (GI) blood flow was followed by a return of GI blood flow to values near or equivalent to pre-stimulation values. However, such regulatory phenomenon seems limited to moderate sympathetic stimulation [5]. As regard to the blood flow distribution within the gut, Shepherd et al. [7] found a redistribution of blood flow within the intestinal wall layers to mucosa during the sympathetic stimulation. However, regulatory capacities of gut mucosa appear limited during intense sympathetic stimulation and splanchnic vasoconstriction. In addition, anatomic factors make the gut mucosa extremely susceptible to the decrease of oxygen delivery (DO₂) during low flow states. The microcirculation of the intestinal virus is supplied by a central arteriole which branches at the tip of the villus into a capillary and veinules network. So, flow in the capillaries and veinules is opposite in direction to the flow in the arteriole. The proximity of ascending and descending vessels permits arterio-venous diffusion of oxygen from arteriole to drainage network. Consequently, oxygen tensions are normally lower at the tips than at the bases of the villus. During low flow states, this countercurrent arterio-venous shunting of oxygen (O₂) is accentuated. Thus, it may be postulated that this phenomenon is important in the development of villus injury under ischemic conditions. The second structural factor favoring mucosal hypoxia during decrease of DO₂ is the right angle origin of the villus arteriole. This arrangement favors the passage of plasma compared to red blood cells (“plasma skimming”) resulting in the villus hematocrit being less than that in arterial blood. Thus, during low flow states, this phenomenon increases and diminishes the O₂ carrying capacity of the blood in villous capillaries [8]. During endotoxic shock, regulatory capacities of gut mucosa are altered [9,10]. Schumacker et al. [9] demonstrated that the ability of the gut to extract O₂ was diminished after endotoxin infusion. Moreover, gut adjustments in perfused capillary density, in response to decrease in DO₂, were impaired after lipopolysaccharide (LPS) administration [11]. In addition, during endotoxemia, tissue hypoxia persisted in the mucosa despite resuscitation, and the increased blood flow within the gut wall was redistributed from the mucosa to the muscularis [10].