Hypothermia is known to improve tissue function in different organs during physiological and pathological conditions. The aim of this study was to evaluate the effects of hypothermia on oral and gastric mucosal microvascular oxygenation (μHbO2) and perfusion (μflow) under physiological and hemorrhagic conditions. Five dogs were repeatedly anesthetized. All animals underwent each experimental protocol (randomized cross-over design): hypothermia (34°C), hypothermia during hemorrhage, normothermia, and normothermia during hemorrhage. Microcirculatory and hemodynamic variables were recorded. Systemic (DO2) and oral mucosal (μDO2) oxygen delivery were calculated. Hypothermia increased oral μHbO2 with no effect on gastric μHbO2. Hemorrhage reduced oral and gastric μHbO2 during normothermia (？36 ± 4% and ？27 ± 7%); however, this effect was attenuated during additional hypothermia (？15 ± 5% and ？11 ± 5%). The improved μHbO2 might be based on an attenuated reduction in μflow during hemorrhage and additional hypothermia (？51 ± 21？aU) compared to hemorrhage and normothermia (？106 ± 19？aU). μDO2 was accordingly attenuated under hypothermia during hemorrhage whereas DO2 did not change. Thus, in this study hypothermia alone improves oral μHbO2 and attenuates the effects of hemorrhage on oral and gastric μHbO2. This effect seems to be mediated by an increased μDO2 on the basis of increased μflow. 1. Introduction The gastrointestinal tract is not only responsible for nutrient absorption but also functions as a metabolic and immunological system, forming an effective barrier against endotoxins and bacteria in the intestinal lumen. Maintenance of this mucosal barrier function by improving perfusion and oxygenation seems to be of vital importance [1–3]. However, during severe illness (e.g., septic or hypovolemic shock) blood flow is redistributed and splanchnic oxygenation is impaired early to preserve perfusion of more vital organs (i.e., heart and brain) [4, 5]. Insufficient microcirculatory oxygen supply impairs mucosal barrier function and has been shown to enable translocation of bacteria and bacterial toxins into portal venous and local lymphatic circulation [6] and to mediate an inflammatory response syndrome [7]. Therefore, adequate splanchnic perfusion and in particular oxygenation of the gastrointestinal mucosa are considered crucial for the prevention and therapy of critical illness [1, 8, 9]. Alterations of the oral microcirculation are an independent predictor of organ failure and associated with a high mortality [10, 11]. Thus, growing effort is made to
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