Intestinal and Cerebral Oxygenation during Severe Isovolemic Hemodilution and Subsequent Hyperoxic Ventilation in a Pig Model

Abstract

During isovolemic hemodilution, the diminished oxygen supply was redistributed in favor of organs with a lower capacity to increase oxygen extraction. It is hypothesized that redirection of the oxygen supply within the intestines resulted in the preservation of oxygen consumption and mucosal muPo(2) compared with serosal muPo(2).

Reassessing the risk of hemodilutional anemia: Some new pieces to an old puzzle

“…A small increase in overall oxygen consumption was attributed, in part, to the increase in myocardial oxygen consumption, while systemic lactate did not increase. Although some variability exists, remarkably similar patterns of response have been observed in other clinical 42 and experimental studies utilizing pig, 43 dog, [44][45][46] and rat 14,47,48 models.…”

“…14,23,43,58,61 Reduced tissue oxygen tension occurs in a hierarchical manner in which organs that are critically important for survival (heart, brain) receive preferential oxygen delivery and maintain tissue ''normoxia'' at very low Hb levels (* 35-50 gÁL -1 ). 14,23,43 This is consistent with the relatively disproportional increases in heart and brain blood flow that have been measured during acute hemodilution. 43,62 Conversely, less vital organs (kidney, intestine) become hypoxic at much higher Hb levels (* 60-70 gÁL -1 ).…”

“…34 In the second proposed mechanism (active-hypoxia), the reduced hematocrit leads to a decrease in blood oxygen content causing a reduction in tissue oxygen delivery that is sensed at the tissue level. 14,23,43 The reduction in tissue PO 2 results in activation of the sympathetic nervous system, which mediates a coordinated increase in cardiac output (CO) and a reduction in SVR 44 by direct (local tissue hypoxia) and remote mechanisms (perivascular innervation). In addition, the increase in the sympathetic nervous system activity reduces venous capacitance, thereby increasing venous return.…”

Plasma methemoglobin as a potential biomarker of anemic stress in humans

“…1). Second, the increase in DeoxyHb in local vascular beds, secondary to increased oxygen extraction, 23,24 would favour the production of NO from nitrite with MetHb as the byproduct (Fig. 2).…”

“…These proposed mechanisms may be particularly favoured during anemia since local production of NO would be supported by an increase in tissue oxyHb extraction which is known to occur in anemic vascular beds. 23,24 For example, in the brain, acute anemia increases Hb O 2 extraction from *30% (Hb * 140 gÁL -1 ) to *50% (Hb * 50 gÁL -1 ), 23 while brain microvascular PO 2 decreases from *70 to *50 mmHg. 6,7 As such, methemoglobin (MetHb) production may be favoured in anemic vascular beds.…”