Can the "brain-sparing effect" be detected in a small-animal model?

Background: Under O(2) imbalance in the body, blood redistribution occurs between more vital organs and less vital organs. This response is defined as the "brain-sparing effect". The study's aim was to develop a new rat model for simultaneous real-time monitoring of tissue viability in a highly vital organ, the brain, and a less vital organ, the small intestine, under various metabolic perturbations and emergency-like situations.

Material/methods: The cerebral cortex and intestinal serosa were exposed in anesthetized rats and a multi-site multi-parametric (MSMP) monitoring system was connected to both. Tissue blood flow (TBF) was monitored using laser Doppler flowmetry and mitochondrial function by NADH fluorometry. The perturbations performed were anoxia (30 sec) and 20 minutes of hypoxia, hypercapnia, or hyperoxia.

Results: Under oxygen deficiency, cerebral blood flow (CBF) increased (315+/-53% in anoxia and 140+/-12% in hypoxia), whereas intestinal blood flow decreased (60+/-11% in anoxia and 56+/-13% in hypoxia). Mitochondrial NADH significantly increased in both organs (119+/-2.8% and 151+/-14% in the brain and intestine, respectively). Under hyperoxia, NADH was oxidized in both organs (up to 9% change). Hypercapnia led to an increase in CBF (143+/-11%) and oxidation of mitochondrial NADH (by 10%), with no significant changes in the intestine.

Conclusions: The two organs respond significantly differently to lack of O(2) by activating the sympathetic nervous system. Monitoring less vital organs may indicate an early response to emergency situations. Therefore, a less vital organ could be used as a surrogate organ to be monitored in order to spare the brain.