Hypoxemia in humans leads to an increase in ventilation, a rise in cardiac output and vasodilation in muscle. In addition, multiple lines of evidence suggest that during hypoxemia, the sympathetic nervous system is activated. In a recent study, we confirmed that during hypoxemia, muscle vasodilation occurs despite increased vasoconstrictor nerve traffic and a rise in norepinephrine release. Thus, vasodilation represents a paradox and local vasodilator mechanisms have been implied though not proven to be responsible. However, when breathing ceases during hypoxia, dramatic vasoconstriction occurs. This raises the question whether a reflex mechanism modulated by ventilation mediates vasodilation. A cholinergic vasodilator system has been recognized in many animal species and was recently demonstrated in humans. Its possible role in the circulatory control during hypoxemia is unexplored.
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