Irwin et al. studied the role of cerebral hypoxia in the development of neurogenic pulmonary edema (NPE). In their elegant study, they showed that infusion of autologous venous hypoxic blood to the brain circulation induced the development of NPE in a canine model.
In addition, these animals had a greater fall in arterial Po2 and Sao2 and higher peak plasma norepinephrine compared to controls, whose brains were perfused with autologous arterial blood. In their discussion, Irwin et al. mentioned a very important problem, that " anesthetic effects such as isofl urane are known to blunt autonomic reflexes thus possibly masking some effects of cerebral-hypoxia-induced activation of sympathetic nervous system. "