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A small number of animal studies have suggested that during the delayed postischemic hypoperfusion state, CO 2  reactivity of the cerebral vasculature is lost whereas autoregulation is retained. These findings, however, are inconsistent with the bulk of experimental evidence which demonstrates that CO 2  reactivity is more robust and may be retained in pathologic circumstances which abolish autoregulation. These opposing viewpoints were therefore further evaluated in 18 dogs in which complete global ischemia was induced by cerebrospinal fluid (CSF) compression for periods of 12 ( n = 12) and 18 ( n = 6) min. Following 45 min of reperfusion and with onset of the delayed postischemic hypoperfusion state, autoregulation and CO 2  reactivity were evaluated using a continuous measurement of CBF (by sagittal sinus outflow). CO 2  reactivity was tested over a P a co 2  range of 20 to 60 mm Hg; autoregulation was tested over a blood pressure range of 60 to 140 mm Hg. Results demonstrated that after both 12 and 18 min of complete global ischemia, autoregulation and CO 2  reactivity of the cerebral vasculature were both present, but attenuated. In the case of CO 2  reactivity, the slope of the CBF response was decreased approximately 75%. In the case of autoregulation, the response in some dogs was incomplete as compared with their preischemic response.

Cerebral Vascular Autoregulation and CO2 Reactivity following Onset of the Delayed Postischemic Hypoperfusion State in Dogs

Cerebral Vascular Autoregulation and CO₂ Reactivity following Onset of the Delayed Postischemic Hypoperfusion State in Dogs