Abstract

The response of spinal cord blood flow (SCBF) to high-dose barbiturate therapy is documented. In nine mongrel dogs with an arterial pCO2 (PaCO2) of 40 mm Hg, sodium thiopental was administered to produce 30, 60, 120, and 240 seconds of electroencephalographic (EEG) burst suppression. At 30-second intervals of EEG suppression, cervical and thoracic cord segments demonstrated a decrease in SCBF of 47% and 39%, respectively, from control values. Isoelectric EEG intervals longer than 30 seconds were not associated with any further significant decrease in SCBF. In 13 other dogs and in the absence of barbiturates, hypocapnia to 20 mm Hg from PaCO2 of 60 mm Hg produced reductions in SCBF of 89% for the cervical and 82% for the thoracic segments. In the presence of thiopental-induced 30- to 60-second intervals of EEG silence, the decrement in SCBF in response to the same degree of hypocapnia was 83% and 75%, respectively, although the absolute value of this reduction was half that without barbiturates. These findings of a significant reduction in SCBF in response to high-dose barbiturate therapy are suggestive of a protective effect of barbiturates upon spinal cord injury as occurs in the brain. Further studies of the influence of barbiturates upon spinal cord compressive syndromes are indicated.

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