Specific hemodynamic changes in acute ischemia were investigated using a middle cerebral artery occlusion primate model and positron emission tomography. The cerebral blood flow (CBF), cerebral blood volume, oxygen extraction fraction (OEF), and cerebral metabolic rate for oxygen were measured 1, 3, and 9 hours after occlusion. OEF showed an increase in ischemic areas, and especially where CBF was below 18 ml/100 gm/min 1 hour after occlusion the OEF increased significantly (0.69 +/- 0.20, p < 0.05). Nine hours after occlusion, the OEF values were lower compared to those 1 and 3 hours after occlusion. Areas where CBF ranged from 18 to 31 ml/100 gm/min showed an increase in OEF at all times (p < 0.05). Clearly, OEF changes remarkably in the acute stage.

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Effects of naloxone and flumazenil on isoflurane activities were examined on dorsal horn neurons in cats. Isoflurane suppressed bradykinin-induced nociceptive responses in transected feline spinal cords. The bradykinin-induced neuronal firing rates were significantly suppressed by 60.0%, 35.3% and 32.2% at 10, 20 and 30 min after isoflurane administration, respectively. The 32.3% suppression on bradykinin-induced neuronal responses at 30 min after isoflurane administration was not reversed 5 min after administration of naloxone (36.4% suppression). The suppressive effects of isoflurane were not reversed by naloxone (0.2 mg.kg(-1), i.v.). Similarly, the benzodiazepine antagonist, flumazenil (0.2 mg.kg(-1), i.v.), did not affect the suppressive effects of isoflurane. Failure of naloxone and flumazenil to reverse the suppressive effects of isoflurane suggests that isoflurane interacts with neither opioid nor benzodiazepine receptors in producing its suppressive action on nociceptive responses in dorsal horn neurons of the feline spinal cord.

The effects of gas composition in the subarachnoid space (injection of air or N(2)O) and in an anesthetic gas mixture (inhalation with or without N(2)O) on cerebrospinal fluid pressure were studied in 22 patients with pneumocisternography for transsphenoidal craniectomy. N(2)O (66%) anesthesia for 10 min increased cerebrospinal fluid pressure by up to 150% in 7 patients who were intrathecally injected with air. Withdrawal of N(2)O from the anesthetic gas mixture for sixty minutes reduced cerebrospinal fluid pressure to the initial pressure. A second N(2)O administration to the anesthetic gas mixture did not elevate cerebrospinal fluid pressure by as much as the first N(2)O administration. In 7 patients receiving subarachnoid air injection, replacing 66% N(2)O with 66% nitrogen prevented the change in cerebrospinal fluid pressure throughout the operation. In 8 patients N(2)O anesthesia and N(2)O intrathecal injection failed to eliminate the rise in cerebrospinal fluid pressure in 8 patients. Withdrawal of N(2)O from the anesthetic gas mixture for 60 min is recommended to prevent an extreme increase in cerebrospinal fluid pressure during pneumocisternography.

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