Summary:The cerebral cortical cup technique was used to monitor changes in adenosine and inosine levels in the rat cerebral cortex during periods of hypoxia, anoxia, or hemorrhagic hypotension. Basal levels of adenosine and inosine in cortical perfusates stabilized within 10 min at concentrations of 30-50 and 75-130 nM, respectively. Comparable levels were observed in normal CSF col lected from the cisterna magna. Reductions in the oxygen content of the inspired air (14, 12, 8, and 5% oxygen) re

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The advent of newer generation high resolution computed tomography (CT) scanners has revolutionized diagnostic evaluation in head and neck cancer. Since the development of conservation surgical techniques for the larynx, a precise preoperative evaluation of the extent of laryngeal involvement by carcinoma has been of prime importance. No single diagnostic study now yields more information regarding the anatomic extent of tumor than high resolution CT scanning. This study was designed to evaluate the reliability of CT scanning in determining extent of disease at several laryngeal levels by comparing preoperative CT scans with corresponding postoperative pathology obtained by serially sectioning laryngeal specimens. We found very good correlation in the inferior larynx and good correlation in the superior larynx. Determination of cartilage invasion proved very difficult, and scanning was unreliable at all levels when severe postradiation reactions were present.

The effects of a potent adenosine deaminase inhibitor, deoxycoformycin, on purine and amino acid neuro-transmitter release from the ischemic rat cerebral cortex were studied with the cortical cup technique. Cerebral ischemia (20 min) was elicited by four-vessel occlusion. Purine and amino acid releases were compared from control ischemic animals and deoxycoformycin-pretreated ischemic rats. Ischemia enhanced the release of glutamate, aspartate, and gamma-aminobutyric acid into cortical perfusates. The levels of adenosine, inosine, hypoxanthine, and xanthine in the same perfusates were also elevated during and following ischemia. Deoxycoformycin (500 micrograms/kg) enhanced ischemia-evoked release of adenosine, indicating a marked rise in the adenosine content of the interstitial fluid of the cerebral cortex. Inosine, hypoxanthine, and xanthine levels were depressed by deoxycoformycin. Deoxycoformycin pretreatment failed to alter the pattern of amino acid neurotransmitter release from the cerebral cortex in comparison with that observed in control ischemic animals. The failure of deoxycoformycin to attenuate amino acid neurotransmitter release, even though it markedly enhanced adenosine levels in the extracellular space, implies that the amino acid release during ischemia occurs via an adenosine-insensitive mechanism. Inhibition of excitotoxic amino acid release is unlikely to be responsible for the cerebroprotective actions of deoxycoformycin in the ischemic brain.

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