[Overestimation of the degree of stenosis in the intracranial internal carotid artery determined by magnetic resonance angiography compared to conventional arteriography]. / Sobreestimación del grado de estenosis de la arteria carótida interna intracraneal por la angiorresonancia respecto a la arteriografía convencional.

INTRODUCTION: In the evaluation of stenoses of the extracranial internal carotid artery (ICA), there are studies that suggest that magnetic resonance angiography (MRA) can be a substitute for conventional arteriography (CA), although it seems it has a tendency to overestimate the degree of stenosis. No similar comparison of the two techniques has been conducted in intracranial ICA. We report the case of a patient suffering from an acute ischemic stroke and symptomatic intracranial stenosis that was overestimated when MRA was used, compared to the results obtained using CA. CASE REPORT: We report the case of a 64-year-old male with a history of arterial hypertension, hypercholesterolemia and intermittent claudication who visited the emergency department because of the sudden onset of paresthesias in the left hemiface and hand. The cranial tomography scan performed in the emergency unit ruled out any acute bleeding or early signs of a stroke. Magnetic resonance (MR) diffusion imaging showed an acute ischemic stroke in the right parietal cortex. Extracranial MRA was normal and in the intracranial area a 73% stenosis was detected in the cavernous segment of the right ICA, whereas the use of CA showed the stenosis to be only 55%. On repeating the MRA to rule out a possible rechanneling of the ICA, the image obtained was exactly the same as the earlier one. CONCLUSIONS: Our observations suggest that, as occurs with the extracranial part, MRA tends to magnify the degree of stenosis in the intracranial vessels, and this technique would therefore appear to be less efficient than CA in the evaluation of intracranial stenoses.

Characterization of a cholecystokinin 8-generating endoprotease purified from rat brain synaptosomes.

An endoproteolytic activity that specifically cleaves CCK 33, producing CCK 8, has been purified from a rat brain synaptosome preparation. The purification, which included anion exchange, chromatofocusing, hydroxyapatite, and gel filtration chromatography, resulted in a greater than 3000-fold increase in specific activity. This neutral endoprotease (pH optimum 8) exists as a 90-kDa species, which can be dissociated into active 40-kDa species. The enzyme is a non-trypsin serine protease, which is inhibited by diisopropyl-fluorophosphate and p-aminobenzamidine but not by soybean trypsin inhibitor, phenylmethylsulfonyl fluoride, aprotinin, or a number of thiol or metalloprotease inhibitors. It is highly substrate-specific and cleaves neither trypsin, enteropeptidase, kallikrein substrates, nor analogues of mono- or dibasic cleavage sites of prohormones other than pro-CCK. The endoprotease will not cleave CCK 12 desulfate or CCK (20-29), although these peptides contain common sequences with CCK-33. The protease does cleave [Glu27]CCK (20-29), a peptide in which the glutamate mimics the negative charge normally present on tyrosine sulfate. This suggests that the negative charge at position 27 is important in substrate recognition. The enzyme will also cleave CCK 33 and CCK (1-21) on the carboxyl-terminal side of a single lysine residue in position 11. The subcellular location and specificity of this endoprotease make it a good candidate for a CCK-processing protease.

Inhibition of potassium-evoked release of cholecystokinin from rat caudate-putamen, cerebral cortex and hippocampus incubated in vitro by phencyclidine and related compounds.

Potassium-evoked release of cholecystokinin (CCK) from slices of caudate-putamen, hippocampus, and cerebral cortex was inhibited in a dose-related fashion by phencyclidine (PCP). In order to further examine this effect, PCP-like ligands (dexoxadrol, levoxadrol, PCMP and MK-801) as well as compounds known to interact with the sigma receptor ((+)-SKF, DTG, (+)-3-PPP, and pentazocine) were tested. While some of these compounds inhibited CCK release, their rank order potency (Dex = Lev greater than PCP = PCMP greater than DTG = MK-801 = (+)-3-PPP) differs from that of known PCP-N-methyl-D-aspartate linked effects or sigma interactions. These results suggest that the mechanism by which PCP acts to inhibit CCK release may involve a novel type of PCP interaction.