Comparison of 40 and 60 milliliters of contrast in assessment of the carotid artery by computed tomography angiography.

BACKGROUND: Although fast acquisition of multidetector-row computed tomography (MDCT) can make it possible to acquire sufficient early vascular enhancement using small volumes and high concentrations of contrast material (CM), there are still some problems with nephrotoxicity and costs related to CM. PURPOSE: To compare the qualitative and quantitative performance in cervicocranial CT angiography (CTA) using two different iodine volumes and concentrations of CM. MATERIAL AND METHODS: CTA ranging from the aortic arch (AA) to distal to the circle of Willis (cW) was performed on a 32-MDCT system. Fifty-eight patients were randomly divided into two groups: group A (29 patients) received 60 ml of 300 mg I/ml CM, and group B (the other 29 patients) received 40 ml of 370 mg I/ml CM. Time to peak arterial enhancement at cW (T(c)) was calculated. As scan speed was 96.9 mm/s and injection rate was 4.0 ml/s, scanning delay was individually decided according to T(c) and scan duration between AA and cW. Arterial attenuation along the z-axis at eight points in the carotid-cerebral artery and venous attenuation of the internal jugular vein (IJV) at carotid bifurcation were measured. Mean attenuation values were then quantitatively analyzed. Postprocessing images were qualitatively assessed. RESULTS: Arterial attenuation profiles revealed maximum attenuation at the distal common carotid artery in both groups. Although there were no significant differences in mean arterial attenuation in group A versus group B (402+/-70 HU vs. 407+/-67 HU; P=0.78), venous attenuation of the IJV was lower in group B than in group A (114+/-57 HU vs. 224+/-81 HU; P<0.001). Although arterial images demonstrated no difference qualitatively between the two groups, the venous contamination of IVC was less prominent in group B. CONCLUSION: Although a different amount of CM was administered in both groups, quantitative and qualitative arterial images did not show significant differences between the two groups.

Effects of 2-tetradecylglycidic acid on rat platelet energy metabolism and aggregation.

We investigated the role of energy supplied by long-chain fatty acid oxidation in rat platelet function. Inhibition of the mitochondrial uptake of long-chain fatty acids was achieved by treating rats with 2-tetradecylglycidic acid (TDGA), a potent inhibitor of the overt form of carnitine palmitoyltransferase (CPT-I). The maximum aggregation rate (MAR), CPT-I activity, lactate production, oxygen consumption and adenine nucleotide content of isolated rat platelets were then studied in vitro. 4 h after the in vivo administration of TDGA, the CPT-I activity in saponin-permeabilized platelets was nearly completely inhibited along with a significant reduction in the MAR induced by ADP, thrombin and ionophore A23187. The ATP level, adenylate energy charge (ATP + 1/2 ADP)/(ATP + ADP + AMP) and ATP/ADP ratio in the platelet cytoplasmic pool were also reduced. Platelets from TDGA-treated rats showed lower oxygen consumption rates in both the basal respiratory and oxygen burst states. These results indicate that mitochondrial long-chain fatty acid oxidation coupled to oxidative phosphorylation is an important energy source in rat platelets and is probably involved in the maintenance of platelet function. Enhanced in vitro lactate production in platelets from TDGA-treated rats may have resulted from a compensatory increase in glycolysis which only partly compensated for impaired long-chain fatty acid oxidation.

Reoxygenation-induced mitochondrial damage is caused by the Ca2+-dependent mitochondrial inner membrane permeability transition.

Anoxia/reoxygenation injury of isolated rat liver mitochondria was investigated. During anoxia of up to 60 min, the membrane potential was largely preserved and mitochondrial swelling was not observed. Reoxygenation of anoxic mitochondria rapidly caused swelling, cyclosporin A-sensitive Ca2+ efflux, [14C]sucrose trapping, and loss of the membrane potential along with increased generation of reactive oxygen intermediates (ROI). Although pretreatment with catalase and superoxide dismutase completely abolished reoxygenation-induced generation of ROI, mitochondrial damage was not prevented, as indicated by swelling, loss of the membrane potential, a decrease of the ATP content, and cyclosporin A-sensitive Ca2+ efflux. However, addition of the immunosuppressant cyclosporin A or addition of ADP completely prevented the mitochondrial damage induced by reoxygenation. The same protective effect was noted when Ca2+ cycling was prevented, either by chelating Ca2+ with EGTA or by inhibiting Ca2+ reuptake with ruthenium red. These findings indicate that mitochondrial anoxia/reoxygenation injury is caused by the cyclosporin A-sensitive and Ca2+-dependent membrane permeability transition. In contrast, reoxygenation injury does not appear to be triggered by the enhanced production of ROI.

Hyperammonemia inhibits platelet aggregation in rats.

The effect of hyperammonemia on ex vivo platelet function and in vivo nitric oxide synthesis was evaluated in rats. In addition, mitochondrial energy production was assessed from the fluorescence intensity of tetramethylrhodamine ethyl ester (TMRE). Continuous ammonium acetate infusion significantly reduced ex vivo platelet aggregation concomitant with a decrease of the platelet cytoplasmic ATP level. The serum level of L-arginine, as well as the levels of nitrite and nitrate (oxidative by-products of nitric oxide), increased with ammonium infusion. Prior administration of N omega-nitro-L-arginine methyl ester, a competitive inhibitor of nitric oxide synthase, did not affect the ammonia-induced rise in L-arginine, but substantially attenuated the associated decrease of platelet ATP and TMRE fluorescence as well as diminishing the anti-aggregatory effect of ammonia infusion. These findings suggest that the synthesis of nitric oxide from L-arginine is accelerated by continuous ammonium infusion and inhibits ex vivo platelet aggregation in the rat, probably by reducing mitochondrial energy production.

Glutathione monoethyl ester and inhibition of the oxyhemoglobin-induced increase in cytosolic calcium in cultured smooth-muscle cells.

OBJECT: The mechanism of arterial vasoconstriction caused by oxyhemoglobin production after subarachnoid hemorrhage was investigated. METHODS: Using a fluorescent Ca++ indicator (fura-2 acetoxymethyl ester), the change in the cytosolic intracellular Ca++ concentration, [Ca++]i. was measured in cultured rat vascular smooth-muscle cells exposed to oxyhemoglobin and other substances. Oxyhemoglobin induced transient elevation of smooth-muscle cell [Ca++]i in either the presence or absence of ethyleneglycol-bis (beta-aminoethylether)-N,N'-tetraacetic acid, indicating that Ca++ released by oxyhemoglobin was derived from [Ca++]i stores. In contrast, methemoglobin had no effect on the smooth-muscle cells. Exposure of the cells to reactive oxygen species generated by xanthine plus xanthine oxidase yielded the same results as with oxyhemoglobin, that is, transient elevation of smooth-muscle cell [Ca++]i. Procaine (a Ca++ channel blocker) failed to inhibit the oxyhemoglobin-induced elevation of [Ca++]i. Ryanodine (a Ca++ channel opener) plus oxyhemoglobin caused markedly greater elevation of [Ca++]i than ryanodine alone, whereas thapsigargin (an adenosine triphosphate [ATP]-dependent Ca++ pump inhibitor) plus oxyhemoglobin had no additional effect when compared with thapsigargin alone. The oxyhemoglobin-induced elevation of [Ca++]i could be blocked by an Fe++ chelator (ferene), but not by an Fe chelator (deferoxamine mesylate). Treatment with either dithiothreitol or glutathione monoethyl ester markedly inhibited the oxyhemoglobin-induced elevation of [Ca++]i. CONCLUSIONS: These results indicate that Fe++-catalyzed hydroxyl radicals generated from oxyhemoglobin-derived free radicals induce the elevation of [Ca++]i by inhibiting the ATP-dependent Ca++ pump rather than the Ca++ channels in the sarcoplasmic reticulum and that thiols may prevent Ca++ pump inactivation by inhibiting the oxidation of membrane sulfhydryl groups.

Biochemical effects of acute stress on energy metabolism in liver damaged rats.

Rats having a non-necrotic damaged liver or a necrotic damaged liver produced by D-galactosamine administration were restrained in water for 0.5, 1, 2, 4, 6, 8 and 12 hours. Serial changes in intrahepatic energy metabolism were compared with those in normal liver. Energy charge, which represents the degree of equilibrium between the energy producing and consuming systems, and cyclic AMP, an intracellular messenger mediating the action of hormones, showed biphasic increases before and after 2 hr in the damaged livers. The lactate/pyruvate ratio, which reflects the cytosolic redox state, markedly increased at 0.5 hr in the damaged livers but returned to the pre-stress level after 1 hr in the non-necrotic damaged liver and after 4 hr in the necrotic damaged liver, showing a transient reduced state. The beta-hydroxybutyrate/acetoacetate ratio, which represents the mitochondrial redox state, decreased at 0.5 hr and returned to the pre-stress level at 1 hr in the non-necrotic damaged liver, exhibiting a transient oxidized state. However, in the necrotic damaged liver, the value decreased at 0.5 hr remained low thereafter, demonstrating a persistent oxidized state. These findings show that, in severely damaged liver, stress has more marked effects on hepatic energy metabolism.

Valproic acid overdose and L-carnitine therapy.

A healthy, nonepileptic 16-month-old child ingested a massive overdose (approximately 4000 mg) of valproic acid (VPA). Upon admission to the hospital, he was in a deep coma and had generalized hypotonicity and no response to pain. His serum and urinary concentrations of VPA were 1316.2 and 3289.5 micrograms/mL, respectively. Urinary concentrations of the beta-oxidation metabolites of VPA were low, whereas concentrations of omega- and omega 1-oxidation metabolites were high. Moreover, 4-en-valproate (a potential hepatotoxin) was detected in the urine. Gastric lavage and general supportive measures were undertaken, including intravenous infusion to increase urine output and oral L-carnitine to correct hypocarnitinemia. Subsequently, the beta-oxidation metabolites increased, the omega- and omega 1-oxidation metabolites decreased, and 4-en-valproate was no longer detected. The patient recovered completely and was discharged on the eighth hospital day without any sequelae. This case suggests that enhanced drug excretion and L-carnitine supplementation may prevent potentially fatal hepatic dysfunction after VPA overdose.

"Spontaneous" pneumocephalus associated with aerobic bacteremia.

Three cases of "spontaneous" pneumocephalus suspected to have resulted from aerobic bacteremia caused by Enterobacter cloacae, Escherichia coli, and Klebsiella aerogenes are reported. In two cases, the E. cloacae and K. aerogenes were isolated from the cerebrospinal fluid. These cases were characterized by a rapid accumulation of air, without niveau, in the subarachnoid space and ventricles.

Anterior dislocation of the subtalar joint: a case report.

We report a very rare case of anterior dislocation of the subtalar joint. Forceful supination of the foot and dorsiflexion of the ankle was considered the cause of the injury in this case. Closed reduction was successful for the talocalcaneal component of subtalar joint, although surgery was subsequently performed because of the residual subluxation of the midtarsal joint including the talonavicular component of subtalar joint and the associated fracture of the lateral process of the talus. Satisfactory results were shown at three-year follow-up.

[Thrombotic thrombocytopenic purpura (TTP) associated with chromosomal aberration and treated with plasma exchange].

We reported a case of 69-year-old female presenting with clinically typical TTP which was treated with Ticlopidine and plasma exchanges four times in total and resulted in successful improvement of her clinical state. The first chromosomal analysis of lymphocytes in the peripheral blood of the patient revealed abnormal patterns of 45, XO/46, XX/47, XXX, the second, 45, XO/46, XX/47, XXX/47.XX, + 21. Measurement of FITC-labelled fibrinogen antibody against the fibrinogen combined with platelet glycoprotein GP IIb/IIIa complex using flow cytometry showed an apparently increased positive rate 76.2% for the platelet of the patient, compared with that of 31.9% for the control. From the comparative study of the platelet agglutination of the platelet rich plasma (PRP) derived from the citrated-added complete blood taken from the patient to whom Ticlopidine was given, added with adenosine-5'-diphosphate (ADP), collagen or acetyl glyceryl ether phosphoryl choline (AGEPC) as the reagents and that of normal control, it was shown that for AGEPC increased. Thus, increased reaction specific to AGEPC in addition to activated platelet was demonstrated in the present study.

[Effects of the administration of urinary trypsin inhibitor on the morphology and function of platelets in the rat septic models].

Effects of urinary trypsin inhibitor (UTI) on the number, morphology and function of platelets under septic state were studied in rat models of cecal ligation and puncture (CLP). At formation of CLP, 5,000 U/kg/h of UTI was serially administered intraperitoneally and blood was sampled after 16 hours. Comparative study among sham-operation group, CLP group, and CLP + UTI group revealed: 1) inhibition of the platelets of platelet counts and appearance of large-sized, active platelets by UTI in the CLP + UTI group, 2) increase of platelet maximum aggregation rate (MAR) by ADP and increase of collagen in the CLP group, while inhibition in the CLP + UTI group and 3) by HPLC evaluation of adenine nucleotide in the platelet, increased levels of total ATP and ADP in the CLP group, particularly, increases of ATP in the metabolic pool and ADP in the granular pool. CLP + UTI group did not show these changes in the adenylate pool. UTI was thus considered to stabilize the platelet cycle in sepsis. Platelets under septic state might be hyperactive, and thrombosis is easy to occur. UTI administration might work for maintaining constancy of the platelet internal environment and improve septic state because adenine nucleotide level in the platelet did not change in the CLP + UTI group through changed in the CLP group.

Cerebral CT angiography using a small volume of concentrated contrast material with a test injection method: optimal scan delay for quantitative and qualitative performance.

OBJECTIVES: The objective of this study was to determine the optimal scan delay quantitatively and qualitatively in cerebral CT angiography (CTA) with a test injection method at the circle of Willis (cW). METHODS: 66 consecutive patients suspected of having unruptured intracranial aneurysms underwent CTA using 40 ml of 370 mg iodine ml(-1) contrast material (CM). After the time until CM arrival at the cW (T(cW)) was calculated, scan delay was divided into three groups according to T(cW) and scan duration (SD) between the second cervical vertebra and cW as follows: [(T(cW)+6)-SD] in 21 patients (Group A); [(T(cW)+8)-SD] in 23 patients (Group B); and [(T(cW)+10)-SD] in 22 patients (Group C). Arterial and venous attenuation in the intracranial vessels was measured. Mean attenuation values were compared quantitatively. The arterial enhancement and venous overlap at the cW and above the cW were qualitatively compared among the three groups. RESULTS: Mean arterial attenuation in Groups B and C was significantly higher than that in Group A. Mean venous attenuation in Group C was significantly higher than those in Groups A and B. Arterial enhancement above the cW showed a significant difference between Groups A and C, and at the cW between Groups A and B, and Groups A and C. There was a significant difference in venous overlap among the three groups, except for that at the cW between Groups B and C. CONCLUSIONS: Setting scan delay as [(T(cW)+8)-SD] s can produce the best performance both quantitatively and qualitatively.

Comparison of different volumes of saline flush in the assessment of perivenous artefacts in the subclavian vein during cervical CT angiography.

OBJECTIVES: The aim of this study was to examine attenuation values in the central vein and perivenous artefacts at the subclavian vein in cervical CT angiography (CTA) when using 40 ml contrast material (CM) followed by different volumes (25 ml vs 40 ml) of saline flush (SF). METHODS: 61 patients underwent CTA between the aortic arch (AA) and distal to the circle of Willis (cW). After calculating test-bolus time to peak enhancement at the cW (Tc), scanning delay was represented as [(Tc + 4) - scan duration between AA and cW] s. 28 patients (Group A) received 40 ml of 370 mg iodine (I) ml(-1) CM followed by 25 ml of SF, and 33 patients (Group B) received the same CM followed by 40 ml of SF, both administered through the right antecubital vein. Arterial attenuation was measured at seven points in the aorto-carotid artery and at three points in the vertebrobasilar artery. Venous attenuation in the central vein was measured at four points. Mean attenuation values were analysed quantitatively. Axial and post-processing three-dimensional images were assessed qualitatively. RESULTS: When Groups A and B were compared, there were no differences in the mean attenuation values in either the aorto-carotid artery (p=0.78) or the vertebrobasilar artery (p=0.82). Mean venous attenuation values were lower (p=0.002) in Group B than in Group A. Although the qualitative assessment of arterial images showed no differences between the two groups overall, perivenous artefacts at the subclavian vein were assessed as less prominent (p<0.01) in Group B. CONCLUSIONS: When compared with CTA followed by 25 ml of SF, CTA followed by 40 ml of SF can reduce venous attenuation values and perivenous artefacts at the subclavian vein.