1.
Optimal contrast medium injection protocols for the depiction of the Adamkiewicz artery using 64-detector CT angiography.
Nakayama, Y, Awai, K, Yanaga, Y, Nakaura, T, Funama, Y, Hirai, T, Yamashita, Y
Clinical radiology. 2008;(8):880-7
Abstract
AIM: To determine the optimal contrast medium injection protocol for demonstrating the Adamkiewicz artery (AKA) using 64-detector CT angiography (CTA). MATERIALS AND METHODS CTA was performed using 64-detector CT. The study population consisted of 80 patients (mean age 67.2 years) with aortoiliac diseases. In the first 60 patients 540 mg I/kg body weight was administered over 25s. The patients were randomly assigned to three protocols with imaging started at 15 (protocol A-1), 18 (A-2), or 21s (A-3) after triggering (threshold 150 HU). The other 20 received 720 mg I/kg body weight with an imaging delay of 18s (protocol B). Two radiologists evaluated the presence of the AKA and measured the attenuation of the aorta and AKA. RESULTS Aortic enhancement was 360.4, 348, 279.3, and 372 HU for protocols A-1, A-2, A-3, and B, respectively. There was no significant difference between the A-1 and A-2 protocols (Tukey-Kramer test, p=0.73); however, aortic enhancement was significantly lower in A-3 than A-1 and A-2 (p<0.01). There was no significant difference between A-2 and B (p=0.40). AKA attenuation was 69.3, 91.9, 94.6, and 105.4 HU for protocols A-1, A-2, A-3, and B, respectively. There was no significant difference between the A-2 and A-3 protocols (p=0.91); however, AKA attenuation was significantly lower with A-1 than A-2 or A-3 (p=0.01). AKA attenuation was significantly lower with A-2 than B (p=0.03) and there was a significant difference between A-2 (50%) and B (95%) in the depiction of the hairpin configuration of the AKA (p=0.02). CONCLUSION For the demonstration of the AKA at CTA, the optimal protocol used an imaging delay of 18s after triggering and an iodine dose of 720 mg I/kg body weight.
2.
Constitutive cyclooxygenase-2 is involved in central nociceptive processes in humans.
Martin, F, Fletcher, D, Chauvin, M, Bouhassira, D
Anesthesiology. 2007;(5):1013-8
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Abstract
BACKGROUND Prostaglandins play a major role in inflammation and pain. They are synthesized by the two cyclooxygenase (COX) isoforms: COX-1, which is expressed constitutively in many cell types, and COX-2, which is induced at the site of inflammation. However, unlike peripheral tissues, COX-2 is expressed constitutively in the central nervous system and may play a role in nociceptive processes. The current study aimed to investigate the role of constitutive COX-2 in the spinal transmission of nociceptive signals in humans. METHODS The authors used 12 healthy volunteers to compare the effects of the specific COX-2 inhibitor sodium parecoxib (1 mg/kg) or placebo, administered intravenously in a double-blind and crossover fashion, on the electrophysiologic recordings of the nociceptive flexion (RIII) reflex. The RIII reflex is an objective psychophysiologic index of the spinal transmission of nociceptive signals and was recorded from the biceps femoris after electrical stimulation of the sural nerve. Two experiments, 7 days apart, were conducted in each volunteer. On each experimental day, the effects of parecoxib or placebo were tested on (1) the RIII reflex threshold, (2) the stimulus-response curves of the reflex up to the tolerance threshold (frequency of stimulation: 0.1 Hz), and (3) the progressive increase of the reflex and pain sensations (i.e., "windup" phenomenon) induced by a series of 15 stimulations at a frequency of 1 Hz (intensity 20% above RIII threshold). RESULTS Parecoxib, but not placebo, significantly reduced the slope of the stimulus-response curve, suggesting a reduction in the gain of the spinal transmission of nociceptive signals. By contrast, the windup phenomenon was not significantly altered after administration of parecoxib or placebo. CONCLUSIONS This study shows that constitutive COX-2 modulates spinal nociceptive processes and that the antiinflammatory and antinociceptive actions of COX-2 inhibitors are not necessarily related.
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Spinal prostaglandin formation and pain perception following thoracotomy: a role for cyclooxygenase-2.
McCrory, C, Fitzgerald, D
Chest. 2004;(4):1321-7
Abstract
STUDY OBJECTIVE Prostaglandins (PGs) generated in the spinal cord may play a major role in pain perception. Consequently, the suppression of spinal cyclooxygenase (COX) and PG formation may contribute to the analgesic effect of nonsteroidal anti-inflammatory drugs (NSAIDs) in pain following surgery. Which isoform of COX is responsible for postsurgical pain and, consequently, should be targeted, is unclear. DESIGN Prospective randomized blinded study. SETTING University teaching hospital. PATIENTS Thirty patients undergoing thoracotomy for lobectomy were recruited. INTERVENTIONS Patients were randomized to receive the COX-2 selective inhibitor nimesulide, 100 mg orally twice daily, or ibuprofen (nonselective), 400 mg orally three times daily, in an open-label study. In addition, there was a randomized control group that received no NSAIDs. Cerebrospinal fluid (CSF) was analyzed for 6-keto-PGF(1)alpha, the principle metabolite of prostacyclin. COX-1 and COX-2 activity was determined by measuring serum thromboxane (TX) B(2) and endotoxin-induced PGE(2) generation in whole blood. MEASUREMENTS Pain perception was measured by visual analog scores, and blinded assessment of opioid analgesic requirements and expiratory peak flow measurements were performed. RESULTS At the doses used, nimesulide was selective for COX-2, while ibuprofen was nonselective based on serum TXB(2) levels. The mean (+/- SEM) levels of 6-keto-PGF(1)alpha in CSF increased following surgery from 32 +/- 4.9 to 127 +/- 29 pg/mL (p < 0.001), and this was suppressed by nimesulide (49 +/- 9.3 pg/mL; p = 0.0025) but not by ibuprofen (122 +/- 35 pg/mL). Pain scores (p < 0.001), morphine requirement (p = 0.0175), and the fall in peak expiratory flow rate (p < 0.001) were significantly lower in the nimesulide group. CONCLUSIONS Increases in spinal PG synthesis after thoracotomy are repressed by a selective COX-2 inhibitor. This suggests that the inducible COX-2 mediates central PG synthesis, which may be important in the generation of pain, as the use of nimesulide also resulted in significant decreases in postoperative pain perception.