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| 2. |
- Hol, P K, et al.
(författare)
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MRI-guided celiac plexus block
- 2000
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Ingår i: Magnetic Resonance Imaging. - 0730-725X .- 1873-5894. ; 12, s. 562-564
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Tidskriftsartikel (refereegranskat)
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| 3. |
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| 4. |
- Jörum, E., et al.
(författare)
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Catecholamine-induced excitation of nociceptors in sympathetically maintained pain
- 2007
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Ingår i: Pain. - : Ovid Technologies (Wolters Kluwer Health). - 0304-3959 .- 1872-6623. ; 127:3, s. 296-301
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Tidskriftsartikel (refereegranskat)abstract
- Sympathetically maintained pain could either be mediated by ephaptic interactions between sympathetic efferent and afferent nociceptive fibers or by catecholamine-induced activation of nociceptive nerve endings. We report here single fiber recordings from C nociceptors in a patient with sympathetically maintained pain, in whom sympathetic blockade had repeatedly eliminated the ongoing pain in both legs. We classified eight C-fibers as mechano-responsive and six as mechano-insensitive nociceptors according to their mechanical responsiveness and activity-dependent slowing of conduction velocity (latency increase of 0.5±1.1 vs. 7.1±2.0ms for 20 pulses at 0.125Hz). Two C-fibers were activated with a delay of several seconds following strong endogenous sympathetic bursts; they were also excited for about 3min following the injection of norepinephrine (10μl, 0.05%) into their innervation territory. In these two fibers, a prolonged activation by injection of low pH solution (phosphate buffer, pH 6.0, 10μl) and sensitization of their heat response following prostaglandin E2 injection were recorded, evidencing their afferent nature. Moreover, their activity-dependent slowing was typical for mechano-insensitive nociceptors. We conclude that sensitized mechano-insensitive nociceptors can be activated by endogenously released catecholamines and thereby may contribute to sympathetically maintained pain. No evidence for ephaptic interaction between sympathetic efferent and nociceptive afferent fibers was found.
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| 5. |
- Rasmussen, H, et al.
(författare)
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Gas supersaturation in the cecal wall of mice due to bacterial CO2 production
- 1999
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Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 86:4, s. 1311-1318
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Tidskriftsartikel (refereegranskat)abstract
- Pco2in the lumen and serosa of cecum and jejunum was measured in mice. The anesthetic used was a fentanyl-fluanisone-midazolam mixture.[Formula: see text] was recorded in vivo and postmortem. [Formula: see text] was 409 ± 32 Torr (55 ± 4 kPa) in the cecal lumen and 199 ± 22 Torr (27 ± 3 kPa) on the serosa in normal mice. Irrigation of the cecum resulted in serosal and luminal [Formula: see text]levels of 65–75 Torr. Cecal [Formula: see text]was significantly lower in germ-free mice (65 ± 5 Torr). Cecal[Formula: see text] increased significantly after introduction of normal bacterial flora into germ-free mice. Introduction of bacterial monocultures into germ-free mice had no effect. After the deaths of the mice, cecal[Formula: see text] increased rapidly in normal mice. The intestinal bacteria produced the majority of the cecal[Formula: see text], and the use of tonometry in intestinal segments with a high bacterial activity should be interpreted with caution. We propose that serosal[Formula: see text] levels >150–190 Torr (20–25 kPa) in the cecum of mice with a normal circulation may represent a state of gas supersaturation in the cecal wall.
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| 6. |
- Rasmussen, H, et al.
(författare)
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PCO(2) in the large intestine of mice, rats, guinea pigs, and dogs and effects of the dietary substrate
- 2002
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Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 8750-7587 .- 1522-1601. ; 92:1, s. 219-224
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Tidskriftsartikel (refereegranskat)abstract
- Pco 2 in the lumen and serosa of cecum and colon was measured in rats, guinea pigs, and dogs to examine the relationship between serosal Pco 2 and the incidence of intestinal necrotic lesions after administration of gas-carrier contrast agents in rodents. The effects of the dietary substrate were tested in a group of mice maintained on a diet based on glucose as the only carbohydrate source. The anesthetic used was a fentanyl-fluanison-midazolam mixture (rodents) and pentobarbital (dogs). Pco 2 was measured in vivo and postmortem, and the kinetics of the postmortem serosal Pco 2 [transmural CO2 flux ( J CO2 )] was calculated. Pco 2 in the cecal serosa and lumen, respectively, was 64 ± 4 and 392 ± 18 Torr in rats, 67 ± 3 and 276 ± 17 Torr in guinea pigs, and 73 ± 6 and 137 ± 7 Torr in mice on glucose-based diet. In the colon serosa and lumen of dogs, Pco 2 was 30 ± 6 and 523 ± 67 Torr, respectively. Serosal Pco 2increased rapidly after death in rats and slower in guinea pigs and mice, and the slowest change was observed in dogs. Compared with dogs, serosal Pco 2 and J CO2 of rats and guinea pigs were significantly higher. Serosal Pco 2 of guinea pigs was similar to that of rats, whereas the J CO2 of guinea pigs was significantly lower. These data suggest a causal relationship between the ability of the cecal and colonic wall to act as a barrier to CO2 diffusion and the presence of characteristic gas-carrier contrast agent-induced intestinal lesions in mice and rats and their absence in guinea pigs, dogs, and other species.
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