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ABSTRACT: Patients suffering from neuropathic pain are difficult to treat and many methods are used to resolve this issue. In this study, we used a model of neuropathic pain comprising rats with chronic constriction injury (CCI) on the left sciatic nerve to investigate the chronic effect of gabapentin via intrathecal administration. We also observed the expression of dorsal spinal protein kinase C gamma subunit (PKCγ) and other pain-related molecules in the spinal area which included cyclooxygenase 2 (COX2), c-Fos and cyclic AMP-dependent transcription factor (ATF3) in the neuropathic pain animals.
Male Sprague-Dawley (SD) rats (250-380 g) were randomly assigned to four groups, i.e., control, gabapentin (Gaba), MK801, and gabapentin plus MK801 (Gaba+M) groups. A PE-5 catheter was inserted into the lumbar spine area via the cervical spine area. CCI was performed the following day after the intrathecal catheter implant surgery. Gabapentin (1.05 μmol/day) was then given the following day after CCI surgery. Intrathecal gabapentin was administrated for 14 consecutive days. Pain-related behavior was assessed every 2 days thereafter by measuring the latency of foot withdrawal elicited by noxious radiant heat or Von Frey microfilament applied to the hind-paw plantar surface. MK801 (30 μg/day), an N-methyl-D-aspartate (NMDA) receptor blocker, was also added for potential effect. The tissue of dorsal horn of the lumbar spine was harvested on the 14(th) day for the expression of COX2, c-Fos, ATF3 and PKCγ with Western blotting, and positive finding protein was then checked on 7(th) day for further evaluation.
The beneficial effect of intrathecal gabapentin of statistic significance on thermal duration and mechanical microfilament appeared after 7-day and 11-day consecutive treatment, respectively. Furthermore, the NMDA receptor blocker also potentiated the effect on the behavior of thermal and mechanical stimulations. Gabapentin had no effect on the expression of COX2, c-Fos and ATF3. Interestingly, the expression of PKCγ in the spinal cord was initially inhibited by gabapentin on the 7(th) day but was potentiated on the 14(th) day.
Our results indicate that chronic intrathecal gabapentin has beneficial effects on the behaviors of both thermal and mechanical stimulations in the neuropathic pain animals and the NMDA blocker can potentiate this effect. Furthermore, gabapentin has biphasic effect on the expression of PKCγ in the spinal cord on Day 7 and Day 14 for the model rats with CCI.
Acta anaesthesiologica Taiwanica : official journal of the Taiwan Society of Anesthesiologists. 12/2011; 49(4):144-8.
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ABSTRACT: The effects of high-dose morphine on vascular endothelial function have not been previously shown. The authors hypothesized that the pro-oxidant effect of high-dose morphine impairs vascular endothelial function.
Mice were subjected to placebo or morphine (20 mg/kg intraperitoneal) injection for consecutive 14 days. Aortas were harvested for assessment of vasomotor function by isometric force recordings. Protein expression p47phox was determined by Western blotting. Generations of superoxide anions were detected under a confocal microscope.
Compared with controls, contraction response to phenylephrine was significantly enhanced in the aorta of mice treated with high-dose morphine (maximal contractions were 150 +/- 26 vs. 261 +/- 32 mg, respectively; n = 5 or 6, P = 0.04). Endothelium-dependent relaxations to acetylcholine (10 to 10 m) were significantly reduced in morphine-treated animals but were normalized by superoxide scavenging. Fluorescent densities of dihydroethidium were increased in the aorta of morphine-treated mice. Aorta of mice treated with morphine expressed higher levels of p47phox (a major subunit of nicotinamide adenine dinucleotide phosphate oxidase). In cultured endothelial cells, morphine enhanced production of reactive oxygen species.
Collectively, the authors' results showed that high-dose morphine impairs vascular endothelial function via attenuation of biologic activity of endothelium-derived nitric oxide. Chemical antagonism between superoxide anions generated by nicotinamide adenine dinucleotide phosphate oxidases may be the molecular mechanism responsible for the inactivation of endogenous nitric oxide after treatment with high-dose morphine.
Anesthesiology 04/2007; 106(3):532-7. · 5.36 Impact Factor
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ABSTRACT: Previous reports suggest that weather changes may affect the attack and pattern of pain. However, a direct relationship between weather and pain attack is yet to be determined, especially when very limited data are currently available in the tropical or subtropical regions.
We studied the patients who visited our clinic for pain management in Tainan, a city in southern Taiwan, in the space from February 2004 to December 2005. Intensity of pain measured by visual analogue scale (VAS) and the weather conditions including temperature, barometric pressure, humidity and wind speed at the time of measurement, were recorded.
Our results indicate that higher scores of the VAS were associated with older age and lower barometric pressure, while the associations with temperature, humidity and wind speed were not statistically significant.
Our results demonstrate a unique pattern of pain, which varies with barometric pressure, in the subtropical region and may provide reference for better pain intervention during change of weather.
Acta Anaesthesiologica Taiwanica 10/2006; 44(3):147-52.
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ABSTRACT: The use of suxamethonium (succinylcholine) for rapid-sequence intubation may be limited by hyperkalaemia. Modest pre-induction hyperkalaemia is usually disregarded. We present a patient who underwent emergency surgery for a perforated peptic ulcer after being bedbound for 26 days because of a head injury. Serum potassium level was 4.0 mmol/L. The patient was intubated after injection of sedative and suxamethonium and, about 3 minutes later, developed ventricular arrhythmia. Blood tests during resuscitation showed a serum potassium level of 8.8 mmol/L. Immobilisation, denervation and intra-abdominal infection were risk factors for hyperkalaemia in this patient. This report reinforces the need to identify risk factors for hyperkalaemia before administration of suxamethonium, even when serum potassium levels are normal.
Critical care and resuscitation: journal of the Australasian Academy of Critical Care Medicine 10/2006; 8(3):213-4. · 1.67 Impact Factor
