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Biomedical subjects

Chih-Shung Wong

Publications and source records attributed to Chih-Shung Wong.

At least 19 recordsLinked to original sources
PubMed2006

Amitriptyline suppresses neuroinflammation and up-regulates glutamate transporters in morphine-tolerant rats.

The present study was performed to evaluate the effects of the tricyclic antidepressant amitriptyline on morphine tolerance in rats. Male Wistar rats were implanted with two intrathecal (i.t.) catheters with or without a microdialysis probe, then received a continuous i.t. infusion of saline (control) or morphine (15 microg/h) and/or amitriptyline (15 microg/h) for 5 days. The results showed that amitriptyline alone did not produce an antinociceptive effect, while morphine alone induced antinociceptive tolerance and down-regulation of spinal glutamate transporters (GLAST, GLT-1, and EAAC1) in the rat spinal cord dorsal horn. Co-administration of amitriptyline with morphine attenuated morphine tolerance and up-regulated GLAST and GLT-1 expression. On day 5, morphine challenge (10 microg/10 microl) resulted in a significant increase in levels of the excitatory amino acids (EAAs), aspartate and glutamate, in CSF dialysates in morphine-tolerant rats. Amitriptyline co-infusion not only markedly suppressed this morphine-evoked EAA release, but also preserved the antinociceptive effect of acute morphine challenge at the end of infusion. Glial cells activation and increased cytokine expression (TNFalpha, IL-1beta, and IL-6) in the rat spinal cord were induced by the 5-day morphine infusion and these neuroimmune responses were also prevented by amitriptyline co-infusion. These results show that amitriptyline not only attenuates morphine tolerance, but also preserves its antinociceptive effect. The mechanisms involved may include: (a) inhibition of pro-inflammatory cytokine expression, (b) prevention of glutamate transporter down-regulation, and even up-regulation of glial GTs GLAST and GLT-1 expression, with (c) attenuation of morphine-evoked EAA release following continuous long-term morphine infusion.

Amino Acid Transport System X-AG↗
PubMed2006

Alterations of postsynaptic density proteins in the hippocampus of rat offspring from the morphine-addicted mother: Beneficial effect of dextromethorphan.

Infants passively exposed to morphine or heroin through their addicted mothers usually develop characteristic withdrawal syndrome of morphine after birth. In such early life, the central nervous system exhibits significant plasticity and can be altered by various prenatal influences, including prenatal morphine exposure. Here we studied the effects of prenatal morphine exposure on postsynaptic density protein 95 (PSD-95), an important cytoskeletal specialization involved in the anchoring of the NMDAR and neuronal nitric oxide synthase (nNOS), of the hippocampal CA1 subregion from young offspring at postnatal day 14 (P14). We also evaluated the therapeutic efficacy of dextromethorphan, a widely used antitussive drug with noncompetitive antagonistic effects on NMDARs, for such offspring. The results revealed that prenatal morphine exposure caused a maximal decrease in PSD-95 expression at P14 followed by an age-dependent improvement. In addition, prenatal morphine exposure reduced not only the expression of nNOS and the phosphorylation of cAMP responsive element-binding protein at serine 133 (CREB(Serine-133)), but also the magnitude of long-term depression (LTD) at P14. Subsequently, the morphine-treated offspring exhibited impaired performance in long-term learning and memory at later ages (P28-29). Prenatal coadministration of dextromethorphan with morphine during pregnancy and throughout lactation could significantly attenuate the adverse effects as described above. Collectively, the study demonstrates that maternal exposure to morphine decreases the magnitude of PSD-95, nNOS, the phosphorylation of CREB(Serine-133), and LTD expression in hippocampal CA1 subregion of young offspring (e.g., P14). Such alterations within the developing brain may play a role for subsequent neurological impairments (e.g., impaired performance of long-term learning and memory). The results raise a possibility that postsynaptic density proteins could serve an important role, at least in part, for the neurobiological pathogenesis in offspring from the morphine-addicted mother and provide tentative therapeutic strategy.

Animals↗
PubMed2006

Hyaluronic acid attenuates osteoarthritis development in the anterior cruciate ligament-transected knee: Association with excitatory amino acid release in the joint dialysate.

We previously reported increased release of the excitatory amino acid (EAA) neurotransmitters, glutamate and aspartate, during the early stage of experimental osteoarthritis (OA). Our present objective was to study the effect of intraarticular injection of hyaluronic acid (HA) on OA development, and to analyze concomitant changes in EAA levels in dialysates of anterior cruciate ligament-transected (ACLT) knee joints. OA was induced in Wistar rats by ACLT of one hindlimb; the knee of the other hindlimb was used as the sham-operated control. HA group (n = 12) were injected intraarticularly in the ACLT knee with 1 mg of HA once a week for 5 consecutive weeks, starting at 8 weeks after surgery. Saline group (n = 12) were injected as above with normal saline. The sham-operated group, underwent arthrotomy, but not ACLT, and received no treatment (n = 14). Twenty weeks after surgery, knee joint dialysates were collected by microdialysis and EAA levels assayed by high-performance liquid chromatography, and gross morphological examination and histopathological evaluation were performed on the medial femoral condyles and synovia. Rats receiving intraarticular HA injections showed a significantly lower degree of cartilage degeneration on the medial femoral condyle at both the macroscopic level and on the Mankin grading scale than rats receiving saline injections. Intraarticular HA treatment also suppressed synovitis. Moreover, glutamate and aspartate levels were significantly reduced in the HA group compared to the saline group. Intraarticular injection of HA limits articular cartilage and synovium damage and OA formation, and, in parallel, reduces EAA levels in ACLT joint dialysates. This study suggests that the underlying mechanism of the anti-inflammatory effect of HA is to inhibit glutamate and aspartate release in ACLT knee joints, which attenuates the early development of OA.

Animals↗
PubMed2006

Anesthetic management of an AAI pacemaker patient with paroxysmal atrial fibrillation during colorectal surgery.

Perioperative management of patients with cardiac pacemakers may be challenging because of the increasing sophistication of these devices. We report a case of a patient with paroxysmal atrial fibrillation (PAF) and with a permanent AAIR (bipolar atrial-inhibited adaptive rate) pacemaker who suffered life-threatening episodes of arrhythmias during operation. The first episode was vagally induced PAF during bowel manipulation; the second, induced by the increased pacing threshold from the external electric cardioversion and hyperkalemia. Transcutaneous pacing provided cardiac pacing and stabilized the patient during the second episode. Thorough preoperative evaluation and prophylactic placement of temporary pacing or at least transcutaneous pacing are important for the avoidance and minimization of intraoperative complications in patients with sick sinus syndrome and with an AAI (atrial inhibited) pacemaker.

Aged↗
PubMed2006

Correlation between changes in regional cerebral blood flow and pain relief in complex regional pain syndrome type 1.

OBJECTIVE: Analyzing changes in regional cerebral blood flow (rCBF) with SPECT in complex regional pain syndrome type 1 (CRPS 1), formerly known as reflex sympathetic dystrophy, is an optimal method for evaluating effective pain relief. We attempted to investigate the correlation of changes in rCBF with pain relief during treatments of sympathetic blockade and multimodal epidural pain control. CASE REPORT: We describe a patient with severe CRPS 1 in whom conventional treatment failed to relieve the pain. Combined repeated lumbar sympathetic blocks and long-term epidural morphine, bupivacaine, and ketamine administration provided satisfactory pain relief and functional activity recovery. Six normal control subjects having one Tc-99m HMPAO scan each and the patient with CRPS having 3 Tc-99m HMPAO scans (once before treatment and twice at 4 months and 6 months after treatment, respectively). The patient with CRPS showed lower rCBF than normal controls in the left thalamus and higher rCBF than normal controls in the right parietal lobe and left frontal lobe. After subsequent treatment, the subtraction images showed increased rCBF in the left thalamus and decreased rCBF in the right parietal and left frontal lobes. CONCLUSIONS: Tc-99m HMPAO SPECT showed a relationship of rCBF in the thalamus, parietal lobe, and frontal lobe with pain relief. rCBF alterations may provide an indicator for the quality of pain management for neuropathic pains. Subtraction analysis between pre- and posttreatment, by using statistical parametric mapping (version 2), can be used as an objective indicator for the effectiveness of therapy.

Adult↗
PubMed2006

Comparing the effects of minimal low-flow desflurane with that of semi-close high flow desflurane on perioperative cytokine response in patients undergoing gastrectomy.

BACKGROUND: Anesthetic techniques may influence the perioperative cytokine response. We investigate two anesthetic techniques: minimal low-flow anesthesia (LFA) and semi-closed high flow anesthesia (HFA) with desflurane on the effect of cytokine response in gastrectomy. METHODS: Forty patients scheduled to undergo elective gastrectomy were randomly allocated to LFA (0.3 mL/min) or HFA (2 L/min) group. Blood was sampled for measurement of tumor necrosis factor (TNF), interleukin (IL)-6, IL-8, and IL-1 receptor antagonist (RA) at scheduled intervals. Hemodynamic responses, desflurane concentrations, numbers of patient using cardiovascular agents, and frequency of vaporizer manipulations were recorded during the operation. RESULTS: For patients in the LFA group, production of IL-8 was significantly less increased at the end of the surgical procedure; however there was no significant difference in total production between groups. There was no significant difference in TNF, IL-6, and IL-1RA production throughout the observed period. The desflurane vaporizer was adjusted more frequently (4 [13-6] versus 2 [1-3] times) for patients in the HFA group, and more patients in this group required the use of cardiovascular agents (10 versus 4) than patients in the LFA group during the operation. CONCLUSIONS: The current study demonstrates that smaller increase in cytokine production in the LFA than HFA with desflurane for the patients receiving gastrectomy.

Aged↗
PubMed2006

Bradycardia and hypotension refractory to ephedrine and atropine treatment: severe autonomic dysfunction with abnormal heart rate variability.

Diabetic patients with autonomic dysfunction are potentially poor risks for anesthesia and particular care is needed during and after surgery. We here report a 48-year-old male patient with diabetes mellitus who suffered from intraoperative hypotension and bradycardia which did not respond to ephedrine and atropine treatment and eventuated in cardiac arrest. A heart rate variability study confirmed the diagnosis of autonomic dysfunction after the event. Possible predisposing mechanisms and anesthetic considerations are discussed.

Atropine↗
PubMed2006

Repeated lumbar sympathetic blockade with lidocaine and clonidine attenuates pain in complex regional pain syndrome type 1 patients--a report of two cases.

Repeated lumbar sympathetic blockade (LSB) with local anesthetics is generally used in complex regional pain syndrome (CRPS) of the lower extremities if the initial block has been successful. However, the symptoms of CRPS may inevitably recur in spite of repeated LSB. Clonidine, an alpha2-adrenoceptor agonist, has both anesthetic and analgesic sparing effects, and when added to local anesthetics may enhance peripheral and central neural block due to its local or central analgesic effects. It is reasonable that clonidine has been used in chronic pain conditions such as neuropathic and sympathetically maintained pain. Here we report two cases of CRPS type 1 who got excellent analgesia and alleviation of clinical symptoms after receiving an LSB with lidocaine and clonidine.

Adult↗
PubMed2006

Utility of the auditory evoked potentials index as an indicator for endotracheal intubation.

BACKGROUND: The A-line ARX Index (AAI) has been used as an indicator of depth of anesthesia. The study examined whether AAI-guided endotracheal intubation (EI), compared with experience guidance, could provide better hemodynamic stability during general anesthesia (GA). METHODS: One hundred and four patients were included in this study. In the control group, EI was performed based on the judgment of the anesthesiologist by clinical experience. In the study groups, EI was performed at an AAI value of either 15, 20, or 30. GA was induced with cisatracurium, lidocaine, fentanyl, thiamylal and succinylcholine. Heart rate (HR) and mean arterial pressure (MAP) were recorded at baseline, 1 min before and 1 and 3 min after intubation. The change of hemodynamics over 20% in the space between 1 min before and after intubation was defined as severe change. RESULTS: The incidences of severe changes of HR and MAP in the AAI-15 and AAI-20 groups were significantly lower than those in the control group (19% and 39% vs. 68%, P < 0.01 and 0.05; 52% and 52% vs. 91%, P < 0.01, respectively). The induction time was significantly shorter in the control group than that in the study groups (183 +/- 47 vs. 366 +/- 151, 248 +/- 53, and 255 +/- 85 sec, P < 0.01). Highest dose of thiamylal and longest induction time were needed in the AAI-15 group. CONCLUSIONS: Compared with the routine clinical practice, AAI monitoring helps to achieve better condition for EI during induction with less hemodynamic changes. The AAI value of 20 is suggested as an optimal indicator for EI.

Adult↗
PubMed2005

Protein kinase C inhibitor chelerythrine attenuates the morphine-induced excitatory amino acid release and reduction of the antinociceptive effect of morphine in rats injected intrathecally with pertussis toxin.

Neuropathic pain syndromes respond poorly to opioid treatment. In our previous studies, we found that intrathecal (i.t.) injection of pertussis toxin (PTX) produces thermal hyperalgesia, which is poorly responsive to morphine and is accompanied by an increase in cerebrospinal fluid (CSF) levels of excitatory amino acids (EAAs) and protein kinase C (PKC) activation. In the present study, rats were implanted with an i.t. catheter for drug injection and a microdialysis probe for CSF dialysate collection. On the fourth day after injection of PTX (2 microg, i.t.), there was a significant reduction in the antinociceptive effect of morphine (10 microg, i.t.) which was accompanied by an increase in levels of EAAs. Pretreatment with the PKC inhibitor, chelerythrine (25 microg, i.t.) one hour before morphine injection markedly inhibited both effects. These results suggest that, in PTX-treated rats, PKC plays an important role in inhibiting the morphine-induced spinal EAA release, which might be related to the reduced antinociceptive effect of morphine.

Alkaloids↗
PubMed2005

Attenuation of morphine tolerance by intrathecal gabapentin is associated with suppression of morphine-evoked excitatory amino acid release in the rat spinal cord.

This study was designed to investigate the effect of acute and chronic intrathecal (i.t.) injection of gabapentin (GBP) on the antinociceptive effect of morphine and tolerance development using a tail-flick latency test. Levels of excitatory amino acids (EAA) in i.t. CSF dialysates were also measured by high performance liquid chromatography. Male Wistar rats were implanted with either one or two i.t. catheters for drug injection or pump infusion and with a microdialysis probe for CSF dialysate collection. The effect of acute GBP (10 microg i.t.) injection on the morphine dose response was examined in both naïve rats and rats made tolerant by continuous infusion of morphine (15 microg/h i.t.) for 5 days. At such a low dose (10 microg i.t.), GBP did not enhance morphine's antinociception in naïve rats. In morphine-tolerant rats, however, acute GBP (10 microg i.t.) injection potentiated morphine's antinociception and yielded a 14.6-fold shift in morphine's dose-response curve. When GBP (10 microg/h i.t.) was co-infused with morphine (15 microg/h i.t.) to examine its effect on the development of morphine tolerance, GBP attenuated the development of morphine tolerance. The effect of GBP and morphine on CSF glutamate and aspartate levels was examined in naïve rats, and the effect of morphine challenge on CSF glutamate and aspartate levels was examined in rats previously infused for 5 days with morphine alone or morphine plus GBP. Acute injection of GBP (10 microg i.t.), morphine (50 microg i.t.), or GBP (10 microg i.t.) followed by morphine (50 microg i.t.) 30 min later had no significant effect on CSF EAA concentration in naïve rats; however, in tolerant rats, morphine challenge (50 microg i.t.) increased aspartate and glutamate levels to 221 +/- 22% and 296 +/- 43%, respectively, of those before morphine challenge, and this phenomenon was inhibited by GBP co-infusion. Our results show that GBP, at a dose without enhanced effect on morphine's antinociception in naïve rats, not only potentiates morphine's antinociceptive effect in morphine-tolerant rats but also attenuates the development of morphine tolerance. The mechanism of the effect of GBP on morphine tolerance might be via suppression of the EAA concentration in spinal CSF dialysate.

Amines↗
PubMed2005

Effect of fentanyl on lidocaine-induced convulsions in mice.

This study was undertaken to examine the effect of fentanyl on lidocaine-induced convulsions in mice. Seventy-five male mice were used and divided into five groups, 15 in each. Convulsions were obtained by lidocaine injection subcutaneously (150 mg/kg), in a dose volume of 0.1 ml/10 g body weight over the upper back. The five groups were: (a) control group: pretreated with normal saline; (b) F50 group: pretreated with fentanyl 50 microg/kg; (c) F100 group: pretreated with fentanyl 100 microg/kg; (d) F200 group: pretreated with fentanyl 200 microg/kg, and (e) F100+N group: pretreated with fentanyl 100 mug/kg plus naloxone 1 mg/kg. The pretreatments were given intraperitoneally (i.p.) 5 min prior to lidocaine injection. After lidocaine injection, the latency to the onset of generalized convulsions was observed for 12 min and recorded. The severity of convulsions was assessed and scored as 1 = mild, 2 = moderate, and 3 = severe. The recovery or death of the mice were also recorded. Student's t, Mann-Whitney U, and Fisher's exact tests were used to analyze the data. Compared with the control group (431.7 +/- 37.3 s), the latencies of onset of convulsions in the fentanyl groups were dose-dependently decreased (F50: 331.0 +/- 37.1 s; F100: 240.3 +/- 28.6 s, p < 0.001; F200: 188.7 +/- 19.4 s, p < 0.001), and the decreased latency was reversed by naloxone (F100+N: 412.9 +/- 34.1 s). Compared with the control group (1.13 +/- 0.19), the severities of convulsions in the fentanyl groups were also increased in a dose-dependent manner (F50: 1.47 +/- 0.19; F100: 1.93 +/- 0.21, p < 0.05; F200: 2.46 +/- 0.17, p < 0.001). Similarly, the increased severity was reversed by naloxone (F100+N: 1.33 +/- 0.16). There was no death in the control and naloxone-treated groups. The incidences of death were 2/15 in F50 group, 5/15 in F100 group, and 7/15 in the F200 group (p < 0.05). The results of this study demonstrated that fentanyl potentiates the lidocaine-induced convulsions in a dose-dependent manner in mice, and this effect may be mediated by an opioid mechanism.

Animals↗
PubMed2005

Increased concentrations of neuro-excitatory amino acids in rat anterior cruciate ligament-transected knee joint dialysates: a microdialysis study.

Changes in excitatory amino acid (EAA) levels were examined in the knee joint dialysates of rats with early osteoarthritis (OA). Early OA was induced by anterior cruciate ligament (ACL) transection in one knee and the contralateral knee was used as the sham-operated control, the side for ACL transection being assigned randomly. Twenty weeks after operation, knee joint dialysates were collected by microdialysis and assayed for EAAs by high performance liquid chromatography. The rats were then sacrificed for histopathological examination. Hematoxylin/eosin and Safranin-O staining showed cartilage fibrillation, clustering of chondrocytes, and a reduction in matrix proteoglycans at week 20 in the ACL-transected knee, but not in the sham-operated knee. Levels of glutamate and aspartate in dialysates from the ACL-transected knee were significantly increased by 92 +/- 20.3% or 57 +/- 17.5%, respectively, compared to those in the contralateral sham-operated knee. This increase may contribute to the pathogenesis of early OA.

Animals↗
PubMed2005

Inhibition of p38 mitogen-activated protein kinase attenuates interleukin-1beta-induced thermal hyperalgesia and inducible nitric oxide synthase expression in the spinal cord.

We have reported recently that intrathecal (i.t.) injection of interleukin-1beta (IL-1beta), at a dose of 100 ng, induces inducible nitric oxide synthase (iNOS) expression and nitric oxide (NO) production in the spinal cord and results in thermal hyperalgesia in rats. This study further examines the role of mitogen-activated protein kinase (MAPK) in i.t. IL-1beta-mediated iNOS-NO cascade in spinal nociceptive signal transduction. All rats were implanted with an i.t. catheter either with or without an additional microdialysis probe. Paw withdrawal latency to radiant heat is used to assess thermal hyperalgesia. The iNOS and MAPK protein expression in the spinal cord dorsal horn were examined by western blot. The [NO] in CSF dialysates were also measured. Intrathecal IL-1beta leads to a time-dependent up-regulation of phosphorylated p38 (p-p38) MAPK protein expression in the spinal cord 30-240 min following IL-1beta injection (i.t.). However, neither the phosphorylated extracellular signal-regulated kinase (p-ERK) nor phosphorylated c-Jun NH2-terminal kinase (p-JNK) was affected. The total amount of p38, ERK, and JNK MAPK proteins were not affected following IL-1beta injection. Intrathecal administration of either selective p38 MAPK, or JNK, or ERK inhibitor alone did not affect the thermal nociceptive threshold or iNOS protein expression in the spinal cord. However, pretreatment with a p38 MAPK inhibitor significantly reduced the IL-1beta-induced p-p38 MAPK expression by 38-49%, and nearly completely blocked the subsequent iNOS expression (reduction by 86.6%), NO production, and thermal hyperalgesia. In contrast, both ERK and JNK inhibitor pretreatments only partially (approximately 50%) inhibited the IL-1beta-induced iNOS expression in the spinal cord. Our results suggest that p38 MAPK plays a pivotal role in i.t. IL-1beta-induced spinal sensitization and nociceptive signal transduction.

Analysis of Variance↗
PubMed2005

Postdural puncture headache with abdominal pain and diarrhea.

Dural puncture or a rent in the dura with prolonged cerebrospinal fluid leakage may cause noninfectious arachnoiditis and may be associated with urinary and fecal incontinence. Visceral dysfunction is common for patients with noninfectious arachnoiditis of the lumbosacral nerve roots after dural puncture. We report a case of postdural puncture headache associated with abdominal pain and diarrhea. An epidural blood patch was performed, and all symptoms resolved after 5 days. After exclusion of organic and psychological disorders, this treatment might be considered for patients who are experiencing abdominal pain and diarrhea after dural puncture.

Abdominal Pain↗
PubMed2005

Intrathecal ketorolac pretreatment reduced spinal cord ischemic injury in rats.

Paraplegia caused by spinal cord ischemic injury remains a potential complication of surgical repair of thoracoabdominal aortic aneurysms. Studies suggest that cyclooxygenase (COX) contributes to ischemic neuronal damage and that COX inhibitors may reduce injury. In this study, we examined whether intrathecal pretreatment with ketorolac, a nonselective COX inhibitor, had a protective effect against ischemic spinal cord injury in rats. Rats were randomized to receive either intrathecal normal saline, ketorolac 30 microg, or ketorolac 60 microg (n = 6 rats per group) 1 h before spinal cord ischemia (intraaortic balloon occlusion combined with proximal arterial hypotension for 11 min). Another 6 rats served as the sham-operated controls. Ischemic injury was assessed by hindlimb motor function and by histopathological changes in the lumbar spinal cord at 24 h after the ischemic insult. The other 20 rats (n = 10 per group) were used in the second experiments to evaluate the safety of this drug. Survival of rats was recorded 28 days after reperfusion. Intrathecal pretreatment with 60 microg of ketorolac significantly reduced neuronal death and improved hindlimb motor function, and the long-term survival was similar to that in the control group. The results suggest that intrathecal ketorolac may be of therapeutic potential for preventing spinal cord ischemic injury during thoracoabdominal aortic surgery.

Animals↗