Baicalin ameliorates neuropathic pain by suppressing HDAC1 expression in the spinal cord of spinal nerve ligation rats.

BACKGROUND/PURPOSE: In a recent study, we found that baicalin exhibited a potent analgesic effect on carrageenan-evoked thermal hyperalgesia. The underlining mechanisms may be associated with inhibition of inflammatory mediator overproduction, including proinflammatory cytokines, nitric oxide (NO), and prostaglandin E2 (PGE2). In the present study, we examined the effect of baicalin on the antinociceptive effect of morphine and histone deacetylase 1 (HDAC1) expression in the spinal cord dorsal horn in neuropathic pain rats. METHODS: Neuropathic pain was induced by tight ligation of the left L5 spinal nerve of the rats. An intrathecal catheter was implanted for drug administration. Nociception was assessed by using the plantar test with the Hargreaves radiant heat apparatus, and the von Frey test with the dynamic plantar anesthesiometer. Spinal cords were removed for histone acetyl-H3 and HDAC1 western blot analysis at the end of the nociceptive assessment. RESULTS: The results showed that hyperalgesia and allodynia were observed in the spinal nerve ligated (SNL) left hindlimb; it was companied by histone-H3 deacetylation and HDAC1 overexpression on the ipsilateral side of the spinal cord dorsal horn. Intrathecal injection of baicalin (10 µg) significantly attenuated the allodynia and hyperalgesia, and enhanced the antinociceptive effect of morphine (15 µg). Moreover, baicalin reversed the histone-H3 acetylation and suppressed HDAC1 expression on the ipsilateral side of the spinal cord dorsal horn of SNL rats. CONCLUSION: The present findings suggest that baicalin can ameliorate neuropathic pain by suppressing HDAC1 expression and preventing histone-H3 acetylation in the spinal cord dorsal horn of SNL rats.

Co-administration of ultra-low dose naloxone attenuates morphine tolerance in rats via attenuation of NMDA receptor neurotransmission and suppression of neuroinflammation in the spinal cords.

Although mechanisms underlying ultra-low dose naloxone-induced analgesia have been proposed, possible interactions with glutamatergic transmission and glial cell activation have not been addressed. In the present study, we examined the effect of ultra-low dose naloxone on spinal glutamatergic transmission and glial cell activity in rats chronically infused with morphine. In male Wistar rats, intrathecal morphine infusion (15microg/h) for 5days induced (1) antinociceptive tolerance, (2) downregulation of glutamate transporters (GTs) GLT-1, GLAST, and EAAC1, (3) increasing of NMDA receptor (NMDAR) NR1 subunit expression and phosphorylation, (4) upregulation of protein kinase C gamma (PKCgamma) expression, and (5) glial cell activation. On day 5, morphine challenge (15microg/10microl) caused a significant increase in the concentration of the excitatory amino acids (EAAs) aspartate and glutamate in the spinal CSF dialysates of morphine-tolerant rats. Intrathecal co-infusion of ultra-low dose naloxone (15pg/h) with morphine attenuated tolerance development, reversed GTs expression, inhibited the NMDAR NR1 subunit expression and phosphorylation, and PKCgamma expression, inhibited glial cell activation, and suppressed the morphine-evoked EAAs release. These effects may result in preservation of the antinociceptive effect of acute morphine challenge in chronic morphine-infused rats. Ultra-low dose naloxone infusion alone did not produce an antinociceptive effect. These findings demonstrated that attenuation of glutamatergic transmission and neuroinflammation by ultra-low dose naloxone co-infusion preserves the lasting antinociceptive effect of morphine in rats chronically infused with morphine.

Mechanical characterization of rabbit pulmonary vein sleeves in in vitro intact ring preparation.

BACKGROUND: Pulmonary vein (PV) sleeves, composed of cardiomyocytes, play certain roles in arrhythmogenesis. In the literature, it has been frequently reported that PV sleeves possess intrinsic spontaneous pacemaking activity and triggered activity in normal dogs and rabbits. In contrast, other research groups presented totally opposite findings which showed absence of such pacemakers in dogs, rabbits and rats. The present study was designed to clarify this puzzle and contradiction. METHODS: A novel methodology using in vitro experimentation was used to examine the electromechanical activity of whole segments of PV sleeves. The ring preparation was composed of a small piece of left atrial (LA) free wall, PV ostium and sleeve from rabbits. A circumferential contraction of the PV sleeve was measured when the preparation was electrically driven from the LA free wall. Mechanical force of the ring preparation was measured using a force transducer. The action potentials were recorded using conventional intracellular recording technique in strip preparation. RESULTS: In 15 rabbits, no spontaneous pacemaking activity or triggered activity was found in the in vitro ring preparation of PV sleeve. The circumferential contraction of PV sleeves was external calcium-dependent. Frequency-force relation displayed a negative staircase at 0.1-0.5 Hz and a positive staircase at 1-5 Hz. Post-rest potentiation was prominent between 15 s and 120 s. Intracellular action potential recording did not display any automaticity or triggered activity in PV sleeves. CONCLUSION: In an intact ring preparation of rabbit PV sleeves, intrinsic spontaneous pacemaking activity or triggered activity was not found.

Myoclonic seizure in the postanesthesia care unit after thoracic laminectomy.

IMPLICATIONS: We report a patient who developed myoclonic seizure in the postanesthesia care unit after thoracic laminectomy. Expeditious diagnostic evaluation of unrecognized dura tear during surgery must be instituted immediately to avoid untoward sequelae. Specific treatment in addition to supportive care is required if the diagnosis is to be clearly identified.

Myofascial pain syndrome induced by malpositioning during surgery--a case report.

It is a real challenge to the anesthesiologists to differentiate brachial plexus injury (BPI) from myofascial pain syndrome (MPS). The possibility of MPS should be suspected in a patient with complaints of pain and dysfunction of the upper arm immediately after surgery. Here we report a case of gallstone with cervical ankylosing spondylitis who sustained myofascial pain syndrome (MPS) immediately after open cholecystectomy. We utilized dry needle stimulation to deactivate the trigger point of the pectoris minor muscle and stretching the muscle to relieve the muscle pain after the diagnosis was made. The patient completely recovered 2 weeks later.

Fentanyl-induced coughing and airway hyperresponsiveness.

BACKGROUND: The tussive effect of fentanyl, in sharp contrast to the antitussive effect that common opioids have, is not rarely seen in clinical anesthesia. Pretreatment with beta 2 agonist inhalation could dramatically suppress fentanyl-induced coughing. We hypothesized that airway hyperresponsiveness might exist in large proportion of the subjects who had experienced fentanyl-induced coughing during previous anesthesia. METHODS: We designed a case-controlled matching study to investigate the correlation between fentanyl-induced coughing and airway hyperresponsiveness. Twenty-six consecutive subjects (ASA I-III), who experienced fentanyl-induced coughing during anesthesia in our hospital from 1999 to 2000, were enrolled in this study as the fentanyl-cough group. In all the subjects baseline spirometry was first obtained. Airway responsiveness was evaluated with either PC20 of methacholine challenge test or bronchodilator test. After matching age and sex, another 26 subjects without history of fentanyl-induced coughing during previous anesthesia were also enrolled in the study as the control group. RESULTS: The proportion of airway hyperresponsiveness in fentanyl-cough group and control group was 30.77% and 19.23% respectively. After pairing of these two groups, McNemar test revealed no significant difference in the proportion of airway hyperresponsiveness between these two groups (P = 0.257). CONCLUSIONS: From the analysis of the present study, we cannot prove that there is a direct correlation between fentanyl-induced coughing and airway hyperresponsiveness.