Articles: hyperalgesia.
-
Several mechanisms of remifentanil-induced hyperalgesia in spinal cord mainly have been explained such as N-methyl-D-aspartate receptors activation, but the mechanism in dorsal root ganglion (DRG) is poorly understood. It has been reported that CCL3 may be a regulator in both inflammatory pain and hyperalgesia. In this paper we explored whether CCL3 and CCR5, the mainly receptor of CCL3, play a role in the remifentanil-induced hyperalgesia in DRG by using a rat model with remifentanil administration. ⋯ The results highlighted the fact that CCL3 and its receptor CCR5 in DRG might contribute to remifentanil-induced hyperalgesia. Thus CCL3/CCR5 signaling may be further considered in the development of new therapeutic strategies.
-
To evaluate widespread pressure pain in patients with chronic plantar heel pain compared with that in healthy controls and to investigate the differences in ultrasound imaging and quality of life between these two groups. ⋯ Patients suffering from chronic plantar heel pain showed widespread and bilateral hypersensitivity, increased thickness of the plantar fascia in the affected foot, and deterioration in quality of life and physical functioning compared with matched controls.
-
Randomized Controlled Trial
Effects of intraoperative high-dose vs low-dose remifentanil for postoperative epidural analgesia after gynecological abdominal surgery: a randomized clinical trial.
To evaluate whether intraoperative high-dose remifentanil infusion increased local anesthetic consumption in postoperative epidural analgesia and postoperative pain scores compared with low-dose remifentanil infusion. ⋯ Intraoperative high-dose remifentanil infusion increased local anesthetic consumption in postoperative epidural analgesia relative to low-dose remifentanil.
-
J. Physiol. Pharmacol. · Aug 2016
Comparative StudyPronociceptive effects induced by cutaneous application of a transient receptor potential ankyrin 1 (TRPA1) channel agonist methylglyoxal in diabetic animals: comparison with tunicamycin-induced endoplastic reticulum stress.
Methylglyoxal (MG) is a reactive carbonyl compound generated in diabetes mellitus. MG is an established transient receptor potential ankyrin 1 (TRPA1) channel agonist that contributes to TRPA1-mediated diabetic pain hypersensitivity. Here we studied whether exposure to diabetes and thereby to elevated endogenous MG modulates hypersensitivity induced by intradermal MG. ⋯ In vitro patch clamp recording indicated that tunicamycin itself (30 μM) is not a TRPA1 agonist. The results indicate that pain hypersensitivity induced by non-diabetic ER stress as well as that induced by diabetes is mediated TRPA1. Reduction of MG-induced hypersensitivity in diabetes or ER stress may, at least partly, be explained by peripheral mechanisms.
-
In the past 2 decades, opioids have been used increasingly for the treatment of persistent pain, and doses have tended to creep up. As basic science elucidates mechanisms of pain and analgesia, the cross talk between central pain and opioid actions becomes clearer. ⋯ Newly revealed basic mechanisms suggest possible avenues for drug development and new drug therapies that could alter pain sensitization through endogenous and exogenous opioid mechanisms. Recent changes in practice such as the introduction of titration-to-effect for opioids have resulted in higher doses used in the clinic setting than ever seen previously. New basic science knowledge hints that these newer dosing practices may need to be reexamined. When pain worsens in a patient taking opioids, can we be assured that this is not because of the opioids, and can we alter this negative effect of opioids through different dosing strategies or new drug intervention?