No abstract

The use of low-volume ultrasound-guided ISBPB is associated with fewer respiratory and other complications with no change in postoperative analgesia compared with the standard-volume technique.

US reduces the number of attempts, LA volume, and postoperative pain when compared with NS for ISB.

Release of inflammatory pain mediators from peripheral sensory afferent endings contributes to the development of a positive feedback cycle resulting in chronic inflammation and pain. Botulinum neurotoxin type A (BoNT-A) blocks exocytosis of neurotransmitters and may therefore block the release of pain modulators in the periphery. Subcutaneous administration of BoNT-A (2.5, 5 and 10U) reduced plasma extravasation (PE) caused by electrical stimulation of the saphenous nerve or capsaicin in the rat hindpaw skin (ANOVA, Post hoc Tukey, p<0.05, n=6). Subcutaneous BoNT-A also reduced blood flow changes evoked by saphenous nerve stimulation (ANOVA, Post hoc Tukey, p<0.05, n=6). Subcutaneous BoNT-A had no effect on PE induced by local injection of substance P (SP) or vasodilation induced by local CGRP injection. Although BoNT-A is an effective treatment for a wide range of painful conditions, the toxin's large size necessitates that it be injected at numerous sites. We found that a short synthetic peptide (TD-1) can facilitate effective transdermal delivery of BoNT-A through intact skin. Coadministration of TD-1 and BoNT-A to the hindpaw skin resulted in a significant reduction in PE evoked by electrical stimulation. The findings show that BoNT-A can be administered subcutaneously or topically with a novel transdermal delivery peptide to reduce inflammation produced by activating nociceptors in the skin. Peptide-mediated delivery of BoNT-A is an easy and non-invasive way of administering the toxin that may prove to be useful in clinical practice.

Activation of the 5-HT(1B/D) receptor inhibits cerebrovascular neurogenic inflammation (NI). The aim of this study was to determine if the 5-HT(1B/D) receptor agonist sumatriptan can also inhibit NI in other regions of the body. NI was assessed by measuring plasma extravasation (PE) and changes in blood flow in the rat hindpaw. Sumatriptan was administered locally (20 microl, 50 or 100 nM, s.c.) into the dorso-medial region of one hindpaw. The other paw was pre-treated with vehicle (20 microl of 0.9% saline) and served as a control. NI was induced after treatment with sumatriptan/vehicle by injecting capsaicin (15 microl, 1%, s.c.) into each paw or by electrically stimulating the saphenous nerve (4 Hz, 30s). Sumatriptan administered locally or systemically (300 microg/kg, i.v.) significantly reduced saphenous nerve and capsaicin-induced PE and vasodilation. The systemic and local inhibitory actions of sumatriptan are mediated by the 5-HT(1B/D) receptor as pre-treatment with the 5-HT(1B/D) antagonist GR127935 (GR; 15 microl, 1 microM, s.c. or 0.2 micromol/kg, i.v.) completely blocked the inhibitory effect of sumatriptan on capsaicin-induced vasodilation and reduced the inhibitory effect of sumatriptan on capsaicin and electrically induced-PE. Neither PE induced by local injection of substance P (SP) (20 pmol, 20 microl, s.c.) nor vasodilation induced by local CGRP injection was affected by pre-treatment with sumatriptan. These findings indicate that both local and systemic activation of the 5-HT(1B/D) receptor by sumatriptan reduce NI induced by nerve stimulation or capsaicin presumably by inhibiting neuropeptide release. 5-HT(1B/D) receptor agonists may be useful for the treatment of non-trigeminal pain conditions involving NI.