ABSTRACT
This report describes a case of spontaneous bleeding from uterine vessels presenting as hyperstimulation and fetomaternal distress at term. A 40-week primigravid woman underwent an emergency caesarean section for fetal distress, which unexpectedly revealed a spontaneous haemoperitoneum. Clinical assessment and investigations postoperatively gave a diagnosis of a right-sided uterine artery aneurysm that, it was believed, had ruptured, causing the haemoperitoneum. This was successfully treated postnatally using interventional radiological techniques leading to expeditious maternal recovery and discharge home.
Subject(s)
Abdominal Pain/diagnostic imaging , Cesarean Section/methods , Fetal Distress/diagnostic imaging , Hemoperitoneum/diagnostic imaging , Pregnancy Complications/diagnostic imaging , Uterine Artery Embolization/methods , Uterine Rupture/diagnostic imaging , Abdominal Pain/etiology , Adult , Anti-Bacterial Agents/administration & dosage , Female , Ferrous Compounds/administration & dosage , Fetal Distress/etiology , Follow-Up Studies , Hemoperitoneum/etiology , Humans , Pregnancy , Pregnancy Complications/surgery , Rupture, Spontaneous/surgery , Term Birth , Tomography, X-Ray Computed , Treatment Outcome , Uterine Rupture/surgeryABSTRACT
To investigate whether the xenon-induced inhibition of the transient receptor potential vanilloid type 1 (TRPV1) ion channel in rat dorsal root ganglion (DRG) neurons reduces nociceptive processing, we examined the effect of xenon in reducing the release of calcitonin gene-related peptide (CGRP) from those neurons. We found that exposure to xenon failed to effect a reduction of capsaicin-evoked CGRP release from cultured primary sensory neurons when stimulated by capsaicin. This finding suggests that xenon acts on several molecular targets on nociceptive primary sensory neurons, and that xenon's action on one, or more, of those targets serves to offset the inhibitory, pro-analgesic, effect of xenon on TRPV1. It is concluded that xenon may not produce any analgesic effect through peripheral nociceptors.
Subject(s)
Calcitonin Gene-Related Peptide/metabolism , Capsaicin/pharmacology , Nociceptors/metabolism , TRPV Cation Channels/metabolism , Xenon/pharmacology , Animals , Calcitonin Gene-Related Peptide/antagonists & inhibitors , Capsaicin/antagonists & inhibitors , Cells, Cultured , Female , Nociceptors/physiology , Rats , Rats, Sprague-Dawley , TRPV Cation Channels/antagonists & inhibitorsABSTRACT
AIMS: Xenon provides effective analgesia in several pain states at sub-anaesthetic doses. Our aim was to examine whether xenon may mediate its analgesic effect, in part, through reducing the activity of transient receptor potential vanilloid type 1 (TRPV1), a receptor known to be involved in certain inflammatory pain conditions. MAIN METHODS: We studied the effect of xenon on capsaicin-evoked cobalt uptake in rat cultured primary sensory neurons and in human TRPV1 (hTRPV1)-expressing human embryonic kidney 293 (HEK293) cells. We also examined xenon's effect on the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) in the rat spinal dorsal horn evoked by hind-paw injection of capsaicin. KEY FINDINGS: Xenon (75%) reduced the number of primary sensory neurons responding to the TRPV1 agonist, capsaicin (100 nM-1 µM) by ~25% to ~50%. Xenon reduced the number of heterologously-expressed hTRPV1 activated by 300 nM capsaicin by ~50%. Xenon (80%) reduced by ~40% the number of phosphorylated ERK1/2-expressing neurons in rat spinal dorsal horn resulting from hind-paw capsaicin injection. SIGNIFICANCE: Xenon substantially reduces the activity of TRPV1 in response to noxious stimulation by the specific TRPV1 agonist, capsaicin, suggesting a possible role for xenon as an adjunct analgesic where hTRPV1 is an active contributor to the excitation of primary afferents which initiates the pain sensation.
