An unusual cause of fetomaternal distress at term: uterine vessel rupture in pregnancy.

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.

Xenon fails to inhibit capsaicin-evoked CGRP release by nociceptors in culture.

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.

Xenon reduces activation of transient receptor potential vanilloid type 1 (TRPV1) in rat dorsal root ganglion cells and in human TRPV1-expressing HEK293 cells.

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.