Cesarean not in labor adds a constant risk of newborn respiratory complications at any gestational age near-term and early-term. The more the planned cesarean is delayed, the better is newborn respiratory outcome.
The influence of pregnancy-induced hypertension (pre-eclampsia) on muscarinic cholinergic receptors and on acetylcholinesterase (AChE) activity was investigated using frozen sections of the umbilical artery and vein. Pre-eclamptic patients undergoing Caesarean delivery and normotensive pregnant control woman undergoing Caesarean delivery with similar parity, gestation length and age were examined. Muscarinic cholinergic receptors were assayed in frozen sections of the umbilical artery and vein by a radioligand binding assay technique, using [3H]-N-methyl scopolamine (NMS) as a ligand. AChE was demonstrated with a histochemical technique associated with microdensitometry. [3H]-NMS was specifically bound to sections of both umbilical artery and vein in a manner consistent with the labelling of muscarinic cholinergic receptors. The affinity of the radioligand was similar in the two vessels, whereas the maximum density of binding sites (Bmax) was higher in the umbilical vein than in the artery. A faint AChE reactivity was observed in the tunica media of both umbilical artery and vein. In pre-eclampsia, a loss of [3H]-NMS binding sites not accompanied by changes in the affinity of radioligand was found. The decrease of muscarinic cholinergic receptors involved to a greater extent the umbilical artery than the vein. No differences in AChE activity were found at the level of umbilical artery and vein between control and pre-eclamptic subjects. These findings suggest that pre-eclampsia is characterized by a loss of muscarinic cholinergic receptors in the umbilical circulation not accompanied by changes of the acetylcholine catabolizing enzyme AChE. It is possible that the decreased density of vascular muscarinic cholinergic receptors in pregnancy-induced hypertension contribute to the increased resistance of the umbilical circulation occurring in pre-eclampsia.
Background
There is a gap between pudendal neuralgia (PN) due to pudendal entrapment syndrome and PN without pudendal entrapment syndrome. The latter could have atypical symptoms.
Aim
Defining a rate of atypical PN from a clinical series of female patients with chronic pelvic‐perineal pain.
Methods
The atypical PN was defined as a pain not meeting clinical criteria for pudendal entrapment syndrome. The effect size was the rate of atypical PN. Such a rate was expected to be found among patients screened for enrollment in clinical series on pudendal neuropathic pain. A systematic search was performed looking for clinical series on PN. Studies must report information on female patients, pelvic‐perineal pain, at least a clinical criterion for diagnosing the pudendal neurogenic origin of pain, the proportion of patients with pain not meeting the clinical criterion/a for diagnosing the pudendal entrapment pain.
Results
From 2637 references, nine studies were included for qualitative analysis. Three of them were not suitable for data synthesis: one assessed the rate of PN after hip arthroscopy; second enrolled miscellaneous patients, a third investigated patients with gynecological diseases. Six studies involved patients with suspicion of pudendal entrapment symptoms (205 patients observed), allowing data synthesis. One of these series was judged as being of good quality. The overall rate of atypical PN is 0.013 (95% confidence interval, 0.008‐0.021), I2 0%. Further analysis suggests the risk of bias for all studies.
Conclusions
Atypical PN in females is low when clinical criteria for pudendal entrapment syndrome are applied.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.