A randomised dose-response study of prophylactic Methoxamine infusion for preventing spinal-induced hypotension during Cesarean delivery.

BACKGROUND: α-receptor agonists have been reported to be safe and effective for treating or preventing spinal-induced hypotension during cesarean delivery. As a pure α1 adrenergic agonist, methoxamine has potential advantages of reducing myocardial oxygen consumption and protecting the heart in obstetric patients compared to phenylephrine. The aim of this study was to determine the optimal prophylactic methoxamine infusion dose that would be effective for preventing spinal-induced hypotension in 50% (ED50) and 95% (ED95) of parturients. METHODS: Eighty parturients with a singleton pregnancy scheduled for elective cesarean delivery were randomly allocated to receive prophylactic methoxamine infusion at one of four different fixed-rates: 1 µg/kg/min (group M1), 2 µg/kg/min (group M2), 3 µg/kg/min (group M3), or 4 µg/kg/min (group M4). An adequate response was defined as absence of hypotension (maternal SBP < 80% of baseline or SBP < 90 mmHg). The values for ED50 and ED95 of prophylactic methoxamine infusion were determined by probit regression model. The outcomes of maternal hemodynamics and fetal status were compared among the groups. RESULTS: The calculated ED50 and ED95 (95% confidence interval) of prophylactic methoxamine infusion dose were 2.178 (95% CI 1.564 to 2.680) µg/kg/min and 4.821 (95% CI 3.951 to 7.017) µg/kg/min, respectively. The incidence of hypotension decreased with increasing methoxamine infusion dose (15/20, 11/20, 7/20 and 2/20 in group M1, M2, M3 and M4 respectively, P <  0.001). 1-min Apgar scores and umbilical arterial PaO2 were lower but umbilical arterial PaCO2 was higher in Group M1. No difference was found in the other incidence of adverse effects and neonatal outcomes among groups. CONCLUSIONS: Under the conditions of this study, when prophylactic methoxamine infusion was given at a fixed-rate based on body weight for preventing spinal-induced hypotension in obstetric patients, the values for ED50 and ED95 were 2.178 µg/kg/min and 4.821 µg/kg/min respectively. CLINICAL TRIAL REGISTRATION: Chinese Clinical Trial Registry (ChiCTR), registry number of clinical trial: ChiCTR-1,800,018,988 , date of registration: October 20, 2018.

Estrogen modulation of visceral pain.

It is commonly accepted that females and males differ in their experience of pain. Gender differences have been found in the prevalence and severity of pain in both clinical and animal studies. Sex-related hormones are found to be involved in pain transmission and have critical effects on visceral pain sensitivity. Studies have pointed out the idea that serum estrogen is closely related to visceral nociceptive sensitivity. This review aims to summarize the literature relating to the role of estrogen in modulating visceral pain with emphasis on deciphering the potential central and peripheral mechanisms.

[Comparative Observation on Electroacupuncture and Manual Acupuncture in Rabbits with Facial Nerve Injury by Electron Microscope].

OBJECTIVE: To observe the effect of manual acupuncture and electroacupuncture (EA) on ultrastructure of facial nerve Schwann cells, myelin sheath and mitochondria in facial nerve injury rabbits, so as to explore its mechanism underlying improving facial palsy. METHODS: A total of 50 New Zealand rabbits were randomly divided into normal, sham-operation, model, MA and EA groups (n=10 in each group). Facial nerve injury model was made by clamping the facial nerve for 5 min using a pair of forceps. Manual needle stimulation (mild reinforcing-reducing) or EA (continuous wave, 20 Hz) was applied to "Dicang" (ST 4), "Xiaguan" (ST 7), "Taiyang" (EX-HN 5) and "Yangbai" (GB 14) on the injured sides for 4 weeks, 30 min each day. The facial nerve motion score was performed every 7 days. The ultrastructure of facial nerve was observed by electron microscope after 28 days' treatment. RESULTS: There were no significant differences in behavioral score and ultrastructure in normal and sham-operation groups (P<0.05). Compared with the normal group, facial nerve motion scores, ultrastructural morphological changes and the number of axons per unit area, myelin sheath thickness and axon area were worse in the model group (P<0.05). After treatment, facial nerve motion scores, ultrastructural morphological changes and the number of axons per unit area, myelin sheath thickness and axon area in the two treatment groups were better than those in the model group (P<0.05), and EA worked better than MA (P<0.05). CONCLUSIONS: In the treatment of facial nerve injury, EA can promote axoplasmic mitochondrial proliferation, myelin sheath recovery and axonal regeneration more effectively than MA, which may be one of the mechanisms that EA therapy is superior to MA.