Gender disparity in organ donation.

Organ donation is affected by legal, cultural, religious, and racial factors, as well as by health considerations. Although organs in and of themselves are gender neutral and can be exchanged between the sexes, women account for up to two thirds of all organ donations. There are no clear reasons why women are more willing to undergo the risks of surgery than are men, nor is this gender disparity mirrored in the demand for donated organs. More men than women are recipients, and women are less likely to complete the necessary steps to receive donated organs. Internationally, ethical concern has been focused on possible human rights violations in the harvesting of organs from prisoners and, in poor countries, on the trafficking of organs from girls and women who are expected to financially help their families by selling their organs.

Vaginocervical stimulation releases oxytocin within the spinal cord in rats.

Vaginocervical stimulation (VS) significantly elevated the concentration of oxytocin (OT) in spinal cord superfusates of 8 intact urethane-anesthetized rats measured 10-15 min after VS (median [interquartile range]: 1.7 [1.00-3.37] pg/ml) compared to that measured 10-15 min before VS (1.1 [1.01-1.40] pg/ml). When VS was administered once (n = 8), it produced a 55% increase over baseline values; when administered a second time 45 min later (n = 6), it produced only a 22% increase over pre-VS values. The effects of estrogen on the VS-induced release of OT were then investigated using ovariectomized rats that were treated either with estradiol benzoate (EB; 10 microg/100 g bw) (n = 6) or with an oil vehicle (n = 6) subcutaneously for 3 days. The EB treatment significantly elevated the basal levels of OT released into spinal cord superfusates above vehicle control levels. Within 5-10 min after the onset of VS, OT concentrations in the superfusates were significantly higher in EB-treated than in vehicle-treated rats. The vehicle-treated rats did not show a significant elevation in OT concentration following VS. To rule out the possibility that the posterior pituitary gland was the source of this OT, the effect of hypophysectomy (HYPOX) was assessed on the VS-induced release of OT into spinal cord superfusates and plasma. The concentration of OT in spinal cord superfusates of both the HYPOX (n = 5) and intact rats (n = 6) increased significantly from 5.8 [4.4-6.5] pg/ml pre-VS to 7.9 [6.7-10.3] pg/ml immediately after VS, and from 4.4 [3.8-5] pg/ml pre-VS to 5.1 [4.6-5.7] pg/ml immediately after VS, respectively. There was no significant difference in baseline levels of OT in cerebrospinal fluid between the two groups. By contrast, plasma OT levels, while significantly elevated in response to VS from 3.42 [2.9-5.34] pg/ml baseline to 7.25 [5.33-15.77] pg/ml in the intact group, failed to respond significantly to VS in the HYPOX group (n = 5). The present findings provide evidence of a direct estrogen-dependent release of OT within the spinal cord in response to VS, presumably via descending oxytocinergic neurons.

Spinal cord monoamines modulate the antinociceptive effects of vaginal stimulation in rats.

Perispinal administration (into the lumbar intrathecal space) of phentolamine (40 micrograms), an alpha-adrenergic receptor blocking agent, reduced the analgesic effect of vaginal stimulation by 39.7% (measured by tail flick latency) and 57.1% (measured by vocalization threshold) as compared to controls. Perispinal administration of methysergide (10 micrograms), a serotoninergic receptor blocking agent, reduced the analgesic effect of vaginal stimulation by 48.5% (measured by vocalization threshold), although it did not significantly affect the tail flick measure. In a separate experiment, vaginal stimulation activated the release of norepinephrine and serotonin into a superfusate of the spinal cord. During vaginal stimulation, levels of norepinephrine and serotonin increased about 2-fold above resting levels. These findings indicate that vaginal stimulation releases norepinephrine and serotonin into the spinal cord, thereby exerting an analgesic effect.