Big pussy lips Massachusetts

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Try out PMC Labs and tell us what you think. Learn More. Sexual dysfunction affects both men and women, involving organic disorders, psychological problems, or both. Overall, the state of our knowledge is less advanced regarding female sexual physiology in comparison with male sexual function.

Female sexual dysfunction has received little clinical and basic research attention and remains a largely untapped field in medicine. The epidemiology of female sexual dysfunction is poorly understood because relatively few studies have been done in community settings. Several studies have shown that the prevalence of female sexual arousal disorders correlates ificantly with increasing age. These studies have shown that sexual arousal and frequency of coitus in the female decreases with increasing age. The pathophysiology of female sexual dysfunction appears more complex than that of males, involving multidimensional hormonal, neurological, vascular, psychological, and interpersonal aspects.

Organic female sexual disorders may Big pussy lips Massachusetts a wide variety of vascular, neural, or neurovascular factors that lead to problems with libido, lubrication, and orgasm. However, the precise etiology and mechanistic pathways of age-related female sexual arousal disorders are yet to be determined. In the past two decades, some advances have been made in exploring the basic hemodynamics and neuroregulation of female sexual function and dysfunction in both animal models and in human studies.

In this review, we summarize neural regulation of sexual function and neurological causes of sexual dysfunction in women. The female genital organs consist of the labia majora, labia minora, clitoris, bulbs of the vestibuleand vagina.

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While there are clearly many homologous structures in the male and female, the anatomy differs very ificantly and should be described in its own right. Due to ificant changes following menopause, many descriptions derived from cadaver dissection are inaccurate for younger and premenopausal women.

The vulva consists of the parts of the female genitals that are visible externally and include the labia majora, the labia minora, the glans of the clitoris, and the vestibule of the vagina. The labia majora represent the cleft female homologue to the male scrotum.

They are two symmetrical folds of skin filled with fat, connective tissue, nerves and lymphatic vessels. The lateral surface is covered with variable amounts of coarse hair while the medial surface is hairless and contains a large of sebaceous glands.

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The function of the labia majora is to protect and enclose the vaginal vestibule. The labia minora are thin, delicate folds of vascular, fat-free, hairless skin located on each side of the vaginal vestibule. The labia minora divide anteriorly to form the prepuce and frenulum of the clitoris. The glans of the clitoris is described below. The vestibule of the vagina is the space enclosed by the labia minora and le into the vagina itself.

Anterior to the vestibule is the external urethral orifice and associated paraurethral Skene's glands. Posteriorly, the vestibule receives the orifices of the greater vestibular Bartholin's glands, which provide lubrication for the vestibule of the vagina and are homologues of the bulbourethral glands of the male. The clitoris is a small midline erectile body that is homologous to the male penis. It consists of a glans, body, and crura. The glans is easily visible at the superior junction of the labia minora.

The body, consisting of paired corpora with an incomplete septum between them, is 1 to 2 cm wide and 2 to 4 cm long [ 1 ]. The crura, 5 to 9 cm in length, are attached to the ischial bone and covered by the ischiocavernosus muscle [ 1 ]. Like the penis, the clitoris is attached to the pubis by specialized Big pussy lips Massachusetts tissue supports.

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The so-called suspensory ligament of the clitoris has both superficial and deep components [ 2 ]. There is a superficial fibro-fatty ligament that extends from within the fatty tissue of the mons pubis to the body of the clitoris and into the labia majora. In addition, there is a deep component that originates on the symphysis pubis itself, extends to the body of the clitoris and then to the bulbs of the clitoris.

The supporting structures of the clitoris thus appear to function less as suspensory ligaments and more as traction ligaments that transmit force from the labia majora, bulbs, and vaginal introitus to the clitoris. Some authors have suggested that the anterior vaginal wall acts to transmit forces generated during intercourse to the clitoris [ 3 ].

Blood supply to the body of the clitoris is supplied by paired pudendal arteries that course lateral to the urethra along the pelvic aspect of the anterior vaginal wall [ 1 ]. These arteries give off the cavernous artery and the artery to the bulb. The body of the clitoris is composed of cavernous tissue surrounded by tough tunica albuginea. However, the clitoris seems to lack the subalbugineal plexus characteristic of the penis [ 4 ]. This finding suggests that, unlike the penis, the clitoris does not have a well developed outflow occlusion mechanism and becomes erect mainly through increased blood flow.

The glans of the clitoris forms a cap that sits on Big pussy lips Massachusetts ends of the corporal bodies and is richly innervated by sensory nerve endings [ 5 ]. The deep dorsal nerves perforate the glans on the dorsal aspect of its junction with the corporal bodies. Recent studies have confirmed that the dorsal nerve of the clitoris is relatively large more than 2 mm in diameter [ 1 ].

The cavernous nerve runs along with the cavernous artery as it enters the bodies of the clitoris. Nerves containing neuronal nitric oxide synthase have been detected in both the body and the glans of the human clitoris [ 6 ], suggesting that nitric oxide is involved in the control of clitoral smooth muscle tone. The female urethra, like the bulbous portion of the male urethra, is surrounded laterally by erectile tissue called the vestibular bulbs in most anatomy texts.

Recent anatomic studies have shown that these erectile bodies are intimately related and lateral to the urethra rather than lateral to the vestibule of the vagina [ 1 ]. They are not, as often depicted in anatomic texts, located within the labia minora. Superiorly, the bulbs continue as the pars intermedia and terminate as the glans of the clitoris [ 9 ]. Thus, the bulbs represent the cleft female homologue to the bulb of the urethra in the male. The entire complex of spongy erectile tissue consisting of bulbs, pars Big pussy lips Massachusetts, and clitoral glans correspond to the corpus spongiosum of the male [ 9 ].

The vagina is a muscular sheath that connects the uterus and the external genitalia. It has both sexual and reproductive functions and this dual function is reflected in various aspects of its structure, especially its vascular supply, its sensory and motor innervation and its marked distensibility.

The wall of the vagina consists of an inner lining of stratified squamous epithelium, an intermediate layer of smooth muscle and an outer adventitial layer.

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The lining of the vagina is folded into numerous rugae which are related to its extreme distensibility. The vaginal entrance is closed by the bulbocavernosus muscle, a striated muscle. Corrosion studies of the rat vagina have shown that the vaginal epithelium is intimately related to a dense capillary network in the subepithelial layer [ 10 ]. This vascular network may be related to the production of transudate during sexual arousal. Somewhat deeper, the loose submucosal layer contains a complex of numerous large veins and smooth muscle fibers that resemble cavernous tissue.

The smooth muscle layer consists of an inner circular layer and a strong external longitudinal layer. The adventitial layer consists of connective tissue and a large plexus of blood vessels. The vagina has a complex innervation that is not well understood. The pelvic nerves appear to subserve sensation from the vagina while the pudendal nerve subserves sensation from the labia and clitoris [ 11 ].

Afferent nerves in the vagina appear to contain substance P in both animal [ 1112 ] and human [ 13 ] tissue samples, although SP-containing nerves appear to be sparse in the human vagina [ 13 ]. Nerves containing nitric oxide synthase NOS have been demonstrated in animal [ 14 ] and human vaginas [ 15 ]. Female sexual arousal is a neurovascular phenomenon involving nerve-regulated vascular reactions. Neurovascular interactions during sexual arousal lead to several hemodynamic phases which affect simultaneously the clitoris, vestibular bulbs, and labia minora as well as the vagina.

In the resting phasethe vagina is a sheath containing a potential space with a minimal blood flow and very low oxygen tension in the wall [ 1718 ]. The earliest detectable of sexual arousal based on studies with experimental models is a ificant increase in vaginal wall and clitoral blood flow [ 19 ]. There is a ificant increase in clitoral cavernosal pressure as well [ 19 ].

With the onset of increased vaginal blood flow, production of vaginal transudate ensues [ 1020 ]. A ificant rise in tissue oxygen tension follows about 20 seconds later which indicates increased inflow of arterial blood. In humans, vaginal and labial oxygen tension increases from 4 to 8 times baseline during sexual stimulation [ 1718 ] and vaginal wall blood flow increases approximately threefold [ 21 - 23 ].

In humans, clitoral blood flow has been estimated to increase from 4 to 11 times baseline during sexual stimulation [ 24 ]. The increased blood flow reaches a plateau phase during which vaginal fluid transudate production continues. The final or resolution phase is characterized by the slow return of blood flow to baseline values.

In women, up to minutes is required for vaginal oxygen tension to return to baseline [ 17 ]. It is believed that the increase of clitoral intracavernosal and vaginal wall blood flow in part from a decrease in vascular resistance and relaxation of clitoral cavernosal and vaginal wall tissues.

The precise identity of the neurotransmitters that control vaginal blood flow is currently unknown. Atropine does not affect the pelvic nerve-stimulated rise in vaginal blood flow in animals [ 1925 ] or the rise in vaginal blood flow seen in human females [ 26 ].

This evidence suggests that muscarinic neurotransmission is probably not involved. The ability of sildenafil to relax clitoral tissue and enhance nerve-stimulated vaginal blood flow has been reported [ 2728 ]. This knowledge, of course, suggests the involvement of the NO-cyclic guanosine monophosphate cGMP pathway [ 2729 ]. At the same time, it has been reported that administration of VIP, either intravenously or by injection in the vaginal wall, increases vaginal blood flow and induces vaginal fluid production [ 1030 ].

Intravaginal prostaglandin E1 can also increase vaginal blood flow [ 32 ]. While some authors have stated that VIP is the primary neurotransmitter in the vaginal circulation [ 2122 ], much more research in this area is required.

A study with a rabbit model has shown Big pussy lips Massachusetts systemic administration of apomorphine had no effect on basal clitoral intracavernosal and vaginal wall blood flow while ificantly increasing blood inflow in Big pussy lips Massachusetts organs during nerve-stimulated vaginal and clitoral engorgement [ 32 ]. The precise mechanism by which apomorphine enhances nerve-stimulated but not basal clitoral intracavernosal and vaginal blood flow remains unknown. Apomorphine at concentrations of 0. This may suggest Big pussy lips Massachusetts involvement of dopaminergic receptors in regulating the hemodynamic mechanism of clitoral and vaginal engorgement.

Vaginal blood flow appears to undergo phasic shifts in conjunction with rapid eye movement REM sleep [ 33 ]. Little is known about the central control of female sexual arousal. Sexual stimulation activates specific areas of the central nervous system such as the medial preoptic region, the anterior hypothalamic region, and the related limbic hippocampal structures.

This stimulates transmission of als via the parasympathetic and sympathetic pathways. The medial amygdala appears to be an important center that utilizes vasopressin as a central neurotransmitter [ 34 ]. Oxytocin is also clearly involved; oxytocin serum levels measured before and after sexual stimulation in 12 healthy women were ificantly elevated [ 35 ]. Although intravenous apomorphine, a centrally acting dopaminergic agent, has been shown to cause increased peak clitoral and vaginal wall blood flow [ 32 ], the role of dopamine in female sexual behavior is not established.

The mechanism of genital arousal and orgasm during sexual stimulation involve spinal cord reflexes that are mediated by genital afferents originating from the pudendal nerve. Interneurons mediating these reflexes are known to be in a column in the central portion of the spinal gray matter. The efferent arm of the spinal reflexes involves sympathetic, parasympathetic, and somatic activity [ 36 ]. Studies with a rabbit model have shown that electrical stimulation of the vaginal branch of the pelvic nerve increases clitoral intracavernosal pressure and blood flow, vaginal wall pressure and blood flow, and vaginal length [ 19 ].

Afferent aling during sexual stimulation enters the spinal cord in the sacral segments, which is then transmitted to supraspinal sites via the spinothalamic and spinoreticular systems [ 36 ]. The spinothalamic pathway contains myelinated fibers that end in the posterolateral nucleus of the thalamus, from which the als are relayed to the medial thalamus. The precise reflex mechanisms of clitoral erection and vaginal engorgement are yet to be studied.

The mechanism of vaginal engorgement during sexual arousal involves vasodilation and ificant changes in vaginal tone.

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