Home | Archive | AJA @ Nature | Online Submission | News & Events | Subscribe | APFA | Society | Links | Contact Us | 中文版 |
 |
Effect of aging on penile ultrastructure
Zhou-Jun SHEN, Xiao-Dong JIN, Zhao-Dian CHEN, Yuan-He SHI
Department of Urology, First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China
Asian J Androl 2001 Dec; 3: 281-284
Keywords:
erectile
dysfunction; penis; aging; scanning electron microscopy
Abstract
Aim:
1
Introduction
The
increasing incidence of impotence with age was acknowledged by NIH Consensus Conference
in 1992[1]. The Massachusetts Male Aging Study has recently
provided a comprehensive
epidemiological report on erectile dysfunction (ED), demonstrating the
determinant role of age on the pathophysiological mechanism of erection.
Men between the ages of 40 and 70 years were asked to categorize their
erectile function
as either totally, moderately, or minimally impotent or potent. Overall,
52% of the people reported certain degrees of ED. Between 40 and 70 years
of age, the probability of complete impotence tripled from 5.1% to 15%.
The probability of moderate impotence doubled from 17% to 34%, whereas
the probability of minimal impotence remained at 17%. By the age of 70
years, only 32% portrayed themselves as being free from ED[2].
Penile erection is a complex neurovascular phenomenon. It involves the coordination of three hemodynamic events: increased arterial inflow, sinusoidal smooth muscle relaxation and decreased venous outflow. It also implies the interaction of the brain, nerves, neurotransmitters, smooth muscles and striated muscles. An alteration in any of these components may affect the response of the erectile tissue and cause ED. The effect of the normal aging process on erectile function is unknown and the cause of age-related dysfunction is likely to be multifactorial in origin[3]. Alterations in blood vessels, hormonal changes, neurologic dysfunction, medication and associated systemic diseases are the main causes[4]. Recently, Iacono et al[5] found that alterations in the microarchitecture of the tunica albuginea, including a decrease in the elastic fibers, may contribute to impotence in men. The present study was designed to observe the penile ultrastructure of rats with different ages in order to help clarifying the age related changes.
2 Materials and methods
2.1
Animals
Seventeen male Sprague-Dawley rats were purchased from the Animal Experimental Center of Zhejiang Medical Research Institute and were divided into three groups based on the age. Group A consisted of six young rats of 9 weeks old (body weight 17545 g); group B, five middle aged rats of 14 weeks old (35445 g); group C, six elderly rats of 62 weeks old (42334 g). The rats were sacrificed by intraperitoneal injection of ketamine and phenobarbital sodium. Samples were obtained from similar sites of the penis from all the animals.
2.2 Scanning Electron Microscopy
Samples for electron microscopy were processed with routine techniques. The tissues were washed with physiological saline solution, fixed in 2.5% glutaraldehyde (pH 7.2-7.4) and washed three times in 0.1 mol/L phosphate buffer saline (PBS). The samples were post-fixed in 1% osmium tetroxide for two hours, dehydrated in graded ethanol solutions and dried by the critical point drying method. Finally, the samples were mounted on suitable carriers and coated with gold. Samples were examined under a scanning electron microscopy (Leica-Stereoscan 260, UK).
2.3 Data processing
Data were expressed in meanSD. Statistical analysis was performed with analysis of variance. Significance of difference was set at P<0.05.
3
Results
3.1 Ultrastructure of tunica albuginea
The tunica albuginea covering the corpora cavernosa was the thickest in Group B and the thinnest in Group C. The thickness of tunica albuginea was significantly thinner in group C than in Groups A and B (P<0.05, Table 1). The elastic fibers of the tunica albuginea in Groups A and B were very rich and arranged regularly and undulated, while in Group C, the elastic fibers were much less and arranged irregularly and the undulated structure was not seen (Figures 1, 2 and 3).
Table 1. The thickness of tunica albuginea (meanSD).
Figure
1. The tunica albuginea of group A, the thickness of which was 0.13
mm; The elastic fibers were rich, arranging regularly and undulated.
300.
Figure 2.
The tunica albuginea of group B, the thickness of which was 0.15
mm; The elastic fibers were more plenty than those of group A, arranging
regularly and undulated. 300.
Figure 3. The
tunica albuginea of group C, the thickness of which was 0.08 mm; The elastic
fibers were less than those of group A and B, while the undulated structure
disappeared. 300.
The elastic fibers of the intracavernous pillars in Group A were rich and contained a few smooth muscle fibers. The structure of the sinusoids was normal, which occupied a large space. The smooth muscles of the intracavernous pillars in Group B were increased and the elastic fibers reduced as compared with Group A. In Group C, the intracavernous pillars were arranged irregularly in which many large collagen fibers could be observed. The smooth muscles of corpora cavernosa in Group C were less than those in Groups A and B (Figures 4, 5 and 6).
Figure 4. The corpora cavernosa of group A with rich elastic and muscle fibers in intracavernous pillars, arranging regularly and the space of sinusoids was big, in which some red cells could be observed. 300 (a), 900 (b).
Figure 5. The corpora cavernosa of group B with rich smooth muscles in intracavernous pillars. The space of sinusoids was smaller than group A . 300 (a), 900 (b).
Figure 6. The corpora cavernosa of group C. Intracavernous pillars were arranged irregularly, in which many bulky collagen fibers could be observed. Elastic and smooth muscle fibers were less than that of group A and B. The space of sinusoids was visible. 300 (a), 900 (b).
4
Discussion
To
date, the mechanisms and etiology of age-related ED has not been clealy
identified. In aging
men, a higher probability of impotence has been directly correlated with
heart disease, hypertension, diabetes, medications, index of anger and
depression. Cigarette smoking is associated with a greater probability
of complete impotence in men with heart disease and hypertension[2].
However, ED occurs frequently
in healthy older men around 70 years of age without major pathological
manifestations, in whom an incidence of 25% has been reported[6].
Chung et al[7] believed that penile hemodynamic changes
occurring in aging
accounted for the age-ralated ED. Changes in the arterial flow velocity
with aging in patients
with a normal response to pharmacological injection were evaluated by
Doppler ultrasonography. A statistically significant decreasing tendency
of peak systolic velocity
with aging was observed. The greatest decrease was seen between patients
in the third and fourth decades. The peak systolic velocity occurred much
later in patients after the fifth decades than in younger patients. These
data indicated that in pharmacological erection in aged men, the cavernous
arterial flow was decreased and the response time of the cavernous artery
or tissue was increased.
The
vascular factor for ED is more or less clearly understood and surgical
revascularization procedures for the treatment of impotence are well established.
However, the erectile capability of more than 50% of the patients underwent
these procedures was not improved, indicating that factors other than
vascular problems might
also have an important role in impotence[8]. Recently, researchers
have paid more attention
to alterations in mechanical and histological properties of the penis with
aging.
Penile
tissue is composed of smooth muscle cells resting on collagen and elastic fibers
limited by the tunica albuginea. Changes in the smooth muscle fiber, elastic
fiber or collagen fiber content may bring about mechanical alterations
of the penis by reducing its elasticity and compliance[9].
The
tunica albuginea of the penis is thought to play a major role in the erection
mechanism[10]. It
compresses the subalbugineal venules, thus decreasing the venous
outflow during erection, and provides an inextensible fibrous frame for
the erectile tissue of the penis. Our study indicated that in elderly
rats, there were structural changes in tunica albuginea, which would
in turn damage its function. Jevtich[8] reported that
there were more interstitial matrix and fewer smooth muscle cells in the
corporeal tissue of impotent individuals compared to normal men. Wespes[9]
measured the percentage of smooth muscle cells in patients of different
ages with normal erection, using computerized image analysis. Under 40
years of age, the percentage was 46%, between 41 and 60 years it was 40%,
and over 60 years it was 35%.
The authors suggested that the decrease in smooth muscle content
would have caused the decline in erection in older men. In the present
study, the reduction of smooth muscle fibers in the elderly rats may affect
the sinusoidal relaxation and arterial dilatation.
The intracavernous fibrous framework has a significant role in maintaining normal corporeal compliance and elasticity. Changes in this framework may influence the optimal function of the corporeal smooth muscle and interfere with the normal filling of the vascular spaces[10]. We found that there were more collagen fibers and less elastic fibers in the corpora cavernosa in the elderly rats than in the young rats, which could lead to the loss of compliance of the penile sinusoids. It may be another factor causing age-related ED. Although a multifold of factors contribute to ED associated with aging, the ultrastructural changes of tunica albuginea and corpora cavernosa could also play an important role.
References
[1]
NIH Consensus Conference: Impotence. NIH Consensus Development Panel on
Conference: Impotence review.
JAMA 1993; 270: 83.
[2] Feldman HA, Goldstein I, Hatzichriston DG, Krane RJ, Mckinlay JB.
Impotence and its medical and psychosocial correlates: results of the
Massachusetts male aging study. J Urol 1994; 151: 54-61.
[3] Melman A, Gingell JC. The epidemiology and pathophysiology of erectile
dysfunction. J Urol 1999; 161: 5-11.
[4] Lue TF. Physiology of penile erection and pathophysiology of erectile
dysfunction and priapism. In: Walsh PC, editor, Cambell's Urology, 7th
edition. Beijing: Science Press; 2001, p 1167.
[5] Iacono F, Barra S, Dirosa G, Boscaino A, Lotti T. Microstructural
disorders of tunica albuginea in patients affected by impotence. Eur Urol
1994: 26: 233-9.
[6] Mersdorf N, Goldsmith PC, Diederichs W, Padula CA, Lue TF, Fishman
IJ, et al. Ultrastructural changes in impotent penile tissue: a
comparison of 65 patients. J Urol 1991; 145: 749-58.
[7] Chung WS, Park YY, Know SW. The impact of aging on penile hemodynamics
in normal responders to pharmacological injection: a Doppler sonographic
study. J Urol 1997; 157: 2129-31.
[8] Jevtich MJ, Khawand NY, Vidic B. Clinical significance of ultrastructural
findings in the corpora cavernosa of normal and impotent men. J Urol 1990;
143: 289-93.
[9] Wespes E. Erectile dysfunction in the aging men. Curr Opin Urol 2000;
10: 625-8.
[10] Goldstein AM, Padma-Nathan H. The microarchitecture of the intracavernous
smooth muscle and the cavernous fibrous skeleton. J Urol 1990; 144: 1144-6.
Correspondence
to:
Prof. Zhou-Jun SHEN, First Affiliated Hospital, Zhejiang University School
of Medicine, Hangzhou 310003, China.
Tel: +86-571-8723 6833,
Fax: +86-571-8723
6628, E-mail: shenzj@mail.hz.zj.cn
Received 2001-08-07
Accepted 2001-11-02
