Clinical evaluation of female sexual function: effects of age and estrogen status on subjective and physiologic sexual responses.

INTRODUCTION: 30-50% of American women complain of sexual dysfunction. Aging, menopause, and a decline in circulating estrogen levels significantly increase the incidence of sexual complaints. Evaluation of physiologic components of the female sexual response has, in the past, been technically challenging and difficult to standardize. We describe methodology for evaluating physiologic and subjective components of the female sexual response in the clinical setting and determine the effects of age and estrogen status on them. METHODS: 48 women with complaints of sexual dysfunction were evaluated. Physiologic measurements include genital blood peak systolic velocity, vaginal pH, intravaginal pressure-volume changes (compliance), and genital vibratory perception thresholds. Measurements were recorded at baseline and following sexual stimulation. Baseline subjective sexual function was assessed using a Female Sexual Function Inventory. Age was then correlated with both physiologic and subjective sexual responses. RESULTS: Sexual stimulation resulted in increased mean genital blood peak systolic velocity, vaginal pressure-volume, and vaginal pH measurements (P < 0.05) in all women. Older women (ages 55-71 y) and menopausal women not on hormone replacement therapy had significantly lower physiologic response sexual complaints. Baseline subjective sexual function complaints included low arousal (67%), low desire (21%), difficulty achieving orgasm (92%), and pain or discomfort during and/or following intercourse (67%). CONCLUSIONS: Clinical evaluation of physiologic and subjective components of the female sexual response are possible using this comprehensive approach. Physiologic measurements were reproducible and easy to perform, and incidence and types of sexual complaints were assessed with the sexual function questionnaire. A comprehensive approach is necessary when evaluating female sexual dysfunction due to the significant emotional and relational factors that can contribute to the problem. This combined subjective/physiologic assessment may also prove useful when evaluating efficacy of pharmacotherapy in the future.

Role of protein kinase C and 72 kDa heat shock protein in ischemic tolerance following heat stress in the rat heart.

Heat stress (HS) and the subsequent expression of 72 kDa heat shock protein (HSP 72) has been shown to enhance post-ischemic functional recovery and reduce infarct size. Because the synthesis of heat shock proteins involves activation of heat shock transcription factors through phosphorylation, we hypothesized that inhibition of protein kinase C (PKC) would block HS mediated protection and expression of HSP 72 in the heart. Five groups of rats were studied (1) Sham anesthetized, (2) HS group--animals were heat shocked by raising the whole body core temperature to 42 degrees C for 15 min, (3) Vehicle group--HS rats treated with 50% DMSO in saline, (4) PKC inhibitor-treated group--specific PKC antagonist, chelerythrine chloride (5 mg/kg, i.p) given 30 min prior to HS and (5) Vehicle treated control--non-HS rats treated with vehicle prior to ischemia/reperfusion. Hearts were subjected to 30 min of regional ischemia and 90 min of reperfusion 24 h after HS. Risk area was delineated by injection of 10% Evan's blue and infarct size determined using computer morphometry of tetrazolium stained sections. Infarct size (% area at risk) reduced significantly from 49.4 +/- 2.3% (n = 7) in sham to 10.0 +/- 2.5% (p < 0.01) and 9.1 +/- 3.0% in HS and vehicle treated HS groups respectively (p < 0.05) Treatment with chelerythrine prior to HS increased infarct size to 49.4 +/- 2.3% (p < 0.05). Infarct size in chelerythrine-treated non-HS ischemic/reperfused heart was 40.7 +/- 5.4%, which did not differ significantly from vehicle-treated sham group. Western blot analysis demonstrated marked increase in HSP 72 in HS groups (with or without vehicle treatment) and pretreatment with chelerythrine chloride failed to inhibit the expression of HSP 72. The results suggest that HS-induced ischemic tolerance is mediated via PKC pathway and this protection does not appear to be directly related to the expression of HSP 72 in rat heart.

Transmission of Chlamydia trachomatis and Neisseria gonorrhoeae among men with urethritis and their female sex partners.

Transmission of Chlamydia trachomatis and Neisseria gonorrhoeae among infected men and their female sex partners was examined using a design enhancing the likelihood that spread was directed from men to women. Chlamydia culture-negative specimens were examined using DNA amplification tests. Infection rates in women exposed to male sex partners with Chlamydia only were 65% (20/31) and with gonorrhea only were 73% (33/45). Infection of women by either agent was not influenced by the number of sexual exposures to or coinfection in men. There was a 98% (40/41) concordance of N. gonorrhoeae isolates among partners by auxotype and serovar. Chlamydia isolates were serotyped using ELISA and immunofluorescence testing and confirmed by nested polymerase chain reaction: 50% (6/12) of men and 57% (8/14) of women yielded mixed serovars. Sixty-four percent of pairs (9/14) were infected with identical serovars and an additional 28% shared at least one serovar. Multiple serovars of C. trachomatis, but not of N. gonorrhoeae, were common in sex partners and exchanged frequently.

Underdiagnosis of Chlamydia trachomatis infection. Diagnostic limitations in patients with low-level infection.

To determine limitations in commonly used methods for detection of Chlamydia trachomatis, 601 genitourinary specimens from patients in a sexually transmitted disease clinic were examined with quantitative cultures and by 2 different direct antigen tests, immunofluorescence (Micro Trak; Syva Company, Palo Alto, CA) and enzyme immunoassay (Chlamydiazyme; Abbott Laboratories, North Chicago, IL). Genital specimens were held no longer than 5 hours (at 4 degrees C) prior to inoculation for culture; 28% (168/601) were positive. To evaluate the effect of storage on culture efficacy, duplicate specimens were also stored at -70 degrees C and brought out subsequently for culture a second time. Only 32% (8/25) of specimens cultured within 5 hours and having less than 10 inclusions were positive on reculture, compared with 98% (49/50) positive for specimens with greater than or equal to 10 inclusions initially (P less than 0.001). Sensitivities of the two antigen tests were similar and taken together diminished significantly (P less than 0.001) as the number of organisms (inclusion forming units) in corresponding cultures decreased: 82% (51/62) sensitivity in cultures with greater than 100 inclusions; 50% (22/44) with 10-100 inclusions; and only 11% (6/53) with less than 10. Lack of urethral discharge in men with C. trachomatis infection (free of Neisseria gonorrhoeae) was associated with low numbers of inclusions (less than 10) and antigen tests failed in 68% (15/22) of these patients.