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Biomedical subjects

Peter Kenemans

Publications and source records attributed to Peter Kenemans.

At least 37 records · Page 2Linked to original sources
PubMed2004

HMR 3339, a novel selective estrogen receptor modulator, reduces total cholesterol, low-density lipoprotein cholesterol, and homocysteine in healthy postmenopausal women.

OBJECTIVE: To investigate the short-term effects of HMR 3339 in comparison with raloxifene and placebo on cardiovascular risk factors. DESIGN: A multicenter, randomized, placebo-controlled, double-blind, dose-ranging study. SETTING: Gynecologic outpatient department. PATIENT(S): One hundred eighteen healthy nonhysterectomized postmenopausal women. INTERVENTION(S): Participants received daily placebo (n = 22), 2.5 mg of HMR 3339 (n = 25), 10 mg of HMR 3339 (n = 24), 50 mg of HMR 3339 (n = 24), or 60 mg of raloxifene (n = 23) for 12 weeks followed by a 2-week washout period. MAIN OUTCOME MEASURE(S): Blood concentrations of lipids measured at baseline, and after 2, 4, 8, 12, and 14 weeks, and of lipoprotein(a), homocysteine, and endothelin-1 measured at baseline, and after 4 and 12 weeks. RESULT(S): After 12 weeks of treatment with HMR 3339, compared with placebo, serum total cholesterol was reduced (10 mg of HMR 3339: -9.7%; 50 mg of HMR 3339: -15.2%), low-density lipoprotein (LDL)-cholesterol (10 mg of HMR 3339: -10.8%; 50 mg of HMR 3339: -24.2%) and plasma homocysteine concentrations (2.5 mg of HMR 3339: -3.9%; 10 mg of HMR 3339: -10.8%; 50 mg of HMR 3339: -13.8%), suggesting a dose-dependent effect of HMR 3339. These effects were already apparent after 2 weeks of treatment for total cholesterol and LDL-cholesterol, and after 4 weeks of treatment for homocysteine. After 12 weeks, raloxifene, compared with placebo, significantly decreased total cholesterol (-10.5%), LDL-cholesterol (-15.0%), and triglycerides (-16.9%), but not homocysteine. High-density lipoprotein-cholesterol, lipoprotein(a), and endothelin-1 showed no significant changes in any of the active treatment groups. CONCLUSION(S): HMR 3339 reduces total cholesterol, LDL-cholesterol, and homocysteine concentrations in postmenopausal women.

Anticholesteremic Agents↗
PubMed2004

Cultures of ovarian surface epithelium from women with and without a hereditary predisposition to develop female adnexal carcinoma.

AIM: Conflicting evidence exists on whether in vivo morphological characteristics can distinguish Ovarian Surface Epithelium (OSE) of ovaries obtained from women with and without a predisposition to develop female adnexal (ovarian and fallopian tube) carcinoma. This study aims to detect differences in growth potential and morphology that are maintained or specifically expressed in vitro. STUDY DESIGN: Ovarian surfaces were scraped to retrieve OSE cells from 56 women at hereditary high risk for female adnexal carcinoma, of whom 33 are BRCA1 and four are BRCA2 mutation carriers (Predisposed OSE, POSE) and from 26 women without such risk (Non Predisposed OSE, NPOSE). Number of passages and total cell yield until last passage, as well as morphology was compared between both groups. To confirm morphology, the expression of epithelial, mesothelial, and fibroblast markers was assessed. RESULTS: Both POSE and NPOSE cultures displayed similar growth potential and morphology. The expression of epithelial markers cyto-keratins 7 and 8 was similar between both groups. Only in cultures in which cells did not uniformly exhibit these markers, the percentage of cells expressing these markers was significantly lower at last passage when compared to the initial culture. In these latter cultures, cells that were morphologically indistinguishable from fibroblasts were observed. Mesothelial marker calretinin was expressed in 75% of cells of both POSE and NPOSE cultures and correlates with cyto-keratins 7 and 8 expression. CA 125 expression was equally low in POSE and NPOSE cultures (4.3%). Fibroblast markers FSM and vimentin were expressed in 100% and collagen IV was expressed in 16% of cells in all cultures. CONCLUSION: OSE cells derived from women with a hereditary predisposition to develop female adnexal cancer possess similar in vitro characteristics as OSE from women without this predisposition. On basis of our results, it seems advisable to study only 100% cyto-keratins 7 and 8 positive OSE cultures, since contamination of fibroblasts in some primary OSE cultures cannot be ruled out.

Adnexa Uteri↗
PubMed2004

Postmenopausal hormone therapy: impact on menopause-related symptoms, chronic disease and quality of life.

Quality of life in climacteric and postmenopausal women is often compromised. This overview addresses the many factors that may interfere with health and well-being in such women. Hormonal changes during the menopausal transition, finally resulting in estrogen deficiency, play a pivotal role in the incidence of climacteric symptoms and also in the development of chronic diseases. Such symptoms and diseases can contribute to impaired quality of life in climacteric and postmenopausal women. Postmenopausal hormone therapy (PHT) is the treatment of first choice to alleviate symptoms of estrogen deficiency. Besides effectively relieving climacteric symptoms and complaints, PHT can also protect against some chronic diseases, such as osteoporosis and colorectal cancer. Presently, available PHTs vary widely in type, estrogen and progestogen dosage, and route and duration of administration. Furthermore, the number of alternatives to treat climacteric symptoms, and/or to prevent chronic diseases, has increased. Therefore, doctors involved in the care of climacteric women in the 21st century are much more able to meet the specific needs of individual patients and improve health and quality of life.

Chronic Disease↗
PubMed2003

Effect of oral and transdermal estrogen replacement therapy on hemostatic variables associated with venous thrombosis: a randomized, placebo-controlled study in postmenopausal women.

OBJECTIVE: The purpose of this study was to investigate whether the effect of transdermal estrogen therapy in postmenopausal women differs from that of oral therapy with regard to resistance to activated protein C (APC), an important risk factor for venous thrombosis, and levels of related proteins, such as protein S, protein C, and prothrombin. METHODS AND RESULTS: In a randomized, double-blind, placebo-controlled study, 152 healthy hysterectomized postmenopausal women received daily either placebo (n=49), transdermal 17beta-estradiol (E2) 50 microg (tE2 group, n=33), oral E2 1 mg (oE2 group, n=37), or oral E2 1 mg combined with gestodene 25 microg (oE2+G group, n=33) for 13 28-day treatment cycles, followed by 4 cycles of placebo for each group. Plasma samples were collected at baseline and in cycles 4, 13, and 17. In cycle 13, significant increases versus baseline and placebo were found in normalized APC sensitivity ratios (nAPCsr) in all treated groups (tE2, +26.9%; oE2, +102.7%; oE2+G, +69.9%). Increases in nAPCsr were significantly higher in the oral treatment groups than in the tE2 group. In addition, compared with baseline and placebo, after 13 cycles, decreases were observed in total protein S (tE2, -4.1%; oE2, -7.9%; oE2+G, -5.8%), free protein S (tE2, -7.1%; oE2, -8.4%; oE2+G, -5.2%), and protein C in the oE2+G group (-6.4%), but these changes did not explain the increase in nAPCsr. Changes in prothrombin were small and also did not affect the nAPCsr. CONCLUSIONS: Increases were observed in resistance to APC, which were more pronounced in the oral treatment groups than in the transdermal group. The increase in resistance to APC was not explained by changes in protein S, protein C, or prothrombin and may contribute to the increased incidence of venous thrombosis in users of hormone replacement therapy.

Activated Protein C Resistance↗
PubMed2003

Effects of oral and transdermal low-dose estrogen therapy on echocardiographic parameters of cardiac function.

OBJECTIVE: To investigate the effects of transdermal 17 beta-estradiol (E(2)) compared with oral unopposed as well as opposed E(2) on echocardiographic parameters of left ventricular (LV) systolic and diastolic function. DESIGN: A prospective, randomized, double-blind, placebo-controlled, multi-center study. SETTING: Gynecologic and cardiologic outpatient departments. PATIENT(S): One hundred fifty-two healthy hysterectomized postmenopausal women. INTERVENTION(S): Participants received daily placebo (n = 49) or transdermal E(2) (50 microg; tE(2) group, n = 33), or oral E(2) (1 mg; oE(2) group, n = 37), or oral E(2) (1 mg) combined with gestodene (25 microg; oE(2)+G group, n = 33) for thirteen 28-day treatment cycles. MAIN OUTCOME MEASURE(S): M-mode, quantitative two-dimensional, and Doppler echocardiographic measurements were performed at baseline and after 1 year. RESULT(S): Compared with placebo, tE(2) and oE(2) showed no statistically significant changes in LV function. oE(2)+G resulted in a statistically significant favorable increase in peak flow velocity, flow velocity integral, and mean acceleration. Furthermore, a favorable decrease was observed in interventricular septum thickness and ejection time. CONCLUSION(S): After 1 year of unopposed E(2), LV function remained unchanged. The oE(2)+G treatment showed a potential beneficial influence on LV systolic function.

Administration, Cutaneous↗
PubMed2003

Laparoscopic detection of sentinel lymph nodes followed by lymph node dissection in patients with early stage cervical cancer.

OBJECTIVE: The purpose of this study was to investigate the feasibility of sentinel node detection through laparoscopy in patients with early cervical cancer. Furthermore, the results of laparoscopic pelvic lymph node dissection were studied, validated by subsequent laparotomy. METHODS: Twenty-five patients with early stage cervical cancer who planned to undergo a radical hysterectomy and pelvic lymph node dissection received an intracervical injection of technetium-99m colloidal albumin as well as blue dye. With a laparoscopic gamma probe and with visual detection of blue nodes, the sentinel nodes were identified and separately removed via laparoscopy. If frozen sections of the sentinel nodes were negative, a laparoscopic pelvic lymph node dissection, followed by radical hysterectomy via laparotomy, was performed. If the sentinel nodes showed malignant cells on frozen section, only a laparoscopic lymph node dissection was performed. RESULTS: One or more sentinel nodes could be detected via laparoscopy in 25/25 patients (100%). A sentinel node was found bilaterally in 22/25 patients (88%). Histological positive nodes were detected in 10/25 patients (40%). One patient (11%) had two false negative sentinel nodes in the obturator fossa, whereas a positive lymph node was found in the parametrium removed together with the primary tumor. In seven patients (28%), the planned laparotomy and radical hysterectomy were abandoned because of a positive sentinel node. Bulky lymph nodes were removed through laparotomy in one patient, and in six patients only laparoscopic lymph node dissection and transposition of the ovaries were performed. These patients were treated with chemoradiation. In two patients, a micrometastasis in the sentinel node was demonstrated after surgery. Ninety-two percent of all lymph nodes was retrieved via laparoscopy, confirmed by laparotomy. Detection and removal of the sentinel nodes took 55 +/- 17 min. Together with the complete pelvic lymph node dissection, the procedure lasted 200 +/- 53 min. CONCLUSION: Laparoscopic removal of sentinel nodes in cervical cancer is a feasible technique. If radical hysterectomy is aborted in the case of positive lymph nodes, sentinel node detection via laparoscopy, followed by laparoscopic lymph node dissection, prevents potentially harmful and unnecessary surgery.

Adult↗
PubMed2003

Histopathological characteristics of BRCA1- and BRCA2-associated intraperitoneal cancer: a clinic-based study.

The aim of the research was to assess possible histopathological differences between BRCA1- and BRCA2-associated malignant intraperitoneal (ovarian/fallopian tube/peritoneal) tumors and their sporadic counterparts. Dutch families harboring pathogenic BRCA1 or BRCA2 mutations were selected. Included were patients who had had malignant primary ovarian, fallopian tube or peritoneal tumors. Histopathological data was compared with data obtained from the Dutch cancer registry between 1989 and 1993 (reference group). A total of 63 with primary intraperitoneal malignant tumors were identified in 41 families. Non-epithelial malignant tumors were not observed in the study group versus 6% (n = 404) in the reference group (n = 6789, P = 0.04). These tumors were excluded from further analysis, as were ovarian adenocarcinomas not otherwise specified, since these were detected in 22% of the study group, and in 19% of the reference group (P = 0.76). Serous carcinomas were detected in 94% (47/50) of the women in the study group in contrast to 62% (3145/5088) of the reference group (P < 0.01). In the study group, mucinous and endometrioid ovarian adenocarcinomas and serous ovarian borderline tumors each comprised 2.0% of the tumors. Clear cell ovarian carcinomas were not detected. In contrast, these percentages were 16% (P < 0.01), 10% (P = 0.07), 7% (P = 0.16) and 5% (P = 0.12), respectively, in the reference group. In the study group, 6.0% of the carcinomas arose in the fallopian tube versus 1.9% in the reference group (P = 0.03). Four percent of the study group developed primary serous peritoneal carcinomas, versus six percent in the reference group (P = 0.57). Serous carcinoma is the predominant type of intraperitoneal malignancy occurring in women harboring BRCA1 or BRCA2 mutations. Non-epithelial cancer does not seem to be part of the tumor spectrum of BRCA mutation carriers. This suggests, therefore, that serous tumors may be the only subtype related to a BRCA1 or BRCA2 mutation. Furthermore, fallopian tube carcinoma occurred more often in BRCA mutation carriers than in the reference population.

Adult↗
PubMed2003

Effects of low-dose oral and transdermal estrogen replacement therapy on hemostatic factors in healthy postmenopausal women: a randomized placebo-controlled study.

OBJECTIVE: This study was undertaken to investigate the effect of transdermal and oral estrogen replacement therapy in healthy postmenopausal women on markers of coagulation and fibrinolysis associated with coronary artery disease. STUDY DESIGN: In a randomized, placebo-controlled, double-blind study, healthy hysterectomized postmenopausal women received daily either placebo (n=49), transdermal 17beta-estradiol (E(2)) 50 microg (tE(2) group, n=33), oral E(2) 1 mg (oE(2) group, n=37), or oral E(2) 1 mg combined with gestodene 25 microg (oE(2)+G group, n=33) for thirteen 28-day treatment cycles. Hemostatic variables were measured in blood samples collected at baseline and in cycles 4 and 13. RESULTS: No significant changes versus baseline and placebo were found in the tE(2) group, except for plasminogen activator inhibitor type-1 (PAI-1) in cycle 13 (-32.4%, P=.01). In the oE(2) group, significant percentage changes from baseline versus placebo in cycle 13 were found in fibrinogen, -5.4% (P<.05); factor VII, -7.3% (P<.05); thrombin-antithrombin III complexes, -13.3% (P<.05); tissue-type plasminogen activator (t-PA), -17.3% (P<.001); and PAI-1, -54.3% (P<.001). In the oE(2)+G group, respective changes were factor VII, -17.6% (P<.001); t-PA, -14.5% (P=.01); PAI-1, -36.4% (P<.01); and D-dimer, +21.8% (P<.05). No significant changes were observed in prothrombin fragment 1+2 and plasmin-alpha(2)-antiplasmin complexes. CONCLUSION: Low-dose oral estradiol therapy was associated with an increase in fibrinolysis and small decreases in procoagulant variables. Transdermal therapy had minor effects.

Administration, Cutaneous↗
PubMed2003

Effect of hormone replacement therapy on plasma levels of the cardiovascular risk factor asymmetric dimethylarginine: a randomized, placebo-controlled 12-week study in healthy early postmenopausal women.

In a prospective, randomized, placebo-controlled 12-wk study, we investigated the effect of oral hormone replacement therapy on asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase (NOS), and an independent risk factor for coronary heart disease. The effects on arginine and symmetric dimethylarginine were also investigated. Sixty healthy early postmenopausal women received daily placebo (n = 16) or oral 17beta-estradiol 2 mg, either unopposed (E(2); n = 16) or sequentially combined with dydrogesterone 10 mg (E(2)+D; n = 14) or trimegestone 0.5 mg (E(2)+T; n = 14). ADMA levels reduced in all active treatment groups. Compared with baseline and placebo, the largest reduction in ADMA levels was observed in the E(2)+T group [-18.7% (95% confidence interval [CI], -25.4 to -11.9%) and -21.1% (95% CI, -26.2 to -16.1%), at 4 and 12 wk, respectively]. At 4 and 12 wk in the E(2)+T group, arginine levels were significantly reduced as well [-30.9% (95% CI, -41.1 to -20.7%) and -36.3% (95% CI, -43.1 to -29.5%), respectively], whereas symmetric dimethylarginine levels were significantly lower in the E(2)+D group after 12 wk [-11.6% (95% CI, -19.9 to -3.3%)]. In conclusion, unopposed oral estradiol and estradiol combined with dydrogesterone or trimegestone reduced plasma levels of the NOS inhibitor ADMA. Whether the reduction of the NOS substrate arginine in the E(2)+T group counteracts the potentially beneficial effect of ADMA reduction or reflects increased NO production remains to be investigated.

Arginine↗
PubMed2003

Clinical and technical evaluation of the ACS:OV serum assay and comparison with three other CA125-detecting assays.

BACKGROUND: In this study the clinical and technical performance of the CA125- detecting Bayer ACS:OV immunoluminometric serum assay was compared with three other well-established CA125-detecting assays. METHODS: A total of 1112 serum samples was included in this evaluation: 462 from apparently healthy women, 153 from patients with benign ovarian disease, 163 from patients with malignant ovarian disease, 10 from patients with borderline ovarian malignancies and 78 samples from 12 ovarian cancer patients during monitoring of disease. Serum samples from women with malignant endometrial (n = 68) and colon (n = 32) diseases were also included. Moreover, serum samples from women with benign uterine disease and endometriosis (n = 136) plus 10 serum samples from men (n = 7) and women (n = 3) with human anti-mouse antibodies (HAMA) after immunoscintigraphy were included. All samples were tested in duplicate with the Bayer ACS:OV, the Centocor CA125 II, the Abbott IMx CA125 and the Roche (formerly Boehringer Mannheim) Enzymun-Test CA125 II assays. RESULTS: The clinical performance of the Bayer ACS:OV assay, assessed in various patient groups, was similar to that of the two other automated assays. In serum from patients with benign diseases the highest values were found in patients with benign ovarian tumours. In the ovarian cancer patients followed during the course of disease we found similar marker patterns with all four assays. In contrast to the Roche Enzymun-CA125 II assay and to a lesser extent the Centocor CA125 II assay, the Bayer ACS:OV assay was less sensitive to interference from HAMA. CONCLUSION: The Bayer ACS:OV assay is a precise and reliable test for the quantification of CA125 in serum.

Biomarkers, Tumor↗
PubMed2002

Cellular and humoral responses after multiple injections of unconjugated chimeric monoclonal antibody MOv18 in ovarian cancer patients: a pilot study.

PURPOSE: Chimeric antibody MOv18 (c-MOv18) mediates antibody-dependent cellular cytotoxicity (ADCC) in vitro. To study the toxicity of c-MOv18 and its immunological effects, five ovarian cancer patients received intravenous injections for 4 weeks. METHODS: ADCC activity of c-MOv18 was tested in a (51)Cr-release assay using IGROV1 and KB cells. Patients' peripheral blood mononuclear cells (PBMC) were phenotyped for CD3, CD4, CD8, and CD25 by FACS analysis and tested for T-cell proliferation in vitro in the presence of c-MOv18 with and without IL-2. RESULTS: Toxicity was mild and transient. No human anti-chimeric antibodies were found. Increased ADCC levels corresponding with a slight increase in CD4+ and CD8+ fractions were observed after the first injection, while the CD4/CD8 ratio and the levels of CD25 remained unchanged. c-MOv18 did not have a mitogenic effect on patients' PBMC and adding IL-2 did not change the degree of proliferation. In three patients stable disease was achieved for up to 4 months, 9 months and 14 months, respectively. CONCLUSION: Immunotherapy aiming at the patient's immunological capacity has minor effects in ovarian cancer patients that have been heavily pretreated with chemotherapy. Such strategies should be evaluated in patients who are more immunocompetent, i.e., before excessive chemotherapy and after achieving microscopic or small volume disease.

Aged↗
PubMed2002

Our history.

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Europe↗
PubMed2002

Our history.

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Female↗
PubMed2002

A 2-year, randomized, comparative, placebo-controlled study on the effects of raloxifene on lipoprotein(a) and homocysteine.

OBJECTIVES: Lipoprotein(a) (Lp(a)) and homocysteine (Hcy) are independent cardiovascular risk factors, which have been shown to be lowered by hormone replacement therapy (HRT). In this 2-year study, the long-term effects of raloxifene (Rlx) in two doses, on Lp(a) and Hcy, were studied and compared with the effects of continuously combined hormone replacement therapy (ccHRT). METHODS: In a prospective, randomized, double-blind, placebo-controlled 2-year study, 95 healthy, non-hysterectomized, early postmenopausal women, received daily either oral Rlx 60 mg (N=24) or 150 mg (N=23), ccHRT (conjugated equine estrogens 0.625 mg plus medroxyprogesterone acetate 2.5 mg; N=24) or placebo (N=24). Fasting serum Lp(a) and plasma Hcy concentrations were measured at baseline and at 6, 12 and 24 months. RESULTS: The mean individual changes compared to baseline after 24 months were for Lp(a): Rlx 60: - 5%, Rlx 150: -7%, ccHRT: -34%, placebo: +1% and for Hcy: Rlx 60: -3%, Rlx 150: -4%, ccHRT: -4%, placebo: +6%. ANCOVA was significant for Lp(a) under ccHRT versus placebo (P=0.001) and for Lp(a) under ccHRT versus each of the two Rlx groups (P<0.05). CONCLUSIONS: Long-term treatment with Rlx was not as effective as ccHRT in lowering Lp(a). Although not significant and without an obvious dose-related response, the Hcy values showed the same trend for each treatment arm, which is in line with data reported earlier.

Cardiovascular Diseases↗
PubMed2002

Increased resistance to activated protein C after short-term oral hormone replacement therapy in healthy post-menopausal women.

As hormone replacement therapy is associated with an early excess risk of venous thrombosis, we investigated the effect of different oral hormone replacement therapies on resistance to activated protein C, and on levels of factor VIII antigen (FVIII:Ag) and factor XI antigen (FXI:Ag). In a prospective, randomized, placebo-controlled 12-week study, 60 healthy post-menopausal women daily received either placebo (n = 16) or 2 mg of micronized 17beta-oestradiol, either alone (E2, n = 16) or sequentially combined with dydrogesterone 10 mg (E2 + D, n = 14) or trimegestone 0.5 mg (E2 + T, n = 14). Medication was given orally. Normalized activated protein C sensitivity ratios (nAPCsr) were determined by quantifying the effect of activated protein C on the endogenous thrombin potential. FVIII:Ag and FXI:Ag were determined by enzyme-linked immunosorbent assay. Compared with baseline and placebo, the nAPCsr increased (92% to 142%; all P < 0.001) in all active treatment groups after both 4 and 12 weeks. Compared with placebo, hormone replacement therapy was not associated with significant changes in FVIII:Ag. After 4 and 12 weeks, FXI:Ag levels were significantly decreased in the E2 group (mean percentage changes from baseline versus placebo: -15.0%, P = 0.001 at 4 weeks and -16.6%, P = 0.003 at 12 weeks) and in the E2 + D group (-10.4%, P = 0.02 and -10.4%, P = 0.02). In conclusion, all hormone replacement regimens were associated with a large increase in resistance to activated protein C. In contrast, hormone replacement therapy had no effect on FVIII:Ag. Oral E2 and E2 + D had a small, favourable effect on FXI:Ag.

Activated Protein C Resistance↗
PubMed2002

Neither long-term treatment with raloxifene nor hormone replacement therapy modulate cardiac function in healthy postmenopausal women: two randomized, placebo-controlled, 2-year studies.

OBJECTIVE: Our purpose was to investigate the long-term effects of raloxifene, compared with opposed and unopposed estrogen replacement therapy, on echocardiographic parameters of left ventricular systolic function in healthy postmenopausal women. A total of 157 women were studied in 2 randomized, double-blind, placebo-controlled, 2-year studies. STUDY DESIGN: In study I, 60 postmenopausal women who had undergone hysterectomy received daily raloxifene, 60 mg (n = 15); raloxifene, 150 mg (n = 15); conjugated equine estrogens (CEE), 0.625 mg (n = 15); or placebo (n = 15). In study II, 97 postmenopausal women who had not undergone hysterectomy received daily raloxifene, 60 mg (n = 24); raloxifene, 150 mg (n = 24); CEE, 0.625 mg, plus medroxyprogesterone acetate (MPA), 2.5 mg (n = 24); or placebo (n = 25). M-mode, quantitative 2-dimensional and Doppler echocardiographic measurements were performed at baseline and after 1 and 2 years. RESULTS: Neither after 1 year nor after 2 years of treatment were echocardiographic parameters found to differ from baseline in both raloxifene groups, as well as in the unopposed CEE and the CEE/MPA groups, compared with the placebo group. CONCLUSION: Within 2 years of raloxifene treatment, no effect on echocardiographic parameters of left ventricular systolic function was found. Unopposed CEE or CEE/MPA also showed no effect.

Double-Blind Method↗
PubMed2002

17 beta-Estradiol induces a rapid, endothelium-dependent, sex-specific vasodilatation in spontaneous constricted rat arterioles.

OBJECTIVE: Our purpose was to resolve the apparent contradiction between the endothelium-dependent and endothelium-independent vasodilator effects of 17 beta-estradiol reported in different studies. STUDY DESIGN: The inner diameters of isolated pressurized spontaneously constricted muscle arterioles (diameter = 63 microm) from Wistar rats (n = 21) were measured during exposure to 17 beta-estradiol, and the role of the endothelium and the influence of sex were assessed. RESULTS: A dose-dependent dilatation was observed during exposure to 17 beta-estradiol concentrations from 10(-10) to 10(-4) mol/L. Arterioles of female rats displayed significantly more dilatation than vessels from male rats. The dilatation was significantly less in endothelium-denuded arterioles or after pretreatment with and in the presence of a nitric oxide synthase inhibitor. CONCLUSIONS: These results provide strong evidence that, in addition to an endothelium-independent effect, 17 beta-estradiol has a dose-dependent, endothelium-mediated, rapid vasodilatory effect on muscle arterioles from the rat, which is stronger in female rats than in male rats.

Animals↗