Biomedical subjects

B Srilatha

Publications and source records attributed to B Srilatha.

7 recordsLinked to original sources

PubMed2006

Characterization of hypertriglyceridemia-induced erectile dysfunction.

OBJECTIVES: To characterize the effects of experimental hypertriglyceridemia on erectile function. METHODS: The daily water intake of 40 sexually mature male rats (groups II to V) was supplemented for 12 weeks with 10% fructose solution to induce hypertriglyceridemia. In addition, animals from three groups (III, IV, and V) were given through daily oral gavage metformin (group III), fenofibrate (group IV), and fish oil (group V) to estimate their therapeutic effects on fructose-induced metabolic alterations. Another group (I) of 10 rats served as controls. At 12 weeks, changes in sexual behavior and cavernous pressure response to nerve stimulation were correlated with serum triglyceride levels and response to preventive measures. RESULTS: After administration of 10% fructose, triglyceride levels increased fourfold to 1.79 +/- 0.31 mmol/L (mean +/- standard deviation) (group II). Coinciding with this elevation was a significant impairment of the copulatory pattern, with prolongation of mount (3.70 +/- 3.44 minutes), intromission (7.09 +/- 4.49 minutes), and ejaculatory latencies and reduced intracavernous pressure (27.56 +/- 2.04 mm Hg) response to nerve electrical stimulation. Whereas similar significant impairment was seen in group III, the other two groups (IV and V) showed beneficial effects of triglyceride reduction on these parameters. CONCLUSIONS: Our results provide the first evidence for an impact of triglycerides on erectile function. This detrimental effect is likely to be due to functional vascular and neuronal deficits related to hypertriglyceridemia.

Animals↗

PubMed2004

Estrogen and phytoestrogen predispose to erectile dysfunction: do ER-alpha and ER-beta in the cavernosum play a role?

OBJECTIVES: To investigate the functional changes in rabbit penile corpus cavernosum (CC) secondary to experimental hyperestrogenism and attempt to identify sites of immunoexpression for estrogen receptor subtypes alpha and beta (ER-alpha and ER-beta) in the CC. Although the role of testosterone in sexual function has been extensively studied in clinical settings and experimental animal models, the effect of hormonal modulation/imbalance arising from estrogenic excess has not been characterized. METHODS: Eighteen New Zealand white male rabbits (2.5-3.0 kg) were divided into control and two treatment groups. The two treatment groups were given orally 0.1 mg of estradiol valerate (estradiol group) or phytoestrogen, daidzein (phytoestrogen group) daily for 12 weeks. Blood and tissue samples were collected for hormone levels and in vitro pharmacologic studies. CC samples from untreated rabbits (n = 4) were cryosectioned and incubated with appropriate mouse monoclonal antibody for identification of ER-alpha and ER-beta. RESULTS: Through immunohistochemistry, color signals for nuclear ER-alpha and ER-beta receptors were localized within the CC. Chronic treatment with estradiol and phytoestrogen significantly reduced the systemic total testosterone levels. In organ bath experiments, relaxant responses to acetylcholine, nitroglycerin, and nitrergic transmission were significantly attenuated compared with the control response. With regard to the contractile effect, both types of estrogen treatments significantly potentiated norepinephrine-induced antierectile contraction of the CC. CONCLUSIONS: These results indicate that estradiol treatment and chronic exposure of phytoestrogen may cause receptor-mediated pathophysiologic changes in erectile function, leading to erectile dysfunction.

Acetylcholine↗

PubMed2003

Oestrogen-mediated hormonal imbalance precipitates erectile dysfunction.

Declining testosterone (T) in an aging male offsets the equilibrium between androgen and oestrogen (oestradiol, E(2)) with a resultant increase in E(2)-T ratio. Similar functional hormone imbalance is existent in clinical states of hypogonadism and is likely to arise from exposure of males to environmental oestrogens. The pathophysiological significance of this derangement on erectile function, hitherto unknown, was estimated in sexually mature male rats following acute and chronic treatment with oestrogen. A total of 60 male Sprague-Dawley rats (200-250 g) were divided into control and two treatment groups, administered 0.01 and 0.1 mg of oestradiol through oral gavage daily for 1 week (n=30, acute study) and 12 weeks (n=30, long-term study), respectively. Sexual activity in the presence of hormonally primed female rats and intracavernous pressure (ICP) response to electrical stimulation estimated treatment-induced changes, which were correlated with hormone levels and penile morphology at 12 weeks. Following two to five-fold elevation in serum E(2) levels (and simultaneous reduction in testosterone), there was a significant prolongation of mount, intromission, ejaculation latencies and some decrease in frequencies. The ICP response to nerve stimulation was also impaired in all the treated groups. Histologically, trichrome staining highlighted the cavernosal connective tissue hyperplasia in the long-term study groups. Results of this investigation indicate that oestradiol causes pathophysiological changes in erectile function. These observations provide an indirect evidence for the possible sexual health hazards in man upon inadvertent exposure to environmental oestrogens, ageing and derangement of E(2)-T ratio.

Administration, Oral↗

PubMed2003

Oestrogen-androgen crosstalk in the pathophysiology of erectile dysfunction.

Ageing in man is associated with a decline in testosterone following changes in the hypothalamo-pituitary-testicular axis. This may offset the physiologic equilibrium between oestrogen and androgen and at some point when the ratio of free testosterone to oestradiol reaches a critical level, the oestrogenic gonadotropin suppressive effect predominates with decreased release of FSH and LH. Adding to this endocrinal complexity is the continued peripheral conversion to oestradiol through aromatisation. Although the androgen deficiency is not the sole cause for impotence in the elderly, there is a gradual decrease in nocturnal penile tumescence (NPT) and spontaneous morning erections with ageing. Despite the age related increase in oestrogen levels, the information on the pathophysiological role of the "female hormone" in erectile dysfunction has been scanty. Together with our identification of oestrogen receptors within the penile cavernosum, we have delineated dysfunctional changes on male erection mediated by oestradiol. These findings parallel the recent concerns over environmental oestrogens on fertility declines in young men. Oestrogenic activity is also present in plants and thereby in human diet. These phytoestrogens are structurally and functionally similar to oestradiol and more potent than the environmental oestrogenic chemicals such as organochlorine and phenolic compounds. Thus in the light of growing concerns of possible compromising effects on sexuality by endogenous and environmental oestrogens, we are faced with the scientific need to delineate their role on the mechanism of male erectile pathway in health and disease for clinical correlates and prognostics.

Aged↗

PubMed1999

Sexual dysfunction related to antihypertensive agents: results from the animal model.

The present investigation elucidates the deleterious effects of three prototypical antihypertensive drugs namely, propranolol, clonidine and captopril on the erectile physiology. In order to delineate the direct drug effects from vascular insufficiency inherent in hypertensive states, the study was conducted on a normotensive animal model. The adverse effects of these drugs were estimated as changes in sexual behaviour and intracavernous pressure response of electrical stimulation in the treated rats compared to normal age-matched controls (n = 10, each group). Copulation studies indicated significant impairment of sexual function in the groups on propranolol and clonidine. The cavernous pressure response to nerve stimulation at the end of sixteen weeks further reinforced the gross compromise on sexual function in these two treated groups. In contrast, the captopril administration produced only marginal alterations to the responses recorded. The results from this study clearly indicate that propranolol and clonidine interfere with sexual behaviour and nerve mediated response to erection whereas captopril which is devoid of significant effects on these parameters, may be a better therapeutic option.

Animals↗

PubMed1999

Elevated low-density lipoprotein cholesterol (LDL-C) enhances pro-erectile neurotransmission in the corpus cavernosum.

Hypercholesterolaemia is thought to foster atherosclerosis and impotence through its effects on vascular endothelium. In this study, we investigated the pharmacological changes in rabbit corpus cavernosum (CC) secondary to incubation with lysolecithin and hypercholesterolaemia. A daily egg yolk dietary supplement induced gross hypercholesterolaemia in our rabbits. Group A of test animals (n-12) was fed with the yolk content of single egg and group B (n-6), that from two eggs for eight weeks. Serum level estimation revealed a progressive elevation of cholesterol to 15 and 30 times respectively, in the two treated groups as compared to values in the control group (n-6). Early histological manifestations of atherosclerosis were perceived as fat cell lesions in the cavernosum of treated animals. In vitro pharmacological studies on CC strips from both groups of test animals demonstrated a profound accentuation of the contractile responses to noradrenaline and histamine and attenuation of relaxant response to acetylcholine. However, in contrast to single-egg treated group, which demonstrated a reduction in the relaxant response to electrical field stimulation (EFS), there was a marked and statistically significant potentiation of this nitrergic transmission, in the two-eggs group. Prior incubation of CC strips of normolipidaemic rabbits (n-7) with lysolecithin, reproduced similar exaggerated response to EFS. Therefore, from the results of our study, it is concluded that oxidised LDL or its major amphiphile lysolecithin, at some critical level or beyond, may be capable of reverting at least some of the adverse effects of hypercholesterolaemia on erectile function, through its mediating effect on nitrergic transmission.

Acetylcholine↗

PubMed1997

Effects of feeding egg yolk on the serum lipid levels in rabbits.

Healthy, nonobese, young rabbits developed hypercholesterolemia following daily intake of fresh egg yolk for 8 weeks. On a quantitative basis, this diet had a profound effect on serum cholesterol level which rose to 15 or 30 times the baseline value depending on whether the test group consumed the yolk content of one or two eggs during the study. Similar drastic changes observed in low density lipoprotein cholesterol levels in these test animals make this a useful method for defining the early pathological changes of atherosclerosis in man. In addition, the present study provides direct evidence of the deleterious effect of hen's egg yolk on the serum cholesterol level in an appropriate and easily reproducible animal model.

Animals↗