The Clinical Safety of Viagra

Lim, Peter Huat Chye; Moorthy, Prayaga N. Srinivas; Benton, Kenneth G.F.

doi:10.1111/j.1749-6632.2002.tb04082.x

Cited by 36 publications

(18 citation statements)

References 33 publications

(77 reference statements)

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“…Besides, the accumulated experience of prescribing Viagra across the broad continuum of men suffering from ED had been sufficient enough for considering its clinical safety and to search for other potential benefits of sildenafil citrate in other disease conditions [11].…”

Section: Discussionmentioning

confidence: 99%

Neuronal angiogenic effect of sildenafil citrate

Kamel¹,

Ali²,

Taha³

et al. 2012

Human Andrology

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BackgroundSildenafil citrate (Viagra) is the most widely prescribed drug for erectile dysfunction. The inhibition of cyclic guanosine monophosphate-specific phosphodiesterase 5 by sildenafil citrate suggests the presence of other systems with effects that might be beneficial or hazardous. Purpose We aimed to study the effect of sildenafil citrate on the vascular supply to striatal neurons of adult albino rats. Methods Thirty adult male albino rats were included in this experimental study, 20 of them were given 2 mg/kg sildenafil citrate orally on alternate days for a month and 10 rats were taken as the control group. At the end of the study, the animals were anaesthetized, decapitated, and their brains were extracted. Slices of striatal neurons were carefully dissected and fixed in 5% buffered glutaraldehyde. Semithin and ultrathin sections were obtained and examined by light and electron microscopy. ResultsThere was significantly marked dilatation and congestion of the blood vessels of rat striatal neurons in the sildenafil group in comparison with the control group. Conclusion Sildenafil citrate induced an angiogenic effect on striatal neurons of adult male rats. This suggests that sildenafil may play a role in the treatment of some neurological disorders associated with angiopathy such as multiple sclerosis and cerebrovascular stroke.

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Section: Discussionmentioning

confidence: 99%

Neuronal angiogenic effect of sildenafil citrate

Kamel¹,

Ali²,

Taha³

et al. 2012

Human Andrology

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“…Because sildenafil has proven to be relatively safe and effective in treating both erectile dysfunction and pulmonary hypertension, 45,46 it is conceivable that sildenafil may provide an additional tool to hematologists and oncologists in preventing cardiotoxicity. Moreover, sildenafil prophylaxis during doxorubicin treatment may potentially allow an increase in the dose of doxorubicin beyond the cumulative limitation of 450 to 600 mg/m 2 , 47 thereby expanding its therapeutic window.…”

Section: Fisher Et Al Sildenafil Prevents Doxorubicin Cardiomyopathymentioning

confidence: 99%

Phosphodiesterase-5 Inhibition With Sildenafil Attenuates Cardiomyocyte Apoptosis and Left Ventricular Dysfunction in a Chronic Model of Doxorubicin Cardiotoxicity

et al. 2005

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Background-Sildenafil, a phosphodiesterase-5 inhibitor, induces cardioprotection against ischemia/reperfusion injury via opening of mitochondrial K ATP channels. It is unclear whether sildenafil would provide similar protection from doxorubicin-induced cardiotoxicity. Methods and Results-Male ICR mice were randomized to 1 of 4 treatments: saline, sildenafil, doxorubicin (5 mg/kg IP), and sildenafil (0.7 mg/kg IP) plus doxorubicin (nϭ6 per group). Apoptosis was assessed with the use of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling and in situ oligo ligation methods. Desmin distribution was determined via immunofluorescence. Bcl-2 expression was analyzed by Western blot. Left ventricular function was assessed by measuring developed pressure and rate pressure product in Langendorff mode. ECG changes indicative of doxorubicin cardiotoxicity were also measured. For in vitro studies, adult ventricular cardiomyocytes were exposed to doxorubicin (1 mol/L), sildenafil (1 mol/L) with or without N G -nitro-L-arginine methyl ester (L-NAME) (100 mol/L), or 5-hydroxydecanoate (100 mol/L) 1 hour before doxorubicin and incubated for 18 hours. Doxorubicintreated mice demonstrated increased apoptosis and desmin disruption, which was attenuated in the sildenafilϩdoxorubicin group. Bcl-2 was decreased in the doxorubicin group but was maintained at basal levels in the sildenafilϩdoxorubicin group. Left ventricular developed pressure and rate pressure product were significantly depressed in the doxorubicin group but were attenuated in the sildenafilϩdoxorubicin group. ST interval was significantly increased in the doxorubicin group over 8 weeks. In the sildenafilϩdoxorubicin group, ST interval remained unchanged from baseline. Doxorubicin caused a significant increase in apoptosis, caspase-3 activation, and disruption of mitochondrial membrane potential in vitro. In contrast, sildenafil significantly protected against doxorubicin cardiotoxicity; however, this protection was abolished by both L-NAME and 5-hydroxydecanoate. Conclusions-Prophylactic

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“…Caution should be excercised in patients with one or more risk factors for cardiovascular or cerebrovascular disease, as cardiovascular events related to sildenafil include myocardial infarction, cardiac arrest, angina, ventricular tachycardia, hypertension, and other cardiac symptoms. 27 Concomitant use with organic nitrates (eg glyceryl trinitrate, isosorbide dinitrate) has resulted in cardiac deaths, possibly due to sildenafil potentiating the nitrate's hypotensive effects. 28,29 Few, if any, nationwide studies profiling sildenafil use are available.…”

Section: Introductionmentioning

confidence: 99%