
|
CIALIS
(brand name: tadalafil) |
 |
|
| |
 |
Reviews |
|
| Cialis |
Expert Opin Pharmacother. 2005 Jan;6(1):75-84.
Comparison of clinical trials with sildenafil, vardenafil
and tadalafil in erectile dysfunction.
Doggrell SA.
Doggrell Biomedical Communications, 47 Caronia Crescent, Lynfield,
Auckland, New Zealand.
Erectile dysfunction (ED) affects up to 50% of men, between 40 and 70years
of age. In the first major trial of sildenafil in ED, at 24weeks, improved
erections were reported by 77 and 84% of men taking sildenafil 50 and
100mg, respectively. Subsequently, sildenafil has been reported to be
effective in men with ED associated with diabetes and prostate cancer,
and in psychogenic ED. Sildenafil is safe in men with coronary artery
disease, provided it is not used with the nitrates (a contraindication).
The most commonly reported adverse effects with sildenafil are headache,
flushing and dyspepsia. Vardena-fil is more potent and more selective
than sildenafil at inhibiting phosphodiesterase-5. Vardenafil is similarly
effective to sildenafil in the treatment of ED. The only advantage that
vardenafil has over sildenafil is that it does not inhibit phosphodiesterase-6
to alter colour perception, a rare side effect which sometimes occurs
with sildenafil. Tadalafil has a longer duration of action than sildenafil
and vardenafil. Tadalafil is similarly effective as sildena-fil in the
treatment of ED. In comparison studies, tadalafil is preferred to sildenafil
(50/100mg) by men with ED, possibly because of its longer duration of
action. Of the phosphodiesterase inhibitors, tadalafil may displace sild-enafil
as the drug of choice among men with ED.
|
Clin Pharmacol Ther. 2005 Jan;77(1):63-75.
Effect of tadalafil on cytochrome P450 3A4-mediated
clearance: studies in vitro and in vivo.
Ring BJ, Patterson BE, Mitchell MI, Vandenbranden M, Gillespie
J, Bedding AW, Jewell H, Payne CD, Forgue ST, Eckstein J, Wrighton SA, Phillips
DL.
Eli Lilly and Company, Indianapolis, IN 46285, USA.
OBJECTIVES: Tadalafil was examined in vitro and in vivo for its ability
to affect human cytochrome P450 (CYP) 3A-mediated metabolism. METHODS: Reversible
and mechanism-based inhibition of CYP3A by tadalafil was examined in human
liver microsomes. The ability of tadalafil to influence CYP3A activity was
also examined in primary cultures of human hepatocytes. The effect of tadalafil
on the pharmacokinetics of CYP3A probe substrates was evaluated in human
volunteers before and after coadministration with either a single dose or
multiple doses of tadalafil (10 or 20 mg). RESULTS: Negligible competitive
inhibition of CYP3A was observed in vitro. Mechanism-based inhibition of
CYP3A was detected, albeit with a low potency. In human hepatocytes, exposure
to 1 micromol/L or greater of tadalafil resulted in increased CYP3A protein
expression; however, as with a combined effect of induction and inhibition,
a corresponding increase in CYP3A activity did not occur. The clinical pharmacokinetics
of midazolam and lovastatin, probe substrates of CYP3A, were unaffected
by up to 14 days of tadalafil administration (90% confidence intervals for
the ratio of least squares means for the pharmacokinetic parameters of tadalafil
were contained within the no-effect boundaries of 0.7 to 1.43). CONCLUSIONS:
In vitro results suggested that tadalafil would have little effect on the
pharmacokinetics of drugs metabolized by CYP3A. Clinical studies demonstrated
that the pharmacokinetics of 2 different CYP3A substrates, midazolam and
lovastatin, were virtually unchanged after tadalafil coadministration. Thus
therapeutic concentrations of tadalafil do not produce clinically significant
changes in the clearance of drugs metabolized by CYP3A. |
| Stroke. 2005 Mar;36(3):557-60.
Epub 2005 Feb 03.
Effects of high altitude exposure on cerebral hemodynamics
in normal subjects.
Van Osta A, Moraine JJ, Melot C, Mairbaurl H, Maggiorini
M, Naeije R.
Laboratory of Physiology, Faculty of Medicine, Free University of
Brussels, Belgium.
BACKGROUND AND PURPOSE: Acute mountain sickness (AMS) may be an early
stage of high altitude cerebral edema. If so, AMS could result from an
alteration of dynamic autoregulation of cerebral blood flow resulting
in overperfusion of capillaries and vasogenic cerebral edema. METHODS:
We measured middle cerebral artery blood flow velocity (Vmca) by transcranial
Doppler and arterial blood pressure by finger plethysmography at 490 m
and 20 hours after arrival at 4559 m in 35 volunteers who had been randomized
to tadalafil, dexamethasone, or placebo in a study on the pharmacological
prevention of high altitude pulmonary edema. A dynamic cerebral autoregulation
index (ARI) was calculated from continuous recordings of Vmca and blood
pressure during transiently induced hypotension. RESULTS: Altitude was
associated with an increase in a cerebral-sensible AMS (AMS-C) score (P<0.001)
and with a decrease in arterial oxygen saturation (Sao2), whereas average
Vmca or ARI did not change. However, at altitude, the subjects with the
lowest ARI combined with the lowest Sao2 presented with the highest AMS-C
score (P<0.03). In addition, a stepwise multiple linear regression
analysis on arterial Pco2, Sao2, and baseline or altitude ARI identified
altitude ARI as the only significant predictor of the AMS-C score (P=0.01).
The AMS-C score was lower in dexamethasone-treated subjects compared with
high altitude pulmonary edema-susceptible untreated subjects. Neither
tadalafil nor dexamethasone had any significant effect on Vmca or ARI.
CONCLUSIONS: High altitude hypoxia is associated with impairment in the
regulation of the cerebral circulation that might play a role in AMS pathogenesis. |
| |
 |
Drug information |
|
| GENERIC NAME: tadalafil
BRAND NAME: Cialis
DRUG CLASS AND MECHANISM: Tadalafil is an oral drug that
is used to treat impotence (the inability to attain or maintain a penile
erection.). It is a phosphodiesterase inhibitor that is similar to sildenafil
(Viagra) and vardenafil (Levitra).
Penile erection is caused by the engorgement of the penis with blood.
This engorgement occurs when the blood vessels delivering blood to the
penis increase in size and increase the delivery of blood to the penis.
At the same time, the blood vessels carrying blood away from the penis
decrease in size and decrease the removal of blood from the penis. Sexual
stimulation that leads to the engorgement and erection causes the production
and release of nitric oxide in the penis. Nitric oxide then activates
the enzyme, guanylate cyclase to produce cyclic guanosine monophosphate
(cGMP). The cGMP is primarily responsible for increasing and decreasing
the size of the blood vessels carrying blood to and from the penis, respectively.
Tadalafil prevents an enzyme called phosphodiesterase-5 from destroying
cGMP so that cGMP persists longer. The longer cGMP persists, the more
prolonged the engorgement of the penis. Tadalafil was approved by the
FDA in November, 2003.
PREPARATIONS: Tablets: 5, 10, and 20 mg.
STORAGE: Store at room temperature between 15-30°C
(59-86°F).
PRESCRIBED FOR: Tadalafil is used for the treatment
of impotence.
DOSING: For most individuals, the recommended starting
dose of tadalafil is 10 mg per day taken before sexual activity. Depending
on the adequacy of the response or side effects, the dose may be increased
to 20 mg or decreased to 5 mg a day. The effect of tadalafil may last
up to 36 hours. Individuals who are taking medications that increase the
blood levels of tadalafil should not exceed 10 mg in 72 hours (See drug
interactions.)
DRUG INTERACTIONS: The breakdown and elimination of
tadalafil from the body may be decreased by erythromycin, ketoconazole
(Nizoral), itraconazole (Sporanox), indinavir (Crixivan) and ritonavir
(Norvir). Therefore, these drugs may increase the concentration of tadalafil
in the blood. If these drugs are being used at the same time as tadalafil,
the dose of tadalafil should be reduced in order to avoid side effects
from high levels of tadalafil. Tadalafil increases the heart rate and
also exaggerates the blood pressure lowering effects of nitrates (e.g.,
nitroglycerin). In patients who take nitrates for chest pain (angina),
tadalafil could cause chest pain by increasing heart rate and lowering
blood pressure. Therefore, patients with angina should not use tadalafil.
Tadalafil also exaggerates the blood pressure lowering effects of some
alpha-blocking drugs e.g., terazosin (Hytrin). Individuals who take these
alpha-blockers should not use tadalafil.
PREGNANCY: Tadalafil is not approved for use in pregnant
women.
NURSING MOTHERS: Tadalafil has not been evaluated in
women who are breastfeeding.
SIDE EFFECTS: The most common side effects of tadalafil
are facial flushing (reddening), headaches, stomach upset, diarrhea, flu-like
symptoms and nausea. Tadalafil also may cause chest pain, low blood pressure,
blurred vision and changes in color vision, abnormal ejaculation and priapism
(prolonged and painful erection).
Caution! Before starting
to take this medicine, it is vital that you should consult your doctor!
Do not use it on your own initiative, without medical advice.
|
| |
 |
Order now ! |
|
Dosage |
Packing |
Price |
Pay now |
10 mg |
50 tab |
USD 0.00 |
|
20 mg |
50 tab |
USD 117.00 |
|
10 mg |
100 tab |
USD 0.00 |
|
20 mg |
100 tab |
USD 198.00 |
|
|
|
| |
| 
|
|