Alprostadil, (PGE1), Prostaglandin E1 video
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Alprostadil, (PGE1), Prostaglandin E1 (745-65-3) usage in steroids cycle
Alprostadil, (PGE1), Prostaglandin E1 (CAS 745-65-3), also called Avastin and Mvasi.
Alprostadil, (PGE1), Prostaglandin E1 Usage
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How Alprostadil, (PGE1), Prostaglandin E1 (745-65-3) works
For the treatment of erectile dysfunction (ED), alprostadil relaxes the smooth muscles of the corpus cavernosum; however, the exact mechanism of action is unknown. It appears that the effects are due to increasing the intracellular concentrations of cyclic AMP. Alprostadil interacts with specific membrane-bound receptors that stimulate adenylate cyclase and elevate intracellular cyclic AMP, leading to activation of protein kinase and resultant smooth muscle relaxation. This action is in contrast to papaverine which inhibits oxidative phosphorylation mediated inactivation of cyclic AMP and interferes with calcium mobilization during muscle contraction. Alprostadil may also antagonize the vasoconstrictive actions of norepinephrine by preventing the neuronal release of norepinephrine and may enhance the actions of nonadrenergic, noncholinergic vasodilatory neurotransmitters. In treating ED, alprostadil induces erection by relaxing trabecular smooth muscle and dilating cavernosal arteries and their branches. Dilation of the cavernosal arteries is accompanied by increased arterial inflow velocity and increased venous outflow resistance. As a result, the lacunar spaces expand and blood becomes entrapped secondary to compression of venules against the tunica albuginea. To achieve adequate tumescence and rigidity, the tunica albuginea must be sufficiently stiff to compress the venules penetrating it and thus block venous outflow. This process is also referred to as the corporal veno-occlusive mechanism. Alprostadil does not directly affect ejaculation or orgasm.
In the treatment of ductus arteriosus-dependent congenital heart defects, alprostadil maintains ductal patency by relaxing the smooth muscles of the ductus arteriosus. Alprostadil is only effective if given prior to complete anatomic closure of the ductus arteriosus. Administration of alprostadil to neonates with cyanotic congenital heart defects (restricted pulmonary blood flow) results in an increase in pulmonary blood flow and/or increase in mixing between the systemic and pulmonary circulation which leads to a temporary increase in arterial oxygen partial pressure (PaO2) and oxygen saturation. The response of the cyanotic neonate to alprostadil therapy is also inversely related to pretreatment PO2. The greatest response appears to be in those neonates with low pretreatment PaO2 (< 20 torr), narrowing ductus arteriosus, and who are 4 days old or younger. Neonates with PaO2 values of 40 torr or more usually have little response to alprostadil.
In neonates with restricted systemic blood flow, administration of alprostadil can result in prevention or correction of acidemia, increased cardiac output with increased systemic blood pressure, increased femoral pulse volume, increased renal blood flow and function, decreased gradient of descending to ascending aortic blood pressures (in neonates with coarctation of the aorta), and/or decreased ratio of pulmonary artery pressure to descending aortic pressure (in neonates with interruption of the aortic arch). Unlike in cyanotic neonates, the efficacy of alprostadil in acyanotic neonates does not depend on age or pretreatment PaO2.
Alprostadil (Prostglandin E1) is used to treat erectile dysfunction (ED) in adult males. The efficacy of alprostadil in treating ED varies with the cause; response rate is generally lower in patients with ED due to mixed etiologies compared to those with ED due to neurogenic, psychogenic, or vasculogenic causes. Two dosage forms are marketed for treating ED: a transurethral product (Muse) which uses a medicated pellet administered into the urethra and an injection (Caverject or Edex) that is directly injected into the corpus cavernosa. Other dosage forms such as a topical gel and a non-invasive liposomal delivery system are under investigation. According to ED treatment guidelines, oral phosphodiesterase type 5 inhibitors (PDE5 inhibitor) are considered first-line therapy. Second-line treatment options include intracavernous injection and intra-urethral therapy. Intracavernous injection therapy is the most effective nonsurgical treatment for ED, with predictable and sustained response. However, it is invasive and caries notable side-effects including priapism and penile fibrosis. FDA approvals are as follows: Caverject in July 1995, MUSE in October 1996, and Edex in June 1997.
Alprostadil and other prostaglandins in the E series are naturally present in the placenta and ductus arteriosus of the fetus. The E-type prostaglandins vasodilate arterioles by direct relaxation of vascular smooth muscle. Other pharmacologic effects include increase in cardiac output, dilation of both systemic and pulmonary vessels, dilation of the ductus arteriosus, inhibition of platelet aggregation, relaxation of bronchial muscle, increase in renal blood flow, and delay of gastric emptying time. Intravenous alprostadil is used in neonates with obstruction of right or left ventricular outflow to maintain the patency of the ductus arteriosus up until the time of corrective or palliative surgery. Alprostadil is generally more effective in those neonates with low pretreatment blood PO2 and who are 4 days old or less. In neonates older than 4 days, there is a decrease in ductal smooth muscle reactivity due to postnatal involutional changes in the wall of the ductus arteriosus. Intravenous alprostadil requires respiratory monitoring during administration because apnea develops in 10—12% of neonates. Alprostadil is FDA approved in pediatric patients as young as neonates. Prostin VR Pediatric was approved by the FDA in 1981.
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