Väitös (farmakologia, lääkekehitys ja lääkehoito): FM Jyrki Lehtimäki
Aika
26.4.2024 klo 12.00 - 16.00
FM Jyrki Lehtimäki esittää väitöskirjansa ”PREMATURE EJACULATION - POTENTIAL ROLEALPHA2-ADRENOCEPTOR AGONISTS FOR SYMPTOMATIC TREATMENT Studies of dexmedetomidine, fadolmidine and tasipimidine” julkisesti tarkastettavaksi Turun yliopistossa perjantaina 26.04.2024 klo 12.00 (Turun yliopisto, Natura, X-luentosali, Turku).
Yleisön on mahdollista osallistua väitökseen myös etäyhteyden kautta: https://echo360.org.uk/section/8fcd9fcb-1f67-459d-b797-9255b0f5887a/public (kopioi linkki selaimeen).
Vastaväittäjänä toimii professori Heikki Ruskoaho (Helsingin yliopisto) ja kustoksena professori Ullamari Pesonen (Turun yliopisto). Tilaisuus on suomenkielinen. Väitöksen alana on farmakologia, lääkekehitys ja lääkehoito.
Väitöskirja yliopiston julkaisuarkistossa: https://urn.fi/URN:ISBN:978-951-29-9671-1 (kopioi linkki selaimeen).
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Tiivistelmä väitöstutkimuksesta:
Ejaculation is a physiological process that results in the expulsion of semen from the male reproduction tract during a sexual climax and is considered an essential component of natural conception. Ejaculation is a delicately orchestrated process controlled by the peripheral nervous system and the central nervous system and involving sympathetic, parasympathetic and somatic neurons. The most common ejaculatory dysfunction is premature ejaculation being also the most common sexual dysfunction in men – with a prevalence rate up to 30% and not much affected by age. Premature ejaculation is associated with reduced satisfaction in sexual life, distress, anxiety, and depression and has a negative impact on relationships with sexual partners. The etiology of premature ejaculation is considered multifactorial, with psychological, relationship and biological factors.
There are limited pharmacological treatment options available. Dapoxetine, an on-demand ive serotonin uptake inhibitor, is the first drug registered for premature ejaculation treatment. A locally administered eutectic mixture of prilocaine/lidocaine, a spray with a local anesthetic effect on the penis, is the other approved medication for premature ejaculation, while others have been used as off-label. Clinical data accumulated in recent years suggests that lifelong premature ejaculation may be associated with increased activity of the sympathetic nervous system. ive a2-adrenoceptors have a key role in regulating sympathetic tone in both the periphery and the CNS. Compounds that activate a2-adrenoceptors decrease sympathetic tonus, and they are widely used in human and veterinary practice. This knowledge of pharmacology prompted us to study the role of a2-adrenoceptor agonists dexmedetomidine, fadolmidine and tasipimidine in the symptomatic treatment of premature ejaculation. The prerequisite for these premature ejaculation studies was the thorough pharmacological profiling of the novel a2-adrenoceptor agonists fadolmidine and tasipimidine studied and presented in this dissertation.
Our observations suggest that centrally acting a2-adrenoceptor agonists might provide symptomatic relief for premature ejaculation by prolonging ejaculation latency without affecting any other parameter of sexual behaviour or sexual incentive motivation. Whether the effects observed in male rats are directly transferrable to men can only be determined through clinical studies.
Yleisön on mahdollista osallistua väitökseen myös etäyhteyden kautta: https://echo360.org.uk/section/8fcd9fcb-1f67-459d-b797-9255b0f5887a/public (kopioi linkki selaimeen).
Vastaväittäjänä toimii professori Heikki Ruskoaho (Helsingin yliopisto) ja kustoksena professori Ullamari Pesonen (Turun yliopisto). Tilaisuus on suomenkielinen. Väitöksen alana on farmakologia, lääkekehitys ja lääkehoito.
Väitöskirja yliopiston julkaisuarkistossa: https://urn.fi/URN:ISBN:978-951-29-9671-1 (kopioi linkki selaimeen).
***
Tiivistelmä väitöstutkimuksesta:
Ejaculation is a physiological process that results in the expulsion of semen from the male reproduction tract during a sexual climax and is considered an essential component of natural conception. Ejaculation is a delicately orchestrated process controlled by the peripheral nervous system and the central nervous system and involving sympathetic, parasympathetic and somatic neurons. The most common ejaculatory dysfunction is premature ejaculation being also the most common sexual dysfunction in men – with a prevalence rate up to 30% and not much affected by age. Premature ejaculation is associated with reduced satisfaction in sexual life, distress, anxiety, and depression and has a negative impact on relationships with sexual partners. The etiology of premature ejaculation is considered multifactorial, with psychological, relationship and biological factors.
There are limited pharmacological treatment options available. Dapoxetine, an on-demand ive serotonin uptake inhibitor, is the first drug registered for premature ejaculation treatment. A locally administered eutectic mixture of prilocaine/lidocaine, a spray with a local anesthetic effect on the penis, is the other approved medication for premature ejaculation, while others have been used as off-label. Clinical data accumulated in recent years suggests that lifelong premature ejaculation may be associated with increased activity of the sympathetic nervous system. ive a2-adrenoceptors have a key role in regulating sympathetic tone in both the periphery and the CNS. Compounds that activate a2-adrenoceptors decrease sympathetic tonus, and they are widely used in human and veterinary practice. This knowledge of pharmacology prompted us to study the role of a2-adrenoceptor agonists dexmedetomidine, fadolmidine and tasipimidine in the symptomatic treatment of premature ejaculation. The prerequisite for these premature ejaculation studies was the thorough pharmacological profiling of the novel a2-adrenoceptor agonists fadolmidine and tasipimidine studied and presented in this dissertation.
Our observations suggest that centrally acting a2-adrenoceptor agonists might provide symptomatic relief for premature ejaculation by prolonging ejaculation latency without affecting any other parameter of sexual behaviour or sexual incentive motivation. Whether the effects observed in male rats are directly transferrable to men can only be determined through clinical studies.
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