Treatment of Pharmacological Priapism with Phenylephrine

“…33,34 Anecdotally, another novel method has been proposed for initiating detumescence during priapism involving physical exercise. In this case, a user of intracavernosal injection therapy experiencing priapism found non-invasive relief with 15 min of rigorous bicycling.…”

Section: Discussionmentioning

confidence: 99%

Development of a rat model of sexual performance anxiety: effect of behavioural and pharmacological hyperadrenergic stimulation on APO-induced erections

et al. 2002

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As part of the multifactorial nature of erectile dysfunction, anxiety associated with sexual performance (SPA) remains a major contributing factor to its progression. In fact, the heightened sympathetic activity associated with sexual performance anxiety may be a key early component of this disruption of normal erectile responses. We are not aware that any animal models have been developed to assess this phenomenon. Using apomorphine (APO, 80 m mg=kg s.c.)-induced erections in rats we characterised the effects of behavioural or pharmacological hyperadrenergic stimulation (that is, anxiety) on erections and hemodynamics. We developed an experimental SPA paradigm by exposing male rats to the stress of being observed by a larger, older male rat placed in close proximity to test rats during APO testing. In a separate group, adrenergic stress was simulated using a sympathomimetic, methoxamine (MXA) given prior to APO testing. In a third group, the changes in circulatory parameters (mean arterial pressure, heart rate) were determined following instrumentation with radiotelemetric transducers for each scenario. APOinduced erections were significantly lower in both the behavioural (1.25 AE 0.8) and pharmacological (0.33 AE 0.5) stressor paradigms compared to controls (2.81 AE 0.9). Further, erections in MXAtreated rats were significantly lower than in the observed scenario. Despite the differences in erections hemodynamic assessments showed no differences in MAP or HR changes between the different experimental conditions. Thus, both the behavioural and pharmacological paradigms of SPA decreased erections, but did not affect the circulation. This suggests that the level of hyperadrenergic input required to induce erectile dysfunction can be subtle, and target only erectogenic pathways.

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“…One explanation pertains to abnormal activation of neural reflexogenic mechanisms involved in erection following genital stimulation. [20][21][22][23][24] Another explanation relates to disturbances in central neurotransmission that mediates penile erection. 25 Knowledge of the traditional autonomic sympathetic nervous system that mediates detumescence and penile flaccidity has supported the general belief that pathogenic failure of this system could readily predispose to the development of priapism.…”

Section: Abnormal Penile Blood Flowmentioning

confidence: 99%

“…Pharmaceutical approaches described to offer benefit include: intracorporal thrombolytic agents, which would support the pathogenic roles of blood stasis and thrombosis, 57,58 oral diethylstilbestrol, which by exerting antiandrogenic effects would imply that androgens permit aberrant penile erection; 35 systemic injections of gonadotropin-releasing hormone analogues, which because they are also anti-androgenic would further hypotheses about the pathogenic role of androgens; 59,60 lidocaine as a penile anesthetic block, which is considered to work by blunting sensory input conveyed in the dorsal nerve of the penis of reflexive erectile pathways; 61 oral and intracorporal alpha-adrenergic agonists, which exert contractile effects on erectile tissue, thus indicating the likely pathogenic role of uncontrolled non-adrenergic factors; 24,60,62,63 intracorporal methylene blue, an antagonist of the nitric oxide/ cyclic guanosine monophosphate/protein kinase G effector mechanism of corporal smooth muscle relaxation, pointing to a possible pathogenic role of this biochemical pathway. 64,65 Basic science investigation Basic research in the field has consisted mainly of identifying and evaluating animal models featuring priapic behavior and molecular studies that suggest possible mechanisms for the disorder.…”

Section: Clinical Studymentioning

confidence: 99%

“…After all, these individuals fit a predictable pattern of progression to erectile tissue destruction in which, it would seem, clinical opportunities exist to gain disease control. Presently, current pharmacologic treatment successes support the roles of androgenic suppressive agents, 59,60 adrenergic agonist therapies, 24,60,62,63 and effectors of the nitric oxide-dependent erection regulatory pathway in the penis such as methylene blue. 64,65 As promising as these therapies have been, they still warrant certain considerations such as when they should be administered, whether they can be administered with minimal penile trauma and without causing adverse extra-penile effects, and whether they can be offered with a regimen that does not impair natural erections long term.…”

Section: Prevention Strategiesmentioning

confidence: 99%

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Priapism pathophysiology: clues to prevention

Burnett

2003

Int J Impot Res

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Priapism, in which penile erection persists in the absence of sexual excitation, is an enigmatic yet devastating erectile disorder. Current endeavors to manage the disorder suffer from a poor fundamental knowledge of the etiology and pathogenesis of priapism. These endeavors have remained essentially reactive, which commonly fail to avert its pathological consequences of erectile tissue damage and erectile disability, not to mention its psychological toll. The role of preventative management seems paramount with respect to priapism. As a prerequisite to formulating prevention strategies, gaining understanding of its pathogenic features and likely pathophysiologic mechanisms is viewed to be quite important. This review combined an analysis of clinicopathologic reports as well as a summary of clinical and basic science investigations on the subject to date. These assessments support the basic classification of priapism into low-flow (ischemic) and high-flow (nonischemic) hemodynamic categories, resulting from venous outflow occlusion and unregulated arterial overflow of the penis, respectively. In addition, consistent with the hypothesis that dysregulative physiology of penile erection accounts for some presentations of priapism, several plausible molecular mechanisms influencing the functional state of the erectile tissue are discussed. Current progress in the field suggests prevention possibilities using androgenic suppressive therapy, adrenergic agonist therapies, and effectors of the nitric oxide-dependent erection regulatory pathway in the penis. New ideas for prevention may emerge from targeting molecular mechanisms involved in regulating erectile tissue function.

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Treatment of Pharmacological Priapism with Phenylephrine

Cited by 52 publications

References 10 publications

Penis lengthening-A retrospective review of 300 consecutive cases

Penis lengthening-A retrospective review of 300 consecutive cases

Development of a rat model of sexual performance anxiety: effect of behavioural and pharmacological hyperadrenergic stimulation on APO-induced erections

Priapism pathophysiology: clues to prevention

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