1,2 The diagnosis of priapism encompasses at least 2 very different pathophysiologic processes. Ischemic priapism (“low flow”) is primarily a disorder of venous outflow and/or stasis. This is primarily due to persistent corporal

smooth muscle relaxation that continually compresses the subtunical veins, thereby preventing any outflow Inhibitors,research,lifescience,medical from the sinusoids. If the intracorporeal pressure is above mean arterial pressure, which it usually is in such a condition, the cavernosal arteries that run through the middle of each corpus cavernosum are also passively compressed such that no inflow of blood is occurring. In contrast, nonischemic priapism (“high flow”) is a disorder of arterial Inhibitors,research,lifescience,medical inflow. This latter condition is due primarily to a high inflow

of blood in tandem where there is very little, if any, smooth muscle relaxation. In this situation, the high inflow of blood clears as rapidly as it can from the sinusoids and the blood only “backs up” into the sinusoids if inflow is greater than outflow. It is this difference in pathophysiology between the 2 conditions that underscores the starkly different etiologies, Inhibitors,research,lifescience,medical presentation, and management of ischemic versus nonischemic priapism. An additional entity, recurrent or stuttering priapism, is a subtype of ischemic priapism reserved for those who experience recurrent painful erections with intervening periods of detumescence. Each of the episodic erections typically Inhibitors,research,lifescience,medical lasts less than 4 hours, often building toward and culminating in a long-standing ischemic erection. The pathophysiology of recurrent priapism was long thought to be repeated episodes of persistent veno-occlusion. Recent work suggests that the cause of this persistent and intermittent disorder of veno-occlusion may be dysregulation of the phosphodiesterase

type 5 (PDE5) within the nitric oxide-cyclic guanosine monophosphate Inhibitors,research,lifescience,medical (cGMP) signaling pathway in the corporal tissue, although definitive scientific proof for this relationship is still lacking. Oxalosuccinic acid Ischemic Priapism Case 1 A 32-year-old black man with a medical history of sickle cell disease presented to the emergency room complaining of a persistent, painful erection for the past 18 hours. Sexual excitement prompted the erection; however, detumescence did not occur after the cessation of intercourse. The patient presented only after the pain became unbearable, and at the time of evaluation was in obvious discomfort. Examination HDAC inhibitor revealed an erect penis with rigid corpora cavernosa. Palpation of the tense corpora exacerbated the pain. Of note, both the glans of the penis and the corpora spongiosum were soft. Laboratory analysis was within normal limits with the exception of an elevated reticulocyte count. Aspiration of the corpora cavernosa demonstrated dark, viscous blood.