ANOXIA AND CORPORAL SMOOTH-MUSCLE DYSFUNCTION - A MODEL FOR ISCHEMIC PRIAPISM

The hemodynamics of penile flaccidity, erection and detumescence requi res corporal smooth muscle to function across a wide variation in pO2. The present study describes the effect of anoxia on corporal smooth m uscle response to field stimulation and pharmacologic agonists and ant agonists of erection. The response of isolated strips of rabbit corpus cavernosal tissue to field stimulation, phenylephrine, bethanechol, A TP and KCL was determined under oxygenated and anoxic conditions. The results can be summarized as follows: 1) Anoxia eliminated spontaneous contractile activity and reduced basal tissue tension to a minimum. 2 ) Neither field stimulation nor pharmacological agents (ATP, bethanech ol, isoproterenol) could relax basal tension below that induced by ano xia alone. 3) Under anoxic conditions alpha-adrenergic agonists produc ed poorly sustained phasic contractile responses; anoxia eliminated to nic contractile responses to phenylephrine. 4) In normoxic conditions field stimulation of smooth muscle precontracted with phenylephrine pr oduced frequency-dependent graded relaxations; under anoxic conditions field stimulation yielded contractile responses at all frequencies. O ur data suggest that corporal smooth muscle tone, spontaneous contract ile activity, the contractile response to alpha-agonists and field sti mulated relaxation depend on the state of corporal oxygenation. The in ability of alpha-stimulation to induce a tonic contraction of corporal smooth muscle under anoxia in vitro parallels the failure of penile i njection of alpha-adrenergic agonists to relax ischemic priapism.