title: The mechanics of corporal veno-occlusion in penile erection: a theory on the effect of stretch-associated luminal constrictability on outflow resistance.
abstract: In order to further our understanding of the physiology of corporal veno-occlusion, we developed a theory of a possible contribution to corporal venous outflow resistance which occurs as the result of venule stretching with resultant luminal narrowing when penile volume increases during the erection process. We stretched non-biological tubes and rabbit abdominal vena cava segments, performed flow-based and volume-based experiments to calculate the magnitude of N, the newly defined 'stretch-associated luminal constrictability' factor. We solved for (R(s)/R(u)), the ratio of the venule fluid resistance in the stretched state (R(s)) to the unstretched state (R(u)), to quantify the projected increases in fluid resistance as well as Q.R(u) where Q is the subtunical venule flow rate. For a given tube, N was found to be essentially constant for different amounts of stretch. A theory was formulated which predicted R(s) and Q as a function of N, DeltaP (intracavernosal pressure increase); V(E)/V(F) (tunical distensibility); X (cavernosal expandability) and R(u). Based on the magnitude of N=2, this theory predicts that patients with the highest values of both V(E)/V(F) and X would have maximal R(s) values, approaching infinity (complete occlusion) at a low DeltaP near 5 mmHg. In contrast, patients with low values of both V(E)/V(F) (eg Peyronie's disease) and X (eg corporal fibrosis), would be predicted to have minimal R(s) values. For example, a hypothetical patient with the lowest values of V(E)/V(F) and X would yield R(s) values only approaching 7.9 times that of unstretched values at a DeltaP increase of 90 mmHg. We concluded to that stretch-associated venule resistance may occur as a result of decreased sub-tunical venule diameter and increased sub-tunical venule length. In individual patients, stretch-associated venule resistance may either dominate or be a minor component of the overall mechanism of corporal veno-occlusion.
authors: Department of Urology, Boston University School of Medicine, MA 02118, USA.
authors: D
authors: D
authors: Udelson
authors: J
authors: J
authors: L'Esperance
authors: A M
authors: AM
authors: Morales
authors: R
authors: R
authors: Patel
authors: I
authors: I
authors: Goldstein
mesh_terms: D000818:Animals; D001698:Biomedical Engineering; D008297:Male; D008954:Models, Biological; D010410:Penile Erection / Q000502:physiology*; D010413:Penis / Q000098:blood supply*; D011817:Rabbits; D012039:Regional Blood Flow / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology*; D014680:Veins / Q000502:physiology; D014684:Venae Cavae / Q000502:physiology; D014699:Venules / Q000502:physiology