Source:http://linkedlifedata.com/resource/pubmed/id/11416835
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2001-6-20
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pubmed:abstractText |
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.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0955-9930
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
12
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
315-27
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pubmed:dateRevised |
2009-11-3
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pubmed:meshHeading |
pubmed-meshheading:11416835-Animals,
pubmed-meshheading:11416835-Biomedical Engineering,
pubmed-meshheading:11416835-Male,
pubmed-meshheading:11416835-Models, Biological,
pubmed-meshheading:11416835-Penile Erection,
pubmed-meshheading:11416835-Penis,
pubmed-meshheading:11416835-Rabbits,
pubmed-meshheading:11416835-Regional Blood Flow,
pubmed-meshheading:11416835-Vascular Resistance,
pubmed-meshheading:11416835-Veins,
pubmed-meshheading:11416835-Venae Cavae,
pubmed-meshheading:11416835-Venules
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pubmed:year |
2000
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pubmed:articleTitle |
The mechanics of corporal veno-occlusion in penile erection: a theory on the effect of stretch-associated luminal constrictability on outflow resistance.
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pubmed:affiliation |
Department of Urology, Boston University School of Medicine, MA 02118, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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