The next line of that quote is important.
"Blood oxygen level-dependent magnetic resonance imaging revealed enlarged, hypoxic corpora cavernosa. Megalophallus probably resulted from permanent loss of elasticity of the tunica albuginea due to severe engorgement during the episode of priapism."
- "Megalophallus as a sequela of priapism in sickle cell anemia:" Urology 2000
While I think the main mechanism for priapism gains is indeed the prolonged physical stress on the tunica of the CC’s, there is some merit to the idea that hypoxia promotes hypertrophy.
Here’s one example.
"Hypoxia increases muscle hypertrophy induced by resistance training."
Hypoxia increases muscle hypertrophy induced by resistance training
There are also many articles on the relationship between hypoxia and cardiac hypertrophy.
Here’s a link to a case study on a sickle cell disease patient who developed a functional megalophallus over the course of 7 years of priapisms. From what I understand, it is very likely for patients to get permanent erectile dysfunction in priapisms lasting beyond 2 days, but this guy did not lose any erectile function.
"AN UNUSUAL CASE OF PRIAPISM"
https://www.ncb i.nlm.nih.gov/p … a00281-0075.pdf
" On the one
end of the spectrum [of sickle-cell] is total venous occlusion
resulting in priapism, cavernous ischemia and subsequent
fibrosis, and impotence, and on the other end is
the minimal venous occlusion with no priapism and no
ischemic changes. In the middle of the spectrum, there
appears to be various degrees of partial venous
obstruction, resulting in priapism associated with
adequate oxygenation of the cavernous tissue because
of continued circulation in the presence of incomplete
venous occlusion. Our patient represents such an
example. Furthermore, repeated episodes of mild
hypoxia resulting from the transient partial venous
obstruction in our patient might have been a stimulus
for the hypertrophy of corpora cavernosa, because
hypoxia is known to result in hypertrophy of tissues.4 It
is interesting to note that the penile hypertrophy was
confined to the corpora cavernosa and that the glans and
the corpus spongiosum were of normal size. It is well
known that the latter structures are not involved in
priapism5-7 and hence they are not subjected to hypoxic
stimulus to under hypertrophy."
In other words, he had a moderate ADC style clamp effect going on, or something like a 7/10 erection as opposed to a 10/10. This guy was an exception.
Priapism patients do routinely get permanent erectile dysfunction when the episodes last too long. Here’s the drill for a priapism at the ER - most of these are sickle cell related, or drug use related (erectile enhancement drugs - usually injectibles)
<4 hour - pain relief, hydration, urination, ejaculation, etc is recommended - also recommended to hear toward an ER if getting close to 4 hours.
4-12 hours - drain the blood from the penis with needles and attempt to chemically stop the erection if it was drug induced, repeat over and over again, blood transfusions as necessary
12+ hours - surgery, if they can’t get the CC’s to stop filling, surgical shunt installed to bypass the venous occlusion mechanism (the way we get erections), permanent ED possible
Priapisms lasting 12-48 hours have a high chance of causing permanent ED - and those lasting 48+ hours have a near certainty of causing permanent ED.
It’s not worth the risks in my opinion. But reading about all this does make me feel better about clamping sets up to 18 minutes, and the benefits of wearing a moderate ADC device for several hours at a time.