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What I see in that study is, in my opinion, a unique & Scientific window into PE - and probably more of one than we’re likely to see in the near future.

While I realize that the “trigger” was pathological (severe priapism resulting from SCA), the mechanism, I believe, explains any type of penile enlargement. Think of the “trigger” as the stimulus - not the end result. A man can get blisters on his hands from grabbing a hot pot or swinging a pick all day (the trigger can be different), but the result (blisters) is the same.

While his “trigger” was illness, ours is PE. And he did what guys here can only dream about: he increased his girth by (probably) 40-50%. * After 3 years of PE, I managed only about a 20% girth increase.

I believe their studies & thermal imaging, and blood work, etc., probably gave them quite a perspective on why his unit ballooned so massively (and “ballooned” is the right word).

This makes me want priapism.

Originally Posted by marinera
The penis was covered with dark brown hypertrophic skin and it had a 6.7 cm in diameter.

I just noticed this. Is this some sort of well-known thing in the medical literature? Is hypertrophic skin dark?

Originally Posted by wadzilla

While he did say “probably,” I would regard it as more than a mere “armchair opinion.” ..

If they said ‘probably’, I think they were meaning ‘probably’.

Originally Posted by wadzilla

……….

(1) That the glans wasn’t enlarged is no surprise at all to me (we’ve had several discussions here about the difficulty of glans enlargement), and my theory is that the glans is so incredibly elastic. Regarding the CS, that is a little surprising, but not greatly. After all, most of us probably recognize that we get the majority of our girth gains from the 2 large chambers - the CC.

……

The problem is:the glans wasn’t enlarged because priapism doesn’t involves glans, not because your theory is true. :)

Originally Posted by wadzilla

……….

(2) marinera, I know that English is not your native language (and I confess that you speak it better than I speak my 2nd or 3rd language), but I think you missed something on your reading of that technical material: You said, “So, they are basing their hypothesis on the fact that the glans wasn’t hypertrophied,” but that is not accurate. They did not “base” their theory on that, they stated that “…The plausibility of this mechanism for megalophallus is supported by…”etc., etc. out the glans & CS.

……

You are splitting hair.

Originally Posted by wadzilla

……

(3) I will concede that they seem to be employing a “generic” reference to hypertrophy, and not always the strict application associated with striated skeletal muscle. Because even though they claim the massive enlargement was due to “loss of elasticity,” they still employed the phrase “hypertrophy” (obviously in a loose manner). Yet the other, 134-yr old, study is far from modern science.

I already explained this point, but I’ll repeat: they reported a case. The case seems genuine and doesn’t accords to your theory. You are facing a fact, not the use of the word ‘hypertrophy’ instead than ‘hyperplasia’ - just a side note, you are the one that is confusing these two different processes in your PDF.

Originally Posted by LongVehicle

I just noticed this. Is this some sort of well-known thing in the medical literature? Is hypertrophic skin dark?

I think the skin was dark because was necrotic.

More on priapism

Hindawi Publishing Corporation
Advances in Urology
Volume 2008, Article ID 549861, 3 pages
doi:10.1155/2008/549861

Idiopathic Low-Flow Priapism in Prepuberty:
A Case Report and a Review of Literature
Ihab A. Hekal1 and Eric J. H. Meuleman2

1Urology Department, Urology and Nephrology Center, Mansoura 35516, Egypt
2Urology Department, Free University Medical Center, 1007 MB Amsterdam, The Netherlands
…….
Priapism is a condition first described by Tripe in 1845.
It has been defined as a pathological condition of
penile erection that persists beyond or is unrelated to sexual
stimulation .
In children and prepubertal boys as well as in adults,
it can be classified according to the aetiology into low-flow
(ischemic) and high-flow priapism. Most common causes
of the former are the use of medications and hematological
conditions. Several medications have been implicated in
ischemic priapism. Most notably, psychiatric drugs as a class
are over represented. Antipsychotics such as chlorpromazine,
phenothiazine, and clozapine are known culprits as well are
the antidepressants such as trazodone [5]. Olanzapine or
methylphenidate therapy (drugs used for attention deficit
hyperactivity disorder) is reported to cause priapism in
children [6]. Total parenteral nutrition, with its high fat
content, is also believed to cause priapism [7].Hematological
diseases that are accompanied by hyperviscosity such as
sickle cell disease or trait and leukemia are well-known causes
of ischemic priapism in children [8].

High-flow (nonischemic) priapism was firstly described
over 40 years ago [9]. It is always the result of a straddle injury
of the corpora cavernosal resulting in an arteriocavernosal
fistula, which on its turn results in an uncontrolled arterial
inflow into the cavernosal sinusoids. Because the cavernosal
smooth muscle is contracted and well oxygenated (on
aspiration, bright red blood with a high PO2 is encountered),
the erection is semirigid and not painful [8].
……….

In low-flow priapism, venous outflow is blocked due
to a complete paralysis of the cavernous smooth muscle.
Due to ischemia, the erection is painful. .
…………….
Various histological studies have been performed to
define the histological changes in relation with the duration
of ischemia. In the early stages at less than 12 hours,
interstitial edema and thickening are the most common
findings. From 12 to 24 hours, thrombocytes start to adhere
to the endothelium such that by 48 hours necrosis of
cavernosal smooth muscle cells and fibroblast proliferation
has occurred. The end result is loss of smooth muscle and
fibrosis of the corpora cavernosa
[12].
Low-flow priapism has been described in men of all ages
including newborns. The peak incidence is bimodal with the
highest incidence occurring between the ages of 5–10, and
20–50 years. Generally in the younger age group, priapism is
secondary to a neoplasm or sickle cell anemia [8]
…..
Link

Originally Posted by marinera
The end result is loss of smooth muscle and
fibrosis of the corpora cavernosa

Loss? I thought this condition left them with massively enhanced penile tissue?

Originally Posted by LongVehicle

Loss? I thought this condition left them with massively enhanced penile tissue?

Quote

In low-flow priapism, venous outflow is blocked due

to a complete paralysis of the cavernous smooth muscle.

Due to ischemia, the erection is painful.

Quote

From 12 to 24 hours, thrombocytes start to adhere

to the endothelium such that by 48 hours necrosis of

cavernosal smooth muscle cells and fibroblast proliferation

has occurred. The end result is loss of smooth muscle and

fibrosis of the corpora cavernosa [12]

The smooth muscle dies (necrosis). The ‘massively enhanced penile tissue’ is not smooth muscle. Some will be fibrotic tissue of the CC’s, some will be swollen lymphatic structures etc.

The long and the short of it is that, while priapism can cause size increase, there is no healthy form of priapism. All forms of priapism will cause irreversable damage to the penis eventually (or very rapidly).


Heat makes the difference between gaining quickly or slowly for some guys, or between gaining slowly instead of not at all for others. And the ideal penis size is 7.6" BPEL x 5.6" Mid Girth.

Basics.... firegoat roll How to use the Search button for best results


Last edited by firegoat : 07-21-2009 at .

Yes. So, I want to add, forget wearing cock-rings while sleeping, inducing erections lasting many hours taking drugs ec.. While very short and incomplete blood-flow occlusion could cause ‘good’ kind of size increase, total or long lasting blood-flow occlusion can make you impotent. You are warned, fellows.

Firegoat and marinera,

Thank you two for clearing that up for me. I did not know much about this prior to this thread.

I wonder then, what is the benefit of having increased blood flow to the penis that isn’t locked off? As in through EVO for example - having larger flaccid sizes daily simply due to blood flow.

Interesting posts.

I don’t know if EVO increases blood flow. But having increased blood flow should be good for many reasons.

In example, an increased blood flow keeps your penis pumped, so in enlarged state, slowly lengthening TA both in circumference and in length.

Also, if one agrees that PE work cause some degree of inflamation/damage, an increased blood flow should help in speeding-up healing; more blood circulating in your penis means more cleaning up of ‘junk’ created by workout and more ‘food’ to repair tissues and make them grow, if it’s clear what I mean.

Originally Posted by marinera
I don’t know if EVO increases blood flow. But having increased blood flow should be good for many reasons.

In example, an increased blood flow keeps your penis pumped, so in enlarged state, slowly lengthening TA both in circumference and in length.

Also, if one agrees that PE work cause some degree of inflamation/damage, an increased blood flow should help in speeding-up healing; more blood circulating in your penis means more cleaning up of ‘junk’ created by workout and more ‘food’ to repair tissues and make them grow, if it’s clear what I mean.

Through my own experience I am 100% certain it does this in me, and not in any minor way either. I also expect that’s why my healing rate has sped up. Good stuff.

Stretching effects at microscope. 1

The Proliferative Response of Isolated Human Tendon Fibroblasts to Cyclic Biaxial Mechanical Strain

  1. Johannes Zeichen, MD,
  2. Martijn van Griensven, MSc and
  3. Ulrich Bosch, MD†
+Author Affiliations

  1. Laboratory of Histology and Cell Biology, Department of Traumasurgery, Hannover Medical School, Hannover, Germany
  1. Presented at the 25th annual meeting of the AOSSM, Traverse City, Michigan, June 1999.

  1. Address correspondence and reprint requests to Ulrich Bosch, MD, Department of Traumasurgery, Hannover Medical School, D-30623 Hannover, Germany
Abstract

At the cellular level, dynamic strain plays a key role in cell stimulation and organization of the extracellular matrix. Although positive effects of physical strain on tendon tissue are well known, little knowledge exists on how mechanical strain affects tendon cells. In this study, human tendon fibroblasts from patellar tendon were cultured on silicone dishes. Subsequently, cyclic biaxial mechanical strain was applied to the dishes for 15, 30, and 60 minutes using a specially developed cell stretching system. After the fibroblasts were strained, cells were tested for proliferation at 6, 12, and 24 hours. As a control, cells were grown on silicone dishes but did not receive any strain. A biphasic response in proliferation was observed for the 15- and 60-minute strain periods: at 6 hours and 24 hours there was more proliferation than at 12 hours. After a strain duration time of 30 minutes, a lower proliferation rate was measured compared with control levels. This study shows that application of mechanical stress to tendon fibroblasts resulted in an alteration of cellular proliferation depending on the stress time. Our results may implicate future modifications in the treatment of ligament and tendon injuries.

Footnotes

Winner of the 1999 Excellence in Research Award

Link

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