Chemical PE: The Long Awaited Evidence

“Big Girtha is know for his extreme PE and liberal use of Liquid C (generic Cialis), and it reportedly did very well for him, but your experience points to something that I have suspected all along: there’s no real substitute for hard work and it doesn’t seem these chemical solutions are actually shortcuts.”

That’s a good point about the Liquid C. It is an excellent way to build up pressure for girth work (Pressure is apparently important for girth work).

I used to use Liquid V, but found it gave me a headache and a ridiculously red face.

Liquid C is much better for people who experience these side effects.

3% of people get facial flushing with Cialis
11% with Levitra
10% with Viagra

People who want a small artificial boost without having to stick needles in their dicks might want to consider pursuing this avenue. It did not work for me unfortunately.

Your post got me thinking. Does anyone actually know why PE leads to growth? What are the current theories? Is it still a mystery?

I have read several “science of PE” type threads, but I cannot remember whether or not this question was ever answered in a satisfactory way.

London100:
The researcher was talking about the increase in girth and length
Was due to oxygenation of the smooth tissue. Do you know what a
Hyperbaric chamber is. It might be worth looking into a hyperbaric
Chamber that we encase the penis in and oxygenate it with pure
Oxygen O2 or Ozone O3. With a hyperbaric chamber the pressure
And temperature could be increased or decreased at will.
What are your thoughts.
I think hard work and consistency is still what it takes but this was just

N idea.

That is an awesome idea. I actually had something like that in the back of my mind.

There are at least three possible interpretations of the emails that I got sent:

(1) Oxygenation leads to hypertrophy and general penile growth

(2) Oxygenation leads to improved erectile function and this somehow leads to general penile growth

(3) The researcher is talking nonsense

I have already gone through my reasons for dismissing (3). This guy is a professor at a famous university and a developer of the “Kiel concept”, which appears to be a well-established cure for ED.

I don’t think (1) is correct either. I went onto google scholar and typed in the word “oxygenation” and the word “hypertrophy”. I could not find any connection between the two things.

I think (2) is probably closest to reality. I went onto google scholar and typed in the words “oxygenation” and “erection”. I have not yet had time to read any of the studies, but there appears to be a good connection between the two things.

Good oxygenation can apparently reverse ED in some patients.

What I am trying to say is that we need more info from professionals and clever people prepared to do a bit of light research.

The idea that you proposed could potentially work, but we need more info before anything like that could be attempted.

Everything that the professor says checks out:

“SILDENAFIL PRESERVES INTRACORPOREAL SMOOTH MUSCLE
AFTER RADICAL RETROPUBIC PROSTATECTOMY”
ERIC J. SCHWARTZ, PHILIP WONG AND R. JAMES GRAYDON

To prevent veno-occlusive dysfunction the focus has
been on the introduction of oxygenated blood to the corpora
cavernosa through the early use of pro-erectile therapy.
Negative pressure vacuum devices and intracorporeal injections
have been used with some success.

Nine of the 11 volunteers
(82%) who completed the study in this treatment arm showed
an absolute increase in smooth muscle content, while only 2
(18%) showed an absolute decrease.

Increased
oxygen tension, testosterone, insulin-like growth
factor 1 and endothelial growth factor have been associated
with protecting or increasing smooth muscle content.

So oxygenation can increase smooth muscle content.

According to the article quoted above:

Our unpublished data confirm this rate with
the finding of an incidence of smooth muscle of about 49% in
normal potent males in the general population.

So roughly half of your dick is smooth muscle and oxygenation can cause an increase in the size of smooth muscle.

I am still struggling to make sense of what the professor said:

The second thing is that I would not expect that the penile in total or the smooth muscle of the corpus cavernosum does induce an increase in penile length and circumference with chronic use of papaverine hydrochloride, because the relaxation of the smooth muscle of the corpora cavernosa becomes evident when it is relaxing and the penile length and circumference is increasing according to the tremendous arterial inflow with initiation of an erection.

This could potentially mean two things:

(1) The monkeys had more smooth muscle and hence more dick

(2) The monkeys had supernormal erectile function. They got so hard that the length and girth went up slightly. They had no more tissue in their dicks, just more blood.

I really hope the answer is (1), but I cannot be sure. I may email him again and try and get him to clarify that for me. I hope that he hasn’t stumbled upon this thread or my posts on pegym.

The article that I just referenced reinforces the testimony of the professor. It demonstrates that his ideas are backed up by independent researchers writing in the Journal of Urology. It demonstrates that his claims do not go against any accepted principle of medicine.

I am not too shore about the hyperbaric chamber BTW. I think that idea is a bit too zainy even for me.

Be careful when fooling around with high levels of O2.. It’s extremely explosive and requires special equipment/flow control to minimise the dangers..

I have no plans to start messing around with O2.

Oxygenation is required to preserve smooth muscle. Smooth muscle hypertrophy observed in people recovering from prostatectomy is just that : a recovery. If they could have spontaneous erections, those would work as well if not better than drug-induced erections.

"Hemodynamics of Penile Erection: III. Measurement of Deep Intracavernosal and Subtunical Blood Flow and Oxygen Tension"

ABSTRACT

Previous studies have shown that intracavernosal blood flow increases during penile erection, but little is known about intracavernosal hemodynamics. Using a previously developed canine model of erection, we measured intracavernosal blood flow and oxygen tension at 2 site s within the corpus cavernosum: directly beneath the tunica albuginea and deep within the cavernous tissue.

We chose to measure oxygen tension as an indicator of arterial blood flow. Penile erection was induced by pelvic nerve stimulation as well as by injection of papaverine and phentolamine. In the flaccid penis, blood flow measured directly under the tunica albuginea was significantly higher than deep intracavernosal blood flow. Subtunical oxygen tension in the flaccid penis was consistent with a largely arterial circulation. These observations provide physiological evidence of an important subtunical circulation that carries most of the intracavernosal blood flow when the penis is flaccid.

With pelvic nerve stimulation, deep intracavernosal blood flow increased significantly followed by an increase in oxygen tension. Oxygen tension deep within the corpus cavernosum increased during penile erection from a level consistent with venous blood to a level consistent with arterial blood. Injection of papaverine and phentolamine caused a significant increase in intracavernosal pressure and a significant decrease in subtunical blood flow but did not cause statistically significant change in intracavernosal blood flow or oxygen tension. In contrast to nerve-induced erection, pharmacologically induced erection appears to depend more on intracavernosal shunting of blood than on increased total arterial blood flow to the penis.

Hypogastric nerve stimulation during established erection caused detumescence by contracting cavernosal smooth muscle, reducing deep cavernosal blood flow and reestablishing blood flow through the subtunical space. Our observations suggest that the subtunical space contains an important circulation that may play a role in the hemodynamics of the flaccid, as well as the erect, penis.

Investigative Urology | Journal of Urology

Even partial spontaneous erections are enough to preserve penile structure:

"CONCLUSIONS:

Significant increases in cavernosal oxygenation occur in the earliest stages of erection at relatively low ICP. These findings suggest that partial erections may be sufficient to oxygenate erectile tissue and protect it from prolonged hypoxia-induced damage."

http://www.ncbi … pubmed/19686425

Hyperoxygenation does not induce hypetrophy; hypoxia is a known cause of hypetrophy; alternating hypoxia with restored oxygenation promotes growth:
Reoxygenation after severe hypoxia induces cardiomyocyte hypertrophy in vitro

Prolonged hypoxia cause pathologic hypetrophy/hyperplasia and in the long run necrosis and atrophy.

Increased oxygenation (which is conceptually different than increased pressure, BTW) does not lead to hypertrophy per se. The very same hyperbaric therapy is doubious at least, but we are divagating now.

Enlarging the tunica albuginea in people who can have erections is all what is needed to enlarge the penis: you don’t need to increase the smooth muscle; and adversely, increasing smooth muscle will not lead to any measurable increase to size, since the limiting factor will always be tunica albuginea (at least in healthy males):

A new technique for augmentation phalloplasty: albugineal surgery with bilateral saphenous grafts—three years of experience.
Austoni E, Guarneri A, Cazzaniga A.
Source

Division of Urology, University of Milan, Ospedale S Giuseppe, Via S Vittore 12, 21123, Milan, Italy. edoardo.austoni@oh-fbf.it
Abstract
OBJECTIVES:

Penile augmentation surgery is a highly controversial issue due to the low level of standardisation of surgical techniques. The aim of the study is to illustrate a new technique to solve the problem of enlarging the penis by means of additive surgery on the albuginea of the corpora cavernosa, guaranteeing a real increase in size of the erect penis.

METHODS:

Between 1995 and 1997, 39 patients who requested an increase in the diameter of their penises underwent augmentation phalloplasty with bilateral saphena grafts. The patients considered eligible for surgery were patients with either hypoplasia of the penis or functional penile dysmorphophobia. All the patients included in our study presented normal erection at screening. The average penis diameter in a flaccid state and during erection was found to be 2.1cm (1.6-2.7 cm) and 2.9 cm (2.2-3.7 cm), respectively. Before surgery the patients were informed of the experimental nature of the surgical procedure. The increase in volume of the corpora cavernosa was achieved by applying saphena grafts to longitudinal openings made bilaterally in the albuginea along the whole length of the penis.

RESULTS:

No major complications and specifically no losses of sensitivity of the penis or erection deficiencies occurred during the post-operative follow-up period. All the patients resumed their sexual activity in 4 months. A measurement of the penile dimensions was carried out 9 months after surgery. No clinical meaningful increases in the diameter of the flaccid penis were documented. The average penis diameter during erection was found to be 4.2 cm (3.4-4.9) with post-surgery increases in diameter varying from 1.1 to 2.1cm (p<0.01).
CONCLUSIONS:

The penile enlargement phalloplasty technique with albuginea surgery suggested by the authors definitely is indicated for increasing the volume of the corpora cavernosa during erection. Albuginea surgery with saphena grafts has been found to be free from aesthetic and functional complications with excellent patient satisfaction.

http://www.ncbi … pubmed/12234509

Similar:
[Experimental study of augmentation phalloplasty using tunica vaginalis grafts in bilateral albuginea of penile corpus].
[Article in Chinese]
Xie J, Liu JH, Fan LC, Wu JT, Wang T, Wang SG, Ye ZQ.
…..
CONCLUSION:

The augmentation phalloplasty technique with bilateral autogenous tunica vaginalis grafts was proved to be effective and reliable with few complications, particularly conspicuous in increasing the volume of the erectile tissues during erection.
http://www.ncbi … pubmed/17201254

So : a) drug induced erections don’t cause more oxygenation than even partial spontaneous erections; b) even if a) wasn’t true, smooth muscle hypertrophy wouldn’t be an outcome; c) even if both a) and b) were false, penis enlargement wouldn’t be a consequence because the limiting factor would alwasy be tunica albuginea.

So what Her Professor said doesn’t makes sense and is consistent with a near complete misunderstanging of the articles and threads reffered by the OP. The ‘He couldn’t check the increase because it wasn’t their starting goal and they didn’t record starting size’ doesn’t makes sense either, since there was a control group of monkeys.

To be honest, I’m starting to be skeptical about the author of those emails.

Good to have you back Marinera!

“Hyperoxygenation does not induce hypetrophy”
“Increased oxygenation (…) does not lead to hypertrophy per se.”

These two statements are contradicted by the quote in the “Sildenafil Preserves…” article:

“Increased oxygen tension… [has] been associated with protecting or increasing smooth muscle content.”

I admit that I don’t know whether or not that is only true for people with damaged or shrunken smooth muscles, but I suspect that it is true of the general population.
In “Sildenafil Preserves…” they give people viagra, which means more blood, which means more oxygen, which means more smooth muscle.

“The very same hyperbaric therapy is doubious at least, but we are divagating now.”
I admit that the hyperbaric chamber thing is a ludicrous idea. It was not my idea.

This quote that you posted is quite troubling for my argument:

“Injection of papaverine and phentolamine caused a significant increase in intracavernosal pressure and a significant decrease in subtunical blood flow but DID NOT CAUSE statistically significant change in intracavernosal blood flow or OXYGEN TENSION. In contrast to nerve-induced erection, pharmacologically induced erection appears to depend more on intracavernosal shunting of blood than on increased total arterial blood flow to the penis.”

The “Sildenafil Preserves…” study says this:

“To prevent veno-occlusive dysfunction the focus has been on the introduction of OXYGENATED BLOOD to the corpora cavernosa through the early use of pro-erectile therapy. Negative pressure vacuum devices and INTRACORPOREAL INJECTIONS have been used with some success.”

So basically, my study says that using injectable ED meds will give the dick more oxygen and this will increase smooth muscle content. Your study appears to be saying the direct opposite. Your study could be considered more authoritative because it is focused directly on measuring oxygen content. My study could be considered more authoritative because it is newer (2004 vs. 1995). I have no idea which study is right and which is wrong (the most likely is that they are somehow both right).

I will try and get my head around this weird contradiction. I will read the first article that you posted.

There actually was no control group of monkeys is the papaverine study.

“To be honest, I’m starting to be skeptical about the author of those emails.”

I will PM you his name so that you can read up on him if you want. I assure you that he looks pretty legit.

I just typed his name into google scholar. He is the author of loads of studies published in good peer-reviewed journals.

Today I paid $20 for an online consultation with a urologist. I tried to ask for his opinion about all this. He closed the chat window and refused to talk to me.

If anyone is currently under the care of a professional urologist they could potentially print the first page of this thread out and show it to them.

It would be excellent to get a professional opinion.

It would help all of us, not just people interested in CPE.

I admire your go-get-it mentality.

There is no contradiction, it is just a matter to understand words : ‘to preserve’ means to avoid loss of what you have - it is not synonimous of ‘to enlarge’. ‘Recovery’ means coming out of an illness - so the subjects where not healthy. If you lay on a bed for 9 months, your muscle get atrophied; then if you simply go out of bed, just standing, your muscles start to get back. The mistake you are doing is like looking at this guy who go out of bed after a prolonged immobilization, and make the conclusion : "Getting out of your bed is enough work to become Mr. Olympia.".

About the control group, right there weren’t in the study you posted. But there were in pretty identical subsequent studies:

Local and systemic effects of chronic intracavernous injection of papaverine, prostaglandin E1, and saline in primates.
Aboseif SR, Breza J, Bosch RJ, Benard F, Stief CG, Stackl W, Lue TF, Tanagho EA.
Source

Department of Urology, University of California School of Medicine, San Francisco 94143.
J Urol. 1989 Aug;142(2 Pt 1):403-8.
Abstract

To compare the local and systemic effects of chronic intracavernous injection of papaverine, prostaglandin E1, and saline on erectile tissue, eight pigtail monkeys underwent 75 injections over a nine-month period. Monkeys were divided into three groups; each group received papaverine (10 mg.), prostaglandin E1 (20 micrograms.), or saline (one ml.).

The erectile response was closely observed for two hours after each injection to monitor the onset, degree, and duration of erection. Liver function tests were performed every three months to detect early systemic metabolic changes. After sacrifice, the simian penises were perfused in situ and examined histologically with both light and electron microscopy. Papaverine resulted in an initially strong erectile response, but this was maintained throughout the length of the study in only two monkeys.
In contrast, prostaglandin E1 resulted in tumescence that was maintained in all monkeys over the nine-month period.

In addition, the papaverine group had elevated liver enzymes and significant histologic changes with loss of normal architecture on both light and electron microscopy. The other two groups showed only minimal histologic changes or none.
http://www.ncbi .nlm.nih.gov/m/ … 3669186/related

Histopathological change of corpora cavernosa after long-term intracavernous injection.
Authors
Hwang TI, Yang CR, Ho WL, Chu HW.
Journal

Eur Urol. 1991;20(4):301-6.
Affiliation

Department of Surgery, Taichung Veterans General Hospital, Taiwan, ROC.
Abstract

Repeated intracavernous injections in healthy monkeys with 2 kinds of vasoactive agents [papaverine and prostaglandin E1 (PGE1) 3 monkeys each] and normal saline (2 monkeys) were conducted in this study.

The purpose was to observe the effect of long-term injection on histopathological changes of the cavernous tissue, as well as the change in drug sensitivity (dosage dependence). Different dosages of the same volume (double, single and half dose) of these 3 agents were injected, twice weekly, 10 times alternatively, with rigidity and maintenance of erection recorded.

After long-term injection (papaverine group: 37, 60, 60 times; PGE1 group: 26, 60, 60 times; normal saline group: 60, 60 times), all monkeys were sacrificed and the penises were collected for light-microscopic (LM) and electron-microscopic (EM) examinations. Dose-dependent response with reversed drug sensitivity was found in the papaverine group, but only elongation to tumescence was found in the PGE1 group, even with double dosage (probably because of scarce PGE1 receptors in monkey’s penile tissue).

Histopathologically, mild to moderate fibrotic changes and distortion of normal architecture were predominant findings in LM while aggregation of mitochondria, irregular shape or atrophy of cells were obvious in EM observation in the papaverine group. On the other hand, limited fibrosis with preservation of corpora cavernosa and hypertrophy of smooth muscle were noted in the PGE1 group. This study indicated that less histopathological change occurred in the PGE1 group after long-term intracavernous injection.

http://www.ncbi .nlm.nih.gov/m/ … 3669186/related

Look that the study you are basing your hopes on is the oldest of them all; it is actually a 25 years ago study. When you read it in light of the subsequent studies, you understand that the ‘hypertrophy of smooth muscle’ they observed in healthy monkeys was instead a pathologic change, consequence of likley too high and frequent dosis - one of the monkeys died after 56 injections, maybe a coincidence maybe not.

In subjects with atrophied penis, drug erections can make recovery easier; but that is not something that you can call ‘growth’ or enlargement - people who don’t get drugs do recovery as well and show ‘smooth muscle increase’, ‘higher oxygenation’ etc. etc.; they are gettin back what they had lost, they are not growing bigger than before.

Look also that no one reported increased size of the penis - differently from what your Professor ‘Thinks.’. After 25 years he ‘think’ the monkeys’ penis increased? You can’t be serious.

Listen, you can sign in one of the many ED forums on the net and see by yoursel how many people are speaking of a bigger penis thanks to viagra, cialis or whatever. Cherry picking studies older than Moyses, trying to make them fit what you hope, this can be funny and nothing else.