This document provides an overview of the physiology of erection. It begins with a brief historical context of erectile dysfunction and theories of erection. The key anatomical structures involved in erection are then described, including the arteries, veins, nerves, smooth muscle, and hormonal factors. The molecular mechanisms of smooth muscle contraction and relaxation are explained, with a focus on the role of nitric oxide signaling. Finally, the types of erection and signaling molecules beyond nitric oxide that can induce smooth muscle relaxation are summarized.
Fundamentals of pelvis, perineum and male genitalia anatomy. contains short notes with atlas. easy for self study of preclinical and clinical students and residents. clinically important common correlations are included. well animated power point presentation.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
2. Moderators:
Professors:
Prof. Dr. G. Sivasankar, M.S., M.Ch.,
Prof. Dr. A. Senthilvel, M.S., M.Ch.,
Asst Professors:
Dr. J. Sivabalan, M.S., M.Ch.,
Dr. R. Bhargavi, M.S., M.Ch.,
Dr. S. Raju, M.S., M.Ch.,
Dr. K. Muthurathinam, M.S., M.Ch.,
Dr. D. Tamilselvan, M.S., M.Ch.,
Dr. K. Senthilkumar, M.S., M.Ch.
Dept of Urology, GRH and KMC, Chennai.
2
3. HISTORICAL ASPECT
• The first description of erectile dysfunction (ED) dates from about 2000 BC and was set
down on Egyptian papyrus. Two types were described: natural (“the man is incapable of
accomplishing the sex act”) and supernatural (evil charms and spells).
• Hippocrates reported many cases of male impotence among the rich inhabitants of
Scythia and ascribed it to excessive horseback riding
• Aristotle - erection is produced by the influx of air.
• Ambroise Paré - accurate account of penile anatomy and the concept of erection.
• Hunter (1787), thought that venous spasm prevented the exit of blood
• Wagner (1981) - increased arterial flow and decreased venous drainage during erection.
3
Dept of Urology, GRH and KMC, Chennai.
4. FUNCTIONAL ANATOMY
• Penis - 2 corpora cavernosa &
corpus spongiosm , encased
with tunica, bucks fascia,
dartos fascia & skin.
• Function – Urinary and
Sexual 4
Dept of Urology, GRH and KMC, Chennai.
5. SKIN OF PENIS
• Penile skin :- Very mobile as its dartos fascia
backing is very loosely attached to Buck fascia.
Highly elastic, without appendages & fat.
• Uncircumcised men:- The prepuce (foreskin) is
the penile skin as it folds over the glans and
attaches below the corona.
5
Dept of Urology, GRH and KMC, Chennai.
6. FASCIA OVER PENIS
DARTOS FASCIA(superficial
fascia)
of colle's fascia in the
• Continuation
perineum
• Extends from base to prepuce
• Loosely attached to skin & deeper buck’s
fascia
• Contains superficial arteries ,veins &
nerves
BUCKS FASCIA (deepfascia)
• Tough elastic layer immediately adjacent to
tunica albuginea.
• The corpora cavernosa are surrounded by Buck
fascia dorsally.
• Buck fascia splits corpus spongiosum
ventrally.
• Deep dorsal vein, Dorsal artery & Dorsal nerve
are contained within bucks fascia.
• Distally attached to glans.
6
Dept of Urology, GRH and KMC, Chennai.
7. TUNICA ALBUGINEA
Bilayered
• Inner layer - Circular, Intra cavernosalpillars
• Outer layer - Longitudinally oriented, Absent between 5- 7° clock
• Emissary veins – between two layers, outer layer compress emissary veins during erection.
W
ithErection,aretightlystretched, and
in theflaccid state theyforman
undulatingmeshwork
Radiating from this inner layer are
intracavernous pillars that act as struts to augment theseptum
and provide essential support to the erectile tissue
The most vulnerable area is located on the ventral groove (between the 5
o’clock and 7 o’clock positions), where the longitudinal outer layer is absent;
most prostheses tend to extrude here
7
Dept of Urology, GRH and KMC, Chennai.
8. CONTENTS OF TUNICA ALBUGINEA
Fibrillar collagen
(mostly type I but also type III)
Collagen has a greater tensile strength
than steel, it is unyielding.
Elastin fibers
• Elastin can be stretched up to 150% of
its length. The elastin content allows
tunical expansion and helps to
determine stretched penile length.
CORPUS SPONGIOSUM
• Lacks an outer layer or intracorporeal struts
• Ensures low pressure structure during
erection
8
Dept of Urology, GRH and KMC, Chennai.
9. • Emissary veins – oblique directed
between two layers compressed
during erection
• Cavernous Artery & branches of dorsal
artery – more direct route and
surrounded by periarterial soft tissue
sheath
• Protects the arteries from occlusion by tunica
albuginea during erection
9
Dept of Urology, GRH and KMC, Chennai.
10. LIGAMENTS
• Suspensory— Arises from Buck fascia and consists of two lateral bundles and one median bundle, which
circumscribe the dorsal vein of the penis. Main function - to attach the tunica albuginea of the corpora
cavernosa to the pubis. Provides support for the mobile portion of the penis
• Fundiform– Arises from Colles’ fascia and is lateral, superficial, and not adherent to the tunica albuginea of the
corpora cavernosa
• Penile elongation surgery –
suspensory ligament is severed
• Congenital deficieny of
suspensory ligament – unstable
penis / drooping penis
10
Dept of Urology, GRH and KMC, Chennai.
11. CORPORA CAVERNOSA
• Paired cylinders & conglomeration of sinusoids
• Sinusoids – separated by smooth muscle cells,
connective tissues, collagen, arterioles, venules and
terminal nerves
• Crura - Proximal ends, covered by ischiocavernosus
muscle, originate at the undersurface of the
puboischial rami as two separate structures but
merge under the pubic arch (distal to pubic
symphysis) and remain attached up to the glans.
CORPUS SPONGIOSUM
• Single, contains urethra
• Extends – bulb to glans
• Sinusoids are larger
• Tunica is thinner, lacks outer layer &
intracorporeal struts
• Bulb - fixed to perineal membrane , covered by
bulbo spongiosus, narrows to form corpus
spongiosum.
11
Dept of Urology, GRH and KMC, Chennai.
12. PENILE COMPONENTS & THEIR
FUNCTION DURING ERECTION
12
Dept of Urology, GRH and KMC, Chennai.
14. ARTERIAL SUPPLY
• Bulbo urethral artery – urethra, spongiousm & glans
• Cavernosal artery -cavernoussinus
• Dorsal artery – below the bucks fascia & between dorsal nerves, supplies glans
• Gives circumflex branches which encircle corpora and provide rich blood supply.
14
Dept of Urology, GRH and KMC, Chennai.
15. ARTERIAL SUPPLY
• Dorsal artery - Engorgement of the
glans during erection
• Cavernous artery effects tumescence of
the corpus cavernosum
• Eners it at the hilum of the penis,
where the two crura merge
• Gives off many helicine arteries
supply the trabecular erectile tissue
and the sinusoids
• Helicine arteries are contracted and
tortuous in the flaccid state
• Dilated and straight during erection
15
Dept of Urology, GRH and KMC, Chennai.
16. ARTERIAL SUPPLY
Three patterns of penile arterial supply:
Type I - airising exclusively from internal pudendal arteries
Type II- arising from both accessory and internal pudendal arteries
Type III - arising exclusively from accessory pudendal arteries
Accessory arteries from
External iliac
Obturator
Vesical
Femoral
• ED - Accessory pudendal artery
• The importance of accessory pudendal artery preservation during radical
prostatectomy was demonstrated by Mulhall and colleagues (2008), who reported
more rapid recovery of sexual function in men who underwent artery-sparing
radical prostatectomy.
16
Dept of Urology, GRH and KMC, Chennai.
20. VENOUS DRAINAGE
• Glans Deep dorsal vein
• C. Spongiosum Circumflex, urethral,& bulbar veins
• C. Cavernosa Mid & distal shafts to Deep dorsal vein
• Proximal to cavernousal & crual veins
• Skin Superficial dorsal vein in turn to saphenous veins
20
Dept of Urology, GRH and KMC, Chennai.
21. NERVESUPPLY
SOMATIC
Primarily responsible for sensation& contraction of bulbocavernous and
ischicavernousmuscle
Sensory receptors – Penile skin, glans, urethra and within corpus cavernosum
FREE NERVE
ENDINGS
Adelta & C fibres
Dorsal nerve of penis
+ Cavernous Nerve
PUDENDAL NERVE
ENTER SPINAL CORD
– S234 ROOTS
21
Dept of Urology, GRH and KMC, Chennai.
22. ONUF’S NUCLEUS – CENTRE
OF SOMATOMOTOR PENILE
INNERVATION
SPINOTHALAMIC &
SPINORETICULUARPATHWAYS
THALAMUS & SENSORY
CORTEX
SENSORY PERCEPTION – PAIN,
TEMPERATURE,TOUCH
Contraction of the ischiocavernosus
muscles produces the rigid-erection
phase.
Rhythmic contraction and compression
of the bulbocavernosus muscle on the
proximal corpus spongiosum helps
semen expulsion
Impairment of bulbocavernosus and
ischiocavernosus muscles may
impair erection
22
Dept of Urology, GRH and KMC, Chennai.
23. NERVE SUPPLY -
SYMPATHETIC
Sympathetic T11-L2
Sympathetic trunk
Inf. Mesentric &
Sup.Hypogastric
plexus
Hypogastric nerves
Pelvic Plexus
vasoconstriction, contraction of
the seminal vesicles and prostate,
and seminal emission
NERVE SUPPLY :-
PARASYMPATHETIC
S2S3S4
Pelvic splanchnic
nerves
(nervi erigentes)
Pelvic plexus
Preganglionic neurons
synapse to give post
ganglionic cavernous
nerves.
Produces vasodilataion
EJACULATION& DETUMESCENCE ERECTION 23
Dept of Urology, GRH and KMC, Chennai.
30. ROLE OF HORMONES
• Androgens
• Act on hypothalamus, important site for modulation of erection.
• Modulate synaptic transmission, synthesis, uptake & release of neurotransmitters
• Deficiency – loss of sexual interest, impaired seminal emission & reduced nocturnal
erection
30
Dept of Urology, GRH and KMC, Chennai.
31. TYPES OF ERECTION
Nocturnal
Occurs Cholinergic neurons in
lateral
Pontine tegmentum is activated
whereas adrenergic neurons in
locus coeruleus & steronergic
neurons in midbrain are silent.
This differential activation
results in nocturnal erection
in REM sleep.
Psychogenic
Fantasy or
audiovisual stimuli.
Impulses from brain
spinal centers
external genitalia
Reflexogenic
Tactile stimuli
pudendal nerves
sacral dorsal horn &
dorsal gray commissure
processed by
interneurons
parasympathetic
cavernous & dorsal
nerves
PRESERVEDIN UPPER SPINAL INJURY
31
Dept of Urology, GRH and KMC, Chennai.
33. MECHANISMOF ERECTION
Smooth muscles relax
Artreial fiow increases
Sunusoidial expansion
Compression of sub tunical &
emissary veins
Reduction of flow Erection
In contrast to many other smooth muscles, corpus cavernosum smooth
muscle is in a contracted state most of the time. 33
Dept of Urology, GRH and KMC, Chennai.
34. MOLECULAR MECHANISM OF SMOOTH
MUSCLE CONTRACTION
1. Cytosolic Free Calcium.
2. Rho Kinase Signaling Pathway
(Calcium Sensitization Pathway)
3. Latch State: A Unique Characteristic of
Smooth Muscle Contraction
4. Pathways Involving Inositol 1,4,5-
Triphosphate, 1,2- Diacylglycerol, and
Protein Kinase C
34
Dept of Urology, GRH and KMC, Chennai.
37. Three isoforms -
nNOS,eNOS, iNOS
nNOS initiating erection
eNOS sustaining erection
NITRIC OXIDE
37
Dept of Urology, GRH and KMC, Chennai.
38. SMOOTHMUSCLE
PHYSIOLOGY:-
• Relaxation of the cavernous smooth muscle
is the key to penile erection.
• On entering the smooth muscle cells, NO
stimulates the production of cGMP.
• cGMP activates PKG, which opens the
potassium channels and closes the calcium
channels.
• Low cytosolic calcium favors smooth muscle
relaxation.
• The smooth muscle regains its tone when
cGMP is degraded by PDE.
38
Dept of Urology, GRH and KMC, Chennai.
39. OTHER SIGNALING MOLECULES
• CARBON MONOXIDE – activates guanylate cyclase by direct binding to heme moiety of the enzyme
• HYDROGEN SULFIDE – relaxation of corpus cavernosal smooth muscle
• NATRIURETIC PEPTIDE – In vitro studies – increases cGMP & relaxes cavernous smooth muscle by
binding to NPReceptor
39
Dept of Urology, GRH and KMC, Chennai.
40. PROSTAGLANDINS
• Eicosanoids capable of initiating numerous biological functions through G-Protein coupled receptors.
• Nine known prostaglandin receptor subtypes
• Four of the subtypes (EP1 to EP4) bind PGE2, two (DP1 and DP2) bind PGD2, and the other three subtypes
(FP, IP, and TP) bind PGF2α (FP), PGI2 (IP), and TXA2 (TP)
. On the basis of signaling attributes, the prostaglandin receptors are classified into three types.
“Relaxant” receptors IP, DP1, EP2, and EP4 are coupled to an αs-containing G protein and are capable of
stimulating adenylyl cyclase to increase intracellular cAMP.
“Contractile” receptors EP1, FP, and TP are coupled to an αq-containing Gprotein, which activates phospholipase C
increase of intracellular calcium
EP3 receptor is also a contractile receptor, but it is coupled to an αi-containing G protein that inhibits adenylyl
cyclase to result in a decrease of cAMP formation.
The erectogenic effects of PGE1 as a pharmaceutic agent have been extensively documented.
Intracavernous injection of PGE1 is one of the safest and most effective treatments for ED;
Transurethral application is an alternative. 40
Dept of Urology, GRH and KMC, Chennai.
41. PHOSPHODIESTERASE
• Termination of cyclic nucleotide signals
• Catalyze the hydrolysis of cAMP and cGMP to AMP and GMP, respectively
• Feedback mechanisms that increase PDE activities and/or expression by the increased cyclic nucleotide level assist cyclic
nucleotide degradation
• 11 families (PDE1 to PDE11) that are encoded from 21 distinct genes
• PDE1, PDE2, PDE3, PDE10, and PDE11 hydrolyze cAMP and Cgmp
• PDE4, PDE7, and PDE8 hydrolyze cAMP
• PDE5, PDE6, and PDE9 hydrolyze cGMP
With the exception of PDE6, which is specifically expressed in photoreceptor cells, all PDEs have been identified in the corpus
Cavernosum
PDE5 is the principal PDE for the termination of cavernous cGMP signaling and inhibition of the cGMP-
catalytic activity by PDE5 inhibitors is highly effective in treating ED.
PDE3 also appears to play a role in erection - erectogenic effect of a PDE3-specific inhibitor, milrinone
41
Dept of Urology, GRH and KMC, Chennai.
42. MOLECULAR OXYGEN AS A
MODULATOR
The PO2 level of cavernous blood in the flaccid state is similar to that of venous blood (≈35 mm Hg).
During erection, the large inflow of arterial blood increases PO2 to approximately 90 mm Hg
Molecular oxygen is a substrate, together with L-arginine, for the synthesis of NO by NOS
flaccid state low oxygen concentration inhibits NO synthesis
erection higher level of substrate induces NO synthesis
Minimal concentration of oxygen in the cavernous bodies necessary to reach full NOS activity is 50 to 60 mm Hg
Prostaglandin H synthase is also an oxygenase (cyclooxygenase) and uses oxygen as substrate for the synthesis of prostanoids.
Production of PGE1 has been shown to be inhibited in flaccidity and stimulated during erection
Endothelin synthesis is also modulated by oxygen
low oxygen concentration promotes production, whereas a high concentration inhibits it.
42
Dept of Urology, GRH and KMC, Chennai.
43. INTERCELLULAR COMMUNICATIONS
Presence of gap junctions in the membrane of adjacent muscle cells
Intercellular channels allow exchange of ions such as calcium and second-
messenger molecules
Connexin-43, a membrane-sparing protein of less than 0.25 μm - Identified between
smooth muscle cells of human corpus cavernosum
Cell-to-cell communication through these gap junctions most likely explains the
synchronized erectile response
43
Dept of Urology, GRH and KMC, Chennai.
48. PHASES OF ERECTION
Flaccid
Phase:
• Minimal arterial and venous flow
• Blood gases values similar to venous blood
Latent
phase
• Increased flow in int.pudendal artery during both systolic and diastolic phases
• Decreased pressure in int.pudendal artery
• Unchanged intracavernous pressure
• Some elongation of penis
Tumescen
t phase
• Rising intracavernous pressure until full erection achieved.
• Penis shows more expansion and elongation with pulsation.
• With rise in pressure arterial flow decrease and flow occurs only during systolic phases.
Full
erection
phase
Skeletal or
Rigid
erection
Phase:
• Intracavernous pressure rises 80-90% of systolic pressure
• Int pudendal atrery pressure increase but remains slightly below systemic pressure
• Arterial flow remains low but still remains higher than flaccid phase
• Venous channels compressed but still higher than flaccid phase. Blood gas values approaches to that of arterial blood
• Ischiocavernous mus contraction causes rise in pressure well above the systolic pressure lead to rigid erection
• Almost no blood flows through cavernous artery
• As the duration is short so no ischemia or tissue damage
Detume
scent
Phase:
• After ejection or cessation of erotic stimuli, sympathetic tonic discharge resumes.
• Result - tonic contraction of smooth muscle against closed venous system slow reopening of venous channels
resumes basal arterial flow fast pressure decrease with fully restored venous outflow from sinusoids.
• Penis returns to it flaccid length and girth. 48
Dept of Urology, GRH and KMC, Chennai.
49. HEMODYNAMIC CHANGES IN CORPUS
SPONGIOSUM & GLANS DURING
ERECTION
Arterial flow increases, BUT Pressure in the corpus spongiosum and glans is
only one third to one half that in the corpora cavernosa because the
tunicalcovering, which is thin over the corpus spongiosum and virtually absent
over the glans, ensures minimal venous occlusion.
Full-erection phase - partial compression of the deep dorsal and circumflex
veins between Buck fascia and engorged corpora cavernosa glanular
tumescence
Rigid-erection phase - ischiocavernosus and bulbocavernosus muscles forcefully
compress the spongiosum and penile veins, resulting in further engorgement
and increased pressure in the glans and spongiosum 49
Dept of Urology, GRH and KMC, Chennai.