Dear listeners! Warning: this course contains shocking materials and is not recommended for viewing to persons with weak psyche, minors and pregnant women. The course describes subject and methods of Pathophysiology, its place within system of biomedical sciences and history. It includes General Nosology (concept of health and disease, general etiology and pathogenesis, pathological processes and states, role of causal factors, conditions, reactivity and somatotype in pathology). It gives systematic of locally and centrally driven typical pathological processes: arterial, venous and combined hyperemiae, stasis, inflammation, immunopathological processes (including allergy and autoimmune disorders) acute phase response, fever, stress, shock, etc. Course deals with functional, metabolic and informational aspects of typical pathologic processes, like disorders of signaling, reception, post – receptor translation, programming and program archiving, conflicts of programs in living systems. It contains the consequent analysis of the injury and defensive responses as regards separate cells, organs and tissues and the whole organism. The lectures based on author’s original three-volumed textbook and workshop in Pathophysiology republished in Russia many times.
4_4 "Arterial (Active) Hyperaemia"
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來自 Saint Petersburg State University 的課程
General Pathophysiology
17 個評分
從本節課中
Locally driven typical pathological processes. Pathophysiology of microcirculation
與講師見面
Churilov Leonid PavlovichAssociate Professor, Full Member of International Academy of Sciences (Health and Ecology)
Department of Pathology, Faculty of Medicine
The next part of our talk is devoted to the pathogenesis of active Hyperaemia.
First, about Methods of Arterial Hyperaemia Registration in Experiment and in Clinics.
Active hyperaemia both in clinics and in experiment can be
investigated and registered visually by means of either biomicroscopy,
as you can see in this picture,
or by means of infrared monitoring or thermovision.
Because in active hyperaemia,
organs or tissues produce much more warm,
much more infrared radiation.
And you can see here,
active hyperaemia and palmer erythema registered in
skin of the hand by means of infrared monitoring.
As you can see, sometimes medical doctor can even evaluate it visually
and oculus without any instruments like in this photo of palmer erythema,
characteristic for a patient with liver cirrhosis.
In liver cirrhosis, liver is not able destroy
rapidly certain circulating vasodilating biogenic amines,
and they produce this symptom palmer erythema in cirrhosis.
And in neighboring picture,
you can see acute conjunctivitis after melogic disease,
inflammation of eye conjunctiva,
and the degree of arterial dilation can be evaluated visually.
Here, you can see thyroid gland.
In left picture, it is normal thyroid, in right picture,
it is thyroid in hyperthyroidism in so-called
"thyrotoxic goiter" or Grave's [inaudible] disease.
You can see that it produces
much more infrared radiation and as a result of active hyperaemia,
it can be registered by means of infrared monitor.
Now, look at this scheme.
This is detailed scheme of the pathogenesis of active hyperaemia.
And the main thing, of course,
is increase of both volumetric and linear blood flow velocity,
as a result of dilatation of arteriolar and opening of precapillary sphincters.
That's why both inflow and outflow of blood are increased and
equal in active hyperaemia arteriolae and venulae are dilated,
number of working capillaries is increased,
but their diameter stays unchanged, remains unchanged.
The Delta P, difference of hydrostatic pressure
between arteriolae and venulae and of the system is increased.
That's why there is increase in blood speed.
You can see all that in dynamics in this movie.
And while you are watching the movie,
let me remind that there are three different pathogenic types of active hyperaemia.
First of them is called myoparalytic,
and it is caused by
so-called myoparalytic mechanism which
is associated with decreased vascular myogenic tone under
the humoral local influence
of either metabolites produced by working organ,
or tissue, or by autacoids of inflammation which are able to
broaden the arteriolae and relax smooth muscle cells of the sphincters.
It is the most common mechanism of active hyperaemia,
because in small arteries and the arteriolar,
myogenic tone prevails over neurogenic one.
And this mechanism is leading in the development of physiological,
functional, working functioning arterial hyperaemia in working organs.
But also, it is prevailing in pathology because in inflammation,
arterial hyperaemia also belongs to myoparalytic mechanism and it is
resulted from the influence of vasodilating mediators of the inflammation.
You can see in this picture the example of
myoparalytic hyperaemia of person's cheek after the slap.
Because slap, as mechanical alteration
produces short and light inflammation of the slapped area.
The next mechanism is neuroparalytic one.
As you can judge upon the name, neuroparalytic,
it is related somehow with nerves and disorder of neuroregulation.
Look at the example cold blush.
Cold blush is typical example of neuroparalytic mechanism of arterial hyperaemia,
because it consists in reducing of
neurogenic constrictor influence and fall of neurogenic vascular tone.
This occurs after transection of nerves,
or it can occur in paralysis,
or in damage of vasoconstrictor nerves,
as well as in damage of their neuro centers.
So, lack of vasoconstrictor neurogenic influence produces
these neuroparalytic arterial hyperaemia in the rated area.
And you know so-called "signs of lightning" in electric shock,
they also belong to the particular example of
neuroparalytic arterial hyperaemia under the influence of electric charge or lighting.
The last mechanism of arterial hyperaemia is neurotonic one.
Neurotonic hyperaemia also is related to
neuroregulation but in different way, in different mode.
Neuroparalytic is lack of vasoconstrictor influence,
and neurotonic mechanism is due to active reflexes with vasodilating nerves.
It can result from increased vasodilator activity or it can result from
active decrease of vasoconstrictor tone by true reflex or axon reflexes.
And it occurs not everywhere in the organism.
You should not over estimate the role of neuroregulation,
especially as regards to local phenomena.
Well, in fact it is actual only for certain organs and tissues
under the influence of the sympathetic vasodilators arterial hyperaemia again no cure.
For example, in pancreas,
and in salivary glands during digestion process,
or it can be involved in phenomenon of erection in cavernous bodies.
Vascular skin reactions used for thermoregulation also use this neurotonic mechanism.
And as you can see in this picture,
neurotonic arterial hyperaemia underlies so-called
"flush of shame or flush of anger."
If you are ashamed,
your cheeks get red already even without slaps because of neurotonic mechanism.
Well, neurotonic hyperaemia, unfortunately, are not nutritive.
So, blood flow through the organ increases,
but there is no adequate increase in metabolic intensity because the major part of
that blood in neurotonic hyperaemia goes through the
arterial venular shunts and bypass the capillary bed,
thus not increasing the tissue metabolism
and not increasing the functional ability of organ.
That's why football players, they
Perform some exercises before the game because they need nutritive hyperaemia.
They need myoparalytic hyperaemia with
the increase of capillary flow and neurotonic mechanism is not enough for them.
And even if every day they will play football the same time,
neural reflex will be not enough to establish functional mobilization,
because neurotonic mechanism can give non-nutritional hyperaemia only.
Nutritional hyperaemia with true increase in organ functional capability is
achieved only by means of myotonic mechanism, humoral mechanism.
Now, few words about those who were pioneers in the studies of active hyperaemia.
You can see Danish scientist, August Krogh.
In 1920, Krogh was awarded the Nobel Prize in Physiology or Medicine,
for the discovery of the mechanisms of regulation of the capillaries in skeletal muscle.
Krogh was the first who described the "functional arterial hyperaemia" in
working muscles and adaptation of
blood perfusion in muscle to the needs of functioning organ.
Krogh describe that by means of biomicroscopy.
But he mistakenly believed that the whole phenomenon of working arterial hyperaemia,
is resulted from neural reflexes.
In fact even if you will perform the narration of certain area,
function will produce dilatation of the arterial,
because the main mechanism for working hyperaemia as you
already know is not neurogenic but humoral myoparalytic one.
The blood vessels are broadened due to effect of
local metabolites produced by working cells and central link.
Central intervention of neural reflexes is not obligatory for that.
Local humoral regulation by myoparalytic mechanism can
establish working active hyperaemia in functioning organs.
The next pioneer in clinical studies of
arterial hyperaemia is a Russian scientist, Abram Solomonovich Zalmanov.
He is world famous,
not only because of his studies of arterial hyperaemia in patients,
but because he was active practitioner.
And he introduced artificial arterial hyperaemia
into the routine clinical practice as a method of physiotherapy.
He performed so-called turpentine baths
by means of turpentine oil added to hot water.
He induced skin Active Hyperaemia in blood vessels of his patients.
By the way, Vladimir Lenin,
the founder of Soviet Union was his patient.
And in our archives there were very positive reply of patients
learning about the methods and activities of Doctor Zalmanov.
Doctor Zalmanov was Krogh's disciple.
He studied Physiology under the guidance of Nobel Prize winner, Krogh.
And he decided to inculcate these methods into practical medicine.
He believed that active hyperaemia is a kind of washout, capillary wash,
for the organism helping to get rid of waste products of metabolism.
And he constructed quite original theory of aging of senescence,
because he insisted that there is a link between senescence and oxygen.
And periodic hyperaemia in his imagination,
was necessary in order to rejuvenate organs and tissues.
Zalmanov lived a very long life.
He started in Soviet Union and finished
as world famous practitioner in the United States,
with his turpentine baths and use of active hyperaemia for physiotherapeutic purposes.
Now, please look at these two persons,
Leon Abgarovich Orbeli and Alexandr Grigorievich Ginetsinsky.
These two scientists collaborating in
my Ama matter in Pediatric University of St. Petersburg.
In 1950, they described a very important phenomenon,
the so-called Orbeli-Ginetsinsky phenomenon.
What was it?
In presence of humoral vasodilating agents,
for example in presence of inflammatory mediators produced locally,
smooth muscle cells of arteriole
become resistant to central neural vasoconstrictive influences.
It was very important discovery.
It means that local humoral vasodilation can
prevail over central neural vasoconstrictor signal.
That's why, in hardwork,
when in overall circulation sympathetic tone is
dominating and activity of sympathetic nervous system is prevailing.
Well, in non-working areas of the organism we have vasoconstriction,
but in working muscles we still have
vasodilation in spite of central sympathetic vasoconstrictor signals.
Because in the working muscle according to Orbeli-Ginetsinsky phenomenon,
local humoral mediators can dominate over central signals.
Now, you can see in this movie,
how to open the access to
nervous ischiadicus in posterior leg of a frog.
When you put it here,
when you put it or there, here is [inaudible].
Doctors, scissors is best friend of part of physiologists, we almost never use a scalpel.
We do that and after that we transect this nerve.
And because in this nerve,
in ischiadicus nerve vasoconstrictor fevers are predominating.
After the dissecting of sciatic nerve,
you can find arterial hyperaemia,
dilation of blood vessels and acceleration of
blood flow in posterior leg inter-digital membrane,
which is recorded here in this photo.
Why after the dissection of sciatic nerve,
blood flow in posterior leg is accelerated and arterial hyperaemia occurs.
That is because the blood vessels get rid of vasoconstrictor neurogenic tonic influence.
It is so-called neural paralytic arterial hyperaemia.
That was for the first time demonstrated by French,
Claude Bernard and Austrian, Solomon Stricker.
And it is called Claude Bernard Solomon Stricker experiment first demonstration,
that there are nerves able to constrict blood vessels.
And you know modification of this experiment was performed by this person.
Recently we celebrated 100 jubilee of his birth.
That is Mauritian born French pathophysiologist, Charles-Edouard Brown-Sequard.
You can see him on postal stamp of his motherland,
now independent Island in Indian Ocean.
Brown-Sequard stimulated the nerve
of the rabbit by electric stimuli.
And by means of that,
he demonstrated that after electric stimulation,
the ear of a rabbit gets pallor
and this is a result of neurogenic ischaemia.
That was first a demonstration that active stimulation of
certain nerve can produce changes of microvascular dynamics.
