- Good morning.
I'd like to thank Rick
and John for inviting me
to speak today.
I said I have no disclosures,
but after listening to
Bob and Anita I realized
that I should disclose that
in the first part of my
career I was fortunate to have
Mike Harrison as my mentor,
in the later part of my
career, Bob Bartlett,
and I've watched Abe Rudolph
operate on fetal lambs.
And when I called him a
few years ago to talk about
the artificial placenta because
I had some questions about
fetal physiology that I didn't understand,
he thought I was pretty crazy, but Anita,
he did say good luck at the
end of the conversation.
So here goes.
So this is a Time
Magazine cover from 2014.
I was in the airport somewhere
already doing work on
the artificial placenta, and
I saw this and I grabbed it,
and I was so curious what
Time Magazine had to say
about prematurity.
And interestingly they
focused on a baby as I recall
who was over 28 weeks
estimated gestational age.
And in fact, neonatologists
should be very proud of
the fact that babies born after 28 weeks,
which are still premature,
they actually do quite well
these days, but babies born
below 28 weeks still have
a lot of problems.
And we call them ELGANs,
who are less than 28 weeks.
There's approximately 40,000 born a year.
To give you some perspective,
there's about 500,000
premature babies defined
as less than 37 weeks
born every year.
As we all know, the mortality
and morbidity is high.
Among long-term survivors
the medical problems
are significant, and it's
a very costly problem.
So I would argue that
ELGANs are still fetuses.
They have significant organ prematurity.
Their growth and development
should occur in a
low pO2 environment, fetal
circulation and no ventilation,
just like it does in the womb.
And the severe complications,
including lung disease,
neural developmental problems, NEC, etc.,
I would argue are largely
iatrogenic in our effort to
support these infants.
So the solution, this is
actually from the Matrix
if anyone remembers that.
This looks really cool.
I'm not sure we can replicate that.
So let me just mention this,
so this is very interesting.
Dr. Bartlett gave a nice
history of ECMO on the heels of
the invention of the heart-lung machine,
and interestingly way back
in the 1960s with the Beetles
on the cover of Life
Magazine work began on the
artificial placenta.
So back in the day before
we had more sophisticated
strategies for infants,
steroids, surfactin,
all types of ventilators,
researchers felt like
the premature infant is
the ideal patient for
extracorporeal support.
So this work off and on has
been going on for over 50 years.
In our iterations of
the artificial placenta
the key elements are maintaining
the fetal circulation,
providing the normal
fetal pO2 level and the
fetal environment.
A critical part is no
mechanical ventilation and
simulated breathing
with fluid filled lungs.
And I'll get to this in a
minute, but our iteration
involves a VV type of
extracorporeal support with inflow
via the umbilical vein and
outflow via the jugular vein.
And this is a picture of
the actual circuit with
jugular drainage.
We have a proprietary M-pump.
We use a commercially
available oxygenator,
umbilical vein reinfusion
and the sweep gas inlet.
This is a picture of the set
up in our experimental lambs,
and you will see an
endotracheal tube in the lamb,
but the lambs, the lungs are fluid filled,
and they're basically capped off.
So I did have early on in
this work a number of people
would ask me how is this
really different from ECMO?
So this is a table showing a
few of the major differences.
Obviously with ECMO the
circulation is postnatal.
We maintain fetal circulation.
A low versus a high pO2.
There's no ventilation.
The environment is
substantially different,
and the anticipated
duration would be long,
three to four weeks.
And as Dr. Bartlett pointed
out, we're working on methods
to avoid heparin, especially
in premature infants.
So this one slide sort
of 10 years of work.
We began this work using a
pumpless model of AV-ECLS,
and you can see in the
picture we cannulated the
umbilical vein and umbilical
artery just like nature does,
but we had lots of issues
with that approach.
So then we went to a pump
driven AV-ECLS approach,
and the major problem we had
was umbilical artery spasm.
And even when we bypassed
the umbilical artery to the
aorta of the animal, we still
had issues with hypotension.
So then we moved to the
cannulation strategy that
I mentioned, VV-ECLS with inflow
through the umbilical vein,
drainage through the jugular.
And we had these animals
submerged, so they were doing
in an amniotic type solution,
so they were doing fetal
breathing movements.
We had a lot of issues
with infection that we
couldn't solve, so we moved
to our current approach
which uses an endotracheal
tube and a variety of
different substances.
Actually most recently
we're using proflora decalin
in these animals, and that
seems to have the best effect
on lung development and
avoidance of trauma.
So next I'd like to just
highlight a few studies.
I won't get into the weeds
of them, but a few studies
that may be of interest to you.
So one of the studies we
did on last several years
was the artificial
placenta after a trial of
mechanical ventilation.
And the reason we did this
study is we thought okay,
what is the clinical
application of this technology?
And what we believe is a
premature infant would be born,
let's say a 24-weeker.
They would be intubated, resuscitated,
and if we had metrics,
which we're developing for
failure of that therapy,
then we would early on
convert them to the artificial
placenta, and we would see
if we could go back to fetal
circulation with no breathing.
So in this study, this
was several years ago,
we used slightly more
mature lambs, 130-day lambs.
We used heparin for anticoagulation.
We used low pressure
mechanical ventilation.
We had definition of ventilatory failure,
and I can tell you all of these
animals, even at 130 days,
they failed mechanical
ventilation within one hour.
They were already cannulated
for the artificial placenta,
so we then transitioned to
artificial placenta support.
So six of seven survived
at least 70 hours,
and the mean duration of
ventilation as I mentioned
was about an hour.
All failed due to hypercapnea,
and these are the mean
ABG values prior to going
on the artificial placenta
with very high pcO2 thoracidotic
with a high lactate.
So then these are the mean
hemodynamic ABG values
you can see on the ventilator
and on the artificial
placenta, and all of the
parameters normalized,
including the lactate.
And if you notice the pO2
of 38, that is actually
what we're targeting because
that's the normal pO2
of the fetus.
So the lessons we learned is
that the artificial placenta
can stabilize a moribund lamb
on mechanical ventilation.
It maintained and reinstituted
fetal circulation.
Gabe Owens was there doing the
echo, so he can confirm that.
Is that right?
True, okay.
They were hemodynamically stable.
They had good gas exchange,
and we also documented
adequate brain profusion.
So we next wanted to, I'll show
you a few more lung studies,
but thus far we've had major
focus on the lungs because
if the lungs don't do well, the baby dies.
The next organ we were very
concerned about was the brain.
So we hypothesized there
would be stable profusion
in this model, and we used
two different methods.
We used the transonic flow
probe on the carotid artery.
We used NIRS on the head.
So we had two different methods to assess
cerebral flow and profusion.
And if you look to the highlighted
areas, the carotid artery
flow was 23 versus 27
baseline on the placenta,
and our NIRS rSO2 was good at 49%.
So basically in these animals
we also studied their brain.
There was no evidence of brain bleeding,
and the data suggested
that brain profusion is
maintained on the artificial placenta.
This is one of our
favorite patients or sheep.
We called her Large Marge
because she was a little bit
large when she came out, and
this was a number of years ago.
She was also 130 days, and
she was maintained on the
artificial placenta only
for three days because
she was more mature.
And these are some of the
hemodynamic and ABG values.
So after three days of support
she was weaned to room air.
She was decannulated, recovered
in the lab for a week.
She was bottle-fed
every one to four hours.
She had some physical therapy.
This is Brian Gray, one of my fellows.
He's a pediatric surgeon
now in Indianapolis.
That's actually Large
Marge there, really cute.
And she went to the farm and survived.
And this is a picture, now
it's very, you can tell how
dated it is because these are my twins,
and they're almost 13 now,
so this is a while ago.
And interestingly Large
Marge had two sets of
her own babies, so she's our
favorite long term survivor.
So then an important point in
our research was developing
a model to simulate the lung
development of a 24-week
human infant.
So I'm not a veterinarian, and
I didn't really realize this,
but different, or in the
sheep I do know this,
different organs mature
at very different levels,
so different stages.
So believe it or not, the
brain matures very early.
You might not think of
sheep as very smart animals,
but relative to the lungs.
So we wanted to find the exact
gestational age in the sheep
where the lungs would match
in the developmental pathway
of a 24-week human infant
in the cannalicular stage.
So we looked in the literature.
We also looked histologically
at these animals,
and we also looked at the
inability to support these animals
with very sophisticated
ventilatory strategies.
And we landed on 118 days
as the equivalent of a
24-week human.
So we did a study comparing
the artificial placenta to
mechanical ventilation controls.
You can see here on the left,
yes, that's an occillator.
I can't remember, Bob, but
somehow we got it donated.
I don't know if it went back to the NICU,
but it's a true oscillator.
There's no sheeps alive on it, though.
We actually had John Barks,
the head of Neonatology.
He was in the lab.
He was given surfactin.
He was helping us with the
critical care management
of these infants.
We wanted to give the MV
control their best shot.
And you can see on this slide
that the artificial placenta,
these animals survived
on average one week.
And the mechanical ventilation
controls, again using an
oscillator, surfactant,
steroids, lasted just a few hours
until they had complete
ventilatory failure.
And this is actually our current lamb,
but it's a great video that shows,
oops.
- [Narrator] AP 922 MA 12.
This is post update two.
- So she's just suckling
on that endotracheal tube
which is filled with perflubron.
And I have others
videos, they move around.
We sedate them, but they move
around, they're hanging out,
and they basically have
fluid-filled lungs.
So then I wanna show you
just a little bit of work
we've done assessing organ development.
So the whole idea behind the
artificial placenta would be
to take a 24-week human
infant who fails mechanical
ventilation, transfer them
to the artificial placenta,
and then our goal would be
to prevent any trauma to
any of the major organs,
but also to allow for
normal development.
So we wanna see normal lung
development during this process.
We wanna see normal brain development.
And the idea would be to
then transition to either
mechanical ventilation or air breathing,
and because the lungs and
other organs are more mature.
So we've done a lot of work on the lung.
These are just a few
representative H&E slides.
You can see on the right the
artificial placenta compared to
mechanical ventilation controls.
The histology looks a lot better.
It's more glandular and
fibrotic in the middle slide.
We've worked with some
lung biologists and U of M
doing a lot of staining for
markers of lung development,
and again we've shown that
even within one week's
time period there's evidence
of lung maturation that's
equivalent to controls at
that same gestational age.
We then have some functional
data of animals who have
been on the artificial
placenta for a week or 10 days,
transitioned to mechanical ventilation,
and then we looked at
compliance for example,
and you can see that on
average compliance this I guess
teal color is the artificial
placenta, and it's equivalent
to 128-day vent control.
So these animals were put on
the artificial placenta at
118 days, stayed on there for
10 days, and their compliance
is equivalent to 128-day vent
controls who were just born.
Also looked at oxygenation
index, and you can see that
it's much lower in the
artificial placenta.
So this is just further
functional physiological data
that these lungs in fact
do mature and work better.
Next we looked at the brain.
Again we were very interested
in injury, bleeding
and development.
Turns out because of
what I mentioned before,
the sheep is not the perfect
model for IVH because
the germinal matrix is present
much earlier in gestation.
However, it turns out
it's an excellent model to
look at white matter injury.
And these are just some cool pictures.
We've been collaborating
with a group at Wash U
who does postmortem MRI, and
it's a very validated tool
for looking at white
matter injury and other
structural problems.
So this is an example
of cortical folding that
we're looking at, and if these
two brains look the same,
it's because they are.
The cortical folding is similar,
virtually identical to controls.
So this was indicating to
us that this is a somewhat
crude measure, but the
development to some degree
looks like it's continuing
with the brain development.
We also looked at particularly
white matter injury,
and we found evidence that
both mylenation continues
with the artificial placenta, and sorry,
and there's no evidence
of white matter injury.
And we saw no evidence of hemorrhage in
any of these animals.
So we concluded that
cortical folding continues
during artificial placenta support,
and does not cause white matter injury.
So our next step in this
is to confirm some of these
findings with neuropathology.
So the future directions
of our work is to continue
evaluating organ function.
We've actually done a lot of
work looking at the kidney,
the heart and GI function and structure.
So far all of that looks very promising.
We're going to evaluate organ
structure and function now
in long term survivors, so
in animals that are on the
artificial placenta for 10
days, are weaned to room air.
They go to the farm, and then
a month later we're gonna be
evaluating all those animals.
We're working in our laboratory
on miniaturization of
the circuit and anticoagulation
as Dr. Bartlett pointed out,
and preparing for a clinical trial.
And it was very difficult to
fit all the acknowledgements
on this one slide, but I
think I'd like to acknowledge
and thank Dr. Bartlett, who
let me work in his lab for
over 12 years now, and has
really provided the culture
in the laboratory for
this work to go forward.
That's a picture above at
one of our local conferences
of just some of the people
involved in this project.
There are tons of postdoc
research fellows who have done
just unbelievable work.
Some faculty, my partner Ron
Hirschl, Gabe Owens here,
John Barks, Raja Rabah, a
pathologist, really key faculty
in this project, and our
many, many lab technicians
and students Dr. Bartlett's
been able to amass.
Is it 100 a year of students,
which is hard to believe.
And it's actually this work,
I'll just end by saying
it's remarkable for these
one-week studies that
the intensivists taking
care of these animals at
two in the morning are
undergraduate students,
and the animals still survive.
So I think that
(audience laughs)
well, it's a testament
to the students and to
the technology I think.
So I'm happy to take any questions.
Thank you very much for our attention.
(applause)
- Invite Anita back for
some questions here.
- [Attendee] So why
doesn't the ductus close?
Are you giving prostaglandin?
Because I know you have the
lower pO2, but you don't have
the maternal factors that...
- That's a good question.
So I think a few things.
One is we give prostaglandins, we do, yes.
So we give prostaglandins,
and we maintain a low
pO2 environment.
And we've had some
difficulties since we're using
proflora carbon in the
airway just because we find
that seems to be kind
of optimal for the lung.
It becomes difficult
for Gabe to do the echo
several days later.
It stays open most of the time,
but it's still a bit of a problem.
It can be a little finicky.
We haven't completely solved that.
Do you think that's fair to say?
- [Gabe] Yeah, I think it
gets more difficult to image,
but for the most part even
that path on the animals
that are nonsurvivors,
we do see it (mumbling).
- Hi, I'm Bob Shadee from
Children's Hospital Los Angeles,
and I have a question for Dr. Grady.
I greatly enjoyed your
presentation, and congratulations
on all your work in the registry.
I thought I saw on one of your
slides that, and I may have
gone by too quickly, but a
32% incidence of fetal demise
in one of the groups that
did the aortic stenosis work.
And my question for you is
two-fold with the AS issue
is number one, how close are
we or confident are you that
the identification of the
patients who are gonna end up
going down the single
ventricle pathway is accurate,
and warrants potential, I
don't think it's that high
most centers obviously, but
whatever fetal demise is,
does occur, whatever the
risk is there, the risk to
the mother, but also to the
fetus, particularly when we have
a not great but a potential
solution to this problem.
And then when you start getting
into the right side as well
even more of an issue of
where does that balance occur
in identifying, making sure,
making confident that you are
identifying the right patients
and at what point is the
risk of fetal demise over,
is too much to be able to
proceed with that?
So I'd like your thoughts on that.
- Great, thank you for asking that.
Some centers do have higher
mortalities reported.
Many of those were very
early in their experience
and had only done three.
So the overall registry
fetal demise rate is closer
to about 10%, and that's
also what Boston reports
in their series.
They say that they're a little lower now,
so there seems to be a learning curve.
One of the things that
we're planning on using the
registry for, I'm very excited
to have so many patients
in it now, is to look at the
volumes outcomes relationship.
And it's gonna be difficult
work for some of these centers
to look at because as you
can imagine we're probably
gonna come to the conclusion
that some of them should stop.
So that's dealing with the 30%.
Yeah, some centers probably
don't have the necessary
expertise and infrastructure
to do this and do it well,
and the diseases are so
rare that we should probably
regionalize where they're done.
Now should they be done at all?
That's another question.
And I think that if you ask
someone like Wayne Teresky
at Boston, he thinks his
ability to predict HLHS is 100%.
If you ask Helen O'Gardner
who is at UT Houston and
was at the Brompton before
that, she feels it's much less.
And I think that in the
registry there are patients
who were referred for
intervention but didn't have it
for some reason, and so we
look at those as well in
these publications.
And I think the answer
is somewhere in between.
Some patients that you
think are gonna have HLHS
do have anatomy that gives
you at least the option of
a neonatal (mumbling)
resection LV rehabilitation
type of pathway without having
undergone a fetal procedure.
Whether or not they would
have been better candidates
for that had they had their
aortic valve opened up
and integrate flow across it
and profusing the coronaries
and better coronary profusion
during the fetal period,
I don't know.
I can hand wave about that,
but depends on the day
of the week how I feel.
Is that actually gonna help them or not?
I'm making it up.
I think working together is
the only way that we're gonna
be able to answer this, but
people are gonna continue
to do it whether we work together or not.
So that's the tactic I've taken.
- [John] So just a brief
question for Dr. Michaliska.
How did I do, okay?
- [George] Awesome.
- Not too bad.
(audience laughs)
You made mention of the
fact that you have avoided
anticoagulation in these
artificial placenta animals.
How are you doing that?
What's--
- [Doctor] I said that's the goal.
- Oh, okay.
- Right, so these animals
we've used heparin,
but we are working other
projects as Dr. Bartlett
pointed out, coded circuits, etc.,
that that would be the next step.
And it's an important step.
I mean, it's a little bit two-fold.
I think the knee jerk
reaction and a reasonable one
by a neonatologist would
be if I came in with this
artificial placenta to your
NICU for a 24-week infant,
your neonatologist would say
you're not giving a 23-weeker
heparin because they already
have an increased risk of IVH.
I think that's legitimate, but
I also think there's a lot of
work in the literature
demonstrating that the risk of IVH
in a premature infant is
also increased significantly
by mechanical ventilation, fluid boluses,
hemodynamic instability, etc.
So in this system we
avoid all of those things.
So there's no positive pressure
ventilation or hemodynamics.
I didn't have a chance
to show you the graphs,
but they're pretty stable.
So probably the risk is lower,
but that is still a hurdle
we have to address, no question.
- [John] And one other
question for your colleague,
Dr. Blum.
What do you think, and
maybe this is way beyond,
but maybe just a little speculation.
Why do you think it is that
we have this problem of
hypoplastic left heart develop?
Do we think it's
primarily a valve problem?
Or do we think it maybe something else,
like something to do with the ventricle?
I'd just be interested in
your thoughts or speculations.
- Yeah, that's really the million
dollar question, isn't it?
So I've talked to Dr. Rudolph
about this quite a bit
because as a first year cardiology fellow,
it's all about the valve, and
if you just unplug the valve,
then everything's gonna get better.
The older I get, the less
I know about fetal aortic
stenosis and evolving
hypoplastic left heart syndrome.
Let's take out the
phenotype where there is no
left ventricle.
We're only talking about
that phenotype with a small
nonfunctional ventricle with
endocardial fibroelastosis
and fibroelastosis involving
the mitral and aortic valves,
and they're hypoplastic.
I mean it's tempting to think
that this is all ischemia,
but there's, the animal
models have not recapitulated
this phenotype, and we don't
see it on the right side.
When you have pulmonary
atresia, you don't see the
same phenotype.
So I think that, you know,
it's probably something a lot
more complex that has to
do with the development of
the heart, but also some
interaction of the fetus with
the placenta and epigenetic
factors controlling development
of the left ventricle in
most of these patients.
- [John] And then the other
sort of tantalizing two
observations are number one,
the incidence of late diastolic
LV dysfunction in patients
who were born with AS
and who had it relieved
in one way or another,
surgically or by catherization,
and who now these kids
are 18 or 20 years of age
and have an LV-EDP of 20
with no significant residual
left ventricle dysfunction.
And then the other interesting
little observation is
the incidence of pulmonary
hypertension seemingly
out of proportion to the
left atrial pressures
in this population as well,
which obviously is a particular
problem for those who
wind up going down a heart
transplant pathway.
You know, it smells to
me, and I won't glorify it
any better than that, there's
gotta be something more
fundamental going on at a
genetic or an extracellular
matrix level, something else
that is well beyond the fact
that you've got a funny
looking valve in there.
- Yeah, I absolutely agree,
and it does seem that the
quote-unquote successes for
fetal aortic valvuloplasty,
they don't have hypoplastic
left heart syndrome at birth.
They have aortic stenosis.
And one of my best patients
had a postnatal aortic
valvuloplasty, stopped the
PGE, went home, was gaining
38 grams a day, saw him in
clinic and then died suddenly
the next day at two months of age.
So that was an aortic stenosis
type of story in the neonate,
and I don't think that just
ballooning open the valve
is gonna be the whole answer.
We have to get at the root
cause of why the alvimyocardium
is abnormal and treat that as well.
- [John] Lot of opportunities
for some great research
adventures or the next generation
of physician scientists
or the providers.
- [Attendee] I'm still the new generation?
- [Attendee] Yes.
- [Attendee] Awesome.
Question over here.
- [Hal] Hal Walters,
Children's Hospital of Michigan
in Detroit, and this
question's for George.
I'll just avoid the last name altogether.
(audience laughs)
So if you have a 120-day-old
fetal lamb, that's about 80%
along in their fetal development
since their gestational
age is about five months.
That would correlate to
about 32 weeks in a human,
but I don't know that
that ratio really holds.
How close is the histology of a--
- Right, so that's a great question.
So I, being a surgeon I can
make fun of myself, right?
I did the same thing.
I just used initially several
years ago, and if you divide
24 by 40, I know.
We're not thinking doctors.
So and then I did the
same thing for the sheep.
It turned out to be a 90-day
lamb, which was actually
very difficult to work with.
We did keep them alive for a few days.
They were like, the
tissue was like, you know,
really difficult to work with.
But turns out when we actually
looked at the histology,
the 118-day is equivalent to a 24-weeker.
- [Hal] Great, thank you.
- [Marcus] I'd like to ask,
I'm Marcus Hall from Devoss.
I'd like to ask Emma a question.
The histology slides were
really fascinating to me
because in a different
life 20, 30 years ago I was
looking at rat lungs and lung injury.
So I think you've got a
spectacular improvement in the
lung histology, which
seems to be the big problem
with the neonates.
Do you think that that's
mainly because of your
placental circulation?
Or because of the fact
you're profusing them with
a fluid rather than
mechanical ventilation?
- I think it's almost
certainly because they're not
being ventilated.
So we have a number of
different experiments,
and those were just a few
slides, but a couple of
interesting things I can tell
you is that in the animals
that we went straight from
the womb to the artificial
placenta, basically we did an
exit procedure in the sheep
where they received no
mechanical ventilation,
a week later those lungs
looked pristine because,
and you know this is quite
clear in the literature.
Even a very short period
of mechanical ventilation,
an hour on a premature
lung, it causes problems,
so we saw that.
There other interesting
observation is that we have
some animals where we instilled
fluids of different types,
and on some of them
that we capped them off,
it's essentially equivalent
to tracheal occlusion.
So what we saw in a week is
that that actually stimulated
lung development.
So it was a little bit
further along in the
developmental pathway.
And then lastly, of the
different fluids we've used
like the actual amniotic
fluid from the mom versus
perflubron or profloradecalan
that we're using,
that seems to be most
protective to the lungs.
So there's less evidence of
injury, but I think it's all
largely due to the absence
of mechanical ventilation.
- [Attendee] A question from Bob.
- [Bob] (mumbling)
- Right, so it's interesting.
So now there you may
have heard the group Chop
has also developed an artificial placenta,
and they published their work recently,
and they've corroborated our findings.
In fact, their work is
impressive for the fact that
they have shown survival
and growth of animals
for one month, which I think is great.
And they have some great
data supporting that.
Their model is different
than our model in that
it does use the umbilical vessels.
They have found a way to
prevent umbilical vein and
artery spasm, but in my mind
it's not clinically relevant
because these patients,
human patients would have to
get an exit procedure during
a precipitous premature
delivery, and once there's
any spasm of those vessels,
their whole machine goes down.
But in the animals it's,
they've done some great work,
I think.
- [Attendee] Sue.
- I'm Sue, I'm from the
University of Michigan,
and I have a question for Dr. B.
So one of the interesting things
about innovational research
to me is that it can have
spillover to other areas.
And Dr. B, I'm wondering if
you could talk a bit about
the nitric oxide generator
that you're working with
in the lab, and the future
implications that could have
an effect on in the ICU cure
environment, OR cath lab
and transport for patients?
- I think that was a
question for you, Bob.
- So you're asking about
a nitric oxide generator.
Thank you.
Yeah, and I must say this
is from my point of view
really exciting stuff,
especially for this audience
because you use a lot of nitric oxide.
And in certain situations,
particularly neonatal pulmonary
hypertension, it's magical.
There's nothing like it,
but it costs a whole lot of
money to do it.
And its concept was
developed and marketed by
a single company, Icaria,
so they could charge
whatever they want, and they
charge a whole lot of money.
Used to cost $12,000
just to open the tank.
I don't know what it is now.
So that company was
acquired by Malencrott.
They charge even more, so that's a factor.
So imagine if every
cardiopulmonary bypass patient
you're gonna put nitric
oxide in, are you kidding?
Thousands of dollars per case.
So because of that we've
got working on other
approach to nitric oxide.
I say we means Mark Meyerhoff,
who is a brilliant chemist.
He used to be Xhairman of
the Chemistry Department.
He and I have been working
on using nitric oxide
to prevent platelets from
sticking to surfaces.
The quick summary is he's
developed a way to put
a reagent in a little cup and
put electric current in it,
and out of it comes pure
nitric oxide in unlimited
quantities for pennies.
So sooner or later maybe
we'll convince the university
to help us develop this,
and if you wanna buy into
that company, let me know.
(audience laughs)
- [Attendee] Great.
(applause)
- [Attendee] Thank you, Dr. B.
