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Letter to Julio Cruz
Morris Rockstein writes: “Thank you for the birthday wishes and
follow-up letter.
“As for my current activities, aside from contact with the APS, AAAS, and
the Gerontological Society, through their publications and newsletters,
having given up driving and living alone, hampered by limited mobility by
osteoarhritis,. I still manage to get up onto the dance floor about once a
week for ballroom and Latin dancing (allowing my overriding cerebral input
to hide the pain through the pleasure of the moment. Needless to say,
tennis, frisbee, and surf fishing are only memories.
“It is interesting to mention that my daughter, in surfing the internet,
found a considerable number of inclusions in Google of my work and
activities, including a recent photo.
“Thank you for your continued interest in the doings of a fellow
Physiologist. (Rocky to my friends).”
Letters to Beverly Bishop
Robert White writes: “Dr.
Robert White was very pleased to receive your notification for APS members
who had reached their 80th birthday. He appreciates very much your
congratulations.
“Professor White is still extremely active in writing and speaking in those
areas of neuroscience that he researched for so many years, i.e., brain
cooling, transplantation and mechanical support of the isolated brain. He
travels considerably outside of the country attending various scientific
meetings and, as a member of the Pontifical Academy of Sciences, each fall
he travels to Rome for their annual meeting.
“You asked for words of wisdoms or advice for colleagues: Biological Science
seems to be fixed on reducing life to its most simple elements. I would
like to suggest that physiology can be reborn by working in system research
and, in the process, begin to put the living organism back together again.”
Walter Ehrlich writes: “I thank you for conveying to me the kind
wishes of the American Physiological Society for my 90th birthday. At your
suggestion, I will try to summarize how experiences from my life and
research contributed to what I think, believe and do today.
“I studied medicine at the Charles University in Prague. In the fall of
1938, when Hitler invaded parts of Czechoslo-vakia, I left the country. In
March 1939, Hitler invaded the rest of the Czech country. This so outraged
the French public, that Czech refugees could now legally stay in France and
I was able to work as a volunteer at the clinics of Professors Fiesinger and
Mondor in Paris. In the afternoons and evenings I had to make a living,
somehow.
“Then on the first of September of the same year, Hitler invaded Poland.
WWII started and a Czechoslovak Army in Exile was created. I volunteered and
was enrolled in an Infantry Battalion in the South of France. In 1940, when
France was invaded from the unsecured North, this Battalion participated in
its badly equipped defense. After the armistice, our units left for England,
where we were integrated into the Costal Defense against the threatened
Invasion. In 1944 we returned as Armored Brigade with the Allied Forces to
France. On a voluntary mission, I was seriously wounded (an open,
complicated fracture of the femur and of the hip joint). Brave comrades
risked their life to bring me back behind the lines. I was taken to a field
hospital. From there I was flown to the special orthopedic hospital in
Basingstoke, England. Fortunately penicillin and conserved blood had just
been introduced in the Army. I had several operations and for the next three
months I received painful penicillin injections every three hours. I and
even my leg survived.
“After the war I was repatriated with the other Czech invalids. Still on
crutches, I got my MD from the Charles University in Prague in 1947. After a
stint in Pathology, I specialized in Internal Medicine and in Cardiology. In
1951, I became a member of the Institute of Cardiovascular Research in
Prague. I studied problems of pathogenesis and therapy of hypertension. For
animal experiments we used intact non-anaesthetized dogs, where we recorded
blood pressure as well as heart rate and their acute changes with a capacity
manometer put on a carotid artery sewn into a skin loop. With K. Fronek we
found, for instance, that ‘nervous hypertension,’ whether it was caused
either by carotid sinus- and aortic arch denervation, or by excitement of
the animal, or by nervous stress, was always accompanied by heart rate
increase. In all presso-receptor denervated animals, this tachycardia was
still maintained 10 months after the denervation, whereas the resting blood
pressure in each animal had returned to the preoperative level. Heart rate
increase is a permanent consequence of presso-receptor denervation, whereas
elevation of blood pressure is not permanent. Nervous abnormality or
dysfunction, therefore, cannot be a pathogenetic factor in essential
hypertension, as was generally assumed, because patients with essential
hypertension have no tachycardia unless cardiac insufficiency develops.
Hypertension in this disease is permanent, unless it is successfully
treated. These clear facts did not convince the reviewers of cardiovascular
journals. The paper appeared in a journal for autonomous nerve physiology,
Acta Neurovegetativa.
“With Z. Harant and others, we clinically analyzed the long-term effect of
various anti-hypertension therapies in use at this time. We also studied the
effect of these therapies on the circulation and the behavior of dogs. In
general, our results did not confirm their therapeutic effectiveness,
claimed in the literature at that time. For instance, the therapy of
hypertension with prolonged sleep was ‘ideologically recommended’ by the
authorities of Soviet Russia and its Satellites. Behind the Iron curtain it
took guts to publish our results that prolonged sleep therapy is totally
ineffective against hypertension. Another example: The Indian plant
‘Rauwolfia’ marketed by Ciba Basel was reported, in many papers from
different countries, to lower the blood pressure of all hypertensive
patients. We followed hypertensive patient during prolonged treatment with
Rauwolfia and found that the initial fall in blood pressure lasted a few
weeks only. Subsequently, the pressure rose again. However the patients
became listless, unmotivated and depressed. In dogs, oral Rauwolfia, in
corresponding doses, also lowered the blood pressure for few weeks only. The
animals lost normal activity and the capacity to differentiate between the
meanings of signals. We were able to publish the experimental results with
dogs. However, our findings about the effect of continuous treatment of
people with Rauwolfia were rejected by the reviewers of every clinical
journal where they were submitted. The reviewers pointed to the praise of
the therapy in the press, where only short term results had been reported so
far, and to the theories of ‘the specialist’ Dr. Bein of Ciba. During the
time we were approaching one journal after another, we read in the press
about suicides of people who had been treated for hypertension. One of these
was the famous writer Hemingway. Hypertension was often suspected to be the
cause of the depression, when it was in reality caused by the treatment with
Rauwolfia. Professor M. Vogt in Scotland described then the real effect of
Rauwolfia. It removes epinephrine and norepi from nervous tissues, specially
also in the brain. Finally, clinical papers from other authors succeeded to
get published, reporting that Rauwolfia is not a suitable drug for the
treatment of hypertension or for any other long-term treatment. I discussed
our experimental findings of the cardiovascular and behavioral effects of
various drugs used then in the treatment of hypertension or of clinical
depression in the monograph ‘Pharmaco-dynamic Analysis of Circulatory
Reactions to Stimuli from the Environment,’ published for countries on both
sides of the Iron Curtain by Gustav Fischer Verlag Jena. It was sold out in
a year.
“In 1966 my family and I left then communist Czechoslovakia in a dangerous
but successful escape in order to live in a democracy. I accepted an
invitation by the extraordinary group of cardiopulmonary physiologists led
by Richard Riley and Solbert Permutt, to continue my research at Johns
Hopkins. From the onset of my experimental work I used mostly intact
animals, as I was aware of the pitfalls caused by the fact that the
generally accepted model of blood circulation was based exclusively on
experiments with anesthetized, open-chest animals. At this time I became
better equipped than I was before to study the laws of blood circulation and
of its regulation in the intact, awake mammal. Indwelling catheters,
implantable flow probes, and computers became available. The electronic
measurement of pressure and, specifically, of flow rendered the previous
necessity, of evaluating steady states only, into a prejudice that prevented
dynamic evaluation of the way steady states are established. In
instrumented, intact, and awake dogs, we could continuously follow cardiac
output, aortic pressure, pressure in cardiac ventricles and atriums,
coronary flow, pleural pressure and values from any circulatory area of
interest.
“The results of many interesting projects, carried out together with several
valuable colleagues and talented students, forced us to recognize that the
mammal organism does not regulate blood pressure, but it regulates blood
flow to serve the metabolic needs of the body at any given moment. The blood
pressure, on the other hand, indicates the degree of filling of the arterial
bed, that is, the relation of the actual blood volume in the arteries to the
actual volume of the arterial bed. It is also the upstream pressure to
arterial flow.
“For the analysis of our findings we had used, during many years of work,
the generally accepted concept of peripheral resistance to arterial flow.
Its values are computed on the assumption that the downstream pressure to
arterial flow is, in all arterial beds and under all conditions, zero. This
assumption was never proven and the concept was not helpful. We became
acquainted with the concept of ‘vascular waterfall’ by Permutt and Riley.
These authors arrived at this concept by connecting several pressure/flow
values into a resistance line. After each flow-change they waited for a few
minutes to reach steady state, before reading the values. In various
experimental arrangements, we carried out ‘instantaneous’ pressure/flow
investigations, where all tested pressure/flow values of one maneuver were
recorded within three seconds. The arterial bed should have practically no
time to adapt to the quick change in flow. Therefore, our pressure flow
lines were straight, indicating that the resistance in the arterial bed did
not change during the short maneuver.
“Using instantaneous pressure/flow investigations, we found in still
standing dogs an intercept of the resistance line with the pressure axis of
about 50mm Hg. We understood that this intercept indicates the mean of the
pressures in all the arterioles which are at this moment open to perfusion.
That was the mean downstream-pressure to flow (dptf) from all the arterial
beds in our still standing dogs. In resting dogs the dptf in the femoral
arteries, mainly delivering blood to skeletal muscles, was also found to be
about 50 mm Hg. The dptf in the renal arteries of resting animals, however,
was about 10 mm Hg. Dptf in coronary arteries of open-chest dogs was about
30 mm Hg. It is the functional state of the arterioles, the opening pressure
in the perfused arterioles which is the dptf in the arterial bed. It
regulates the blood flow to the supplied organs in accordance with the
actual needs of the organs in any given moment.
“F. Schrijen, a French Fulbright Scholar in our lab, found in awake, intact
dogs that deep inspiration lowers stroke volume and is followed by an
increase in coronary flow. The lower pressure in the chest and, therefore,
in the heart, against the unchanged pressure in the rest of the organism,
elevates the after-load to the left ventricle and lowers, therefore, the
stroke volume. The bigger workload for the heart muscle elevates coronary
flow. However, no US journal in the field accepted the manuscript. After it
was published in Pflugers Archive in Germany, it became our most quoted
paper, even in the journals which had originally rejected it.
“Such results and their interpretation led to a new understanding of blood
circulation and its regulation. At rest dptf in arterial beds of abdominal
organs is far lower than the dptf in most other arterial beds of the mammal.
The cardiac output is relatively small and a relatively large part of it is
directed to abdominal organs for house-keeping. When an animal has to move
suddenly, the pressure in the aorta falls precipitously, because far more
arterioles in skeletal muscles open quickly, to serve the far greater
metabolic needs of the exercising muscles. The outflow from the arterial bed
is greater then the inflow. The blood volume in the arterial bed and,
therefore, the blood pressure fall. The backpressure to the ejection from
the left ventricle falls. The aortic valve opens earlier, closes later and
the ventricle empties more thoroughly. The end-diastolic- and the atrial
pressures fall. The cardiac output increases. The rising cardiac output, the
quicker return of more blood through the beds in the muscles as the supply
of the house-keeping organs is limited, and the lower end-diastolic pressure
increase the venous return to the heart progressively. The progressively
rising cardiac output fills the enlarged arterial bed. The blood pressure
reaches the original values or gets slightly higher. This stops further
increase in cardiac output. A steady state, appropriate to the degree of
muscular work, is established. These intrinsic circulatory mechanisms can
adapt the cardiac output to the metabolic needs of the mammal even if the
heart is denervated and the sympathetic nervous branches are severed. The
intact nervous system makes it only possible to anticipate the need of
regulatory change and to speed it up.
“The reaction to excitement, however, needs intact innervation, at least of
the heart. The excited heart increases the rate and strength of
contractions. The increased output into the unchanged or diminished arterial
bed, increases filling of the arterial bed and elevates, therefore, the
blood pressure. The elevated after-load limits the further increase of
cardiac output. A steady state is induced where a small increase of cardiac
output is accompanied by a marked blood pressure elevation. This is
different from the circulatory reaction in exercise, where a substantial
increase of cardiac output is not accompanied by a marked pressure
elevation, as long as excitement is not involved too. Fight or flight
reactions are certainly combinations of both kinds of reactions.
“After retiring from the lab at 70, I followed my interest in History of
Medicine. I found that the pacemaker in the mammal heart was not discovered
by Keith and Flack to whom the discovery is attributed. It was instead
discovered by McWilliams (1888) and published at the time when Keith was a
medical student taught by McWilliams in Edinburgh. The pacemakers were
investigated later by Hering (1900), Wenckebach (1898, 1903) and others,
before the publication of Keith and Flack (1907) appeared. I found that the
muscular connection between the right atrium and both ventricles was found
by Kent and Hiss (1893). Tawara (1907) called this connection later the
atrioventricular node. Tawara’s original discovery, however, was that the
atrioventricular pathway is connected with the muscles at the tip of heart
by the Purkynje fibers.
“With my wife Helli we had three children and seven grandchildren. After we
had been married for 62 years, Helli died in 2002. Later, two
great-grandchildren were born. I married Francine Schrijen, the retired
French scientist who had worked in our lab 34 years ago.
“I thank you for your interest and for giving me the chance to tell you and
other members of APS about life and physiological research in my time.”
Letters to Peter Lauf
Allan M. Lefer writes: “Thank you for your kind letter which arrived
on my 70th birthday Feb. 1, 2006. I have some thoughts which I would like to
share with colleagues both young and old. My story of retirement is a bit
different from most of those I have read in The Physiologist.
“I retired in September 2001, at the age of 65, for two major reasons.
Firstly, I promised my wife Mary that I would step down while I was still
close to my peak level of quality and vigor. Towards that end, I retired
while I still had two research grants and a training grant, still published
ten or more peer reviewed papers annually, still mentored two postdoctoral
fellows, and still chaired the Department of Physiology at Thomas Jefferson
University. During my 39 years of academic life, I published 638 peer
reviewed papers and co-edited eight books. Therefore, I felt that I had made
sufficient contributions to the scientific literature to feel comfortable in
stepping down.
“Secondly, I strongly felt and still feel that many of us senior scientists
should move over and make room for the younger generation of scientists
coming along. I felt that way after talking to my two sons who are academic
scientists and too many of my former fellows and students. I am very proud
that both of my sons chose academic research and education as a career path.
Some of you know my older son David, who is a Professor of Medicine at
Albert Einstein College of Medicine and is engaged in cardiovascular
physiologic research there. My younger son, Barry, is an Assistant Professor
at The University of Houston in Environmental Sciences. He is an atmospheric
chemist working on air pollution. Interestingly, we all three have an
interest in nitric oxide albeit from different perspectives. Further-more,
many of my former students and fellows keep in touch, and one recently wrote
that he is a student of mine ‘forever.’ I considered all of my 20
predoctoral students and 28 postdoctoral fellows as sons or daughters.
Although many of my contemporaries eschewed retirement to continue their
work, I strongly feel that we need to afford our ‘scientific offspring’ a
full opportunity to develop and thrive, much like we did in the ‘Golden Age’
of science. Toward this end, we need to step down and free up both line item
budget positions and laboratory space to them.
“I actually planned my retirement over two years before I stepped down. I
went to my Dean and suggested that I stage a gradual retirement over two
years, progressively working fewer days each year until I fully retired two
years later. I had an excellent administrative assistant so that the
department ran smoothly and I cut down to two senior postdoctoral fellows
who could carry the research effort with only moderate supervision. In this
manner, I prepared myself for retirement with only minimal disruption to my
colleagues and associates.
“Whereas most of my contemporary colleagues still work in the lab and keep
up the good fight with grant review panels and editorial boards, I chose to
take up golf a year before I retired. Four years ago, Mary and I moved to
Hilton Head Island, SC where we live in a lovely gated community on a
beautiful golf course to which we belong. We play golf about five times a
week and thoroughly enjoy it. Any of my old friends who are in the area,
come join us for a pleasant round of golf. We have made many new friends
from our golf club and the neighborhood and we love living here in a corner
of paradise, while many of our old friends still in science indicate that
their frustration level seems to be increasing with time. I salute and
applaud my colleagues still ‘toiling in the vineyards’ of science. However,
perhaps we should heed the advice Tennyson, who wrote in his epic poem
Ulysses ‘Come my friends, ’Tis not too late to seek a newer world.’”
Mortimer Levy writes: “Thank you for your kind inquiry concerning my
present activities.
“Your letter reminded me that I will be age 70 on June 20th of this year. On
January 1, I completed 37 years of service here at Mcgill University, with a
dual appointment in both the departments of Physiology and Medicine. I have
spent most of my career as an academic clinician, with my laboratory in the
physiology dept. (situated in Mcgill`s medical bldg.), while serving as a
Nephrologist in the Royal Victoria Hospital, a teaching hospital of the
McGill Univ. Health Centre. My laboratory was heavily involved in a study of
the factors determining sodium retention in dogs with edema formation, i.e.,
the dog with partial thoracic caval constriction and the dog with
experimental liver cirrhosis. It was findings in our laboratory that have
led most physiologists to realize that sodium retention in Generalized edema
formation is a biphasic phenomenon, i.e., that sodium retention begins in a
pre-edematous phase where the ECF becomes ‘overfilled’ and in a second phase
where Starling forces become sufficiently perturbed, edema occurs by
‘overflow’ and the effective arterial volume becomes ‘underfilled.’
“After 33 years, I finally closed my laboratory in 2002, after spending the
last 15 years examining the actions of ANP in models of canine edema.
Working with dogs was becoming prohibitively expensive, and studies of whole
organ integrative physiology were not looked upon with favour by study
committees.
“Like many other senior physiologists, I am now saddened that current
graduate students in our department while being expert in many aspects of
molecular biology and cell physiology, seem to have little knowledge of how
intact organs actually function.
“While not actually engaged in the laboratory, I spend a great deal of time
mentoring younger colleagues, serving on thesis committees and completing
various scientific writings. I am very involved in Kidney physiology
teaching, lecturing in an elementary and intermediate course to Science
students. I also direct an advanced course in renal and epithelial transport
physiology, offered to final year Physiology students and postgraduate
students. After lecturing to first year medical students for 35 years, I
have given this up, but still serve as a small group tutor for 12 hours.
Physiology lecture time has been reduced with added emphasis on interactive
and self-learning (computer-based), a maneuver that does not seem to be
conducive to more knowledge acquisition.
“After serving as chairman of our Nephrology division for 15 years, I
stepped down at the end of 1998, but I am still very active in clinical
work, serving on our very busy Consult service, our hemodialysis service,
and I am currently serving as acting director of our peritoneal dialysis
service. I am heavily involved in the teaching of medical students in the
hospital as well as nephrology and medical residents. I am particularly
interested in teaching these groups to bring a physiological perspective to
their clinical reasoning.
“I still serve on several faculty committees, e.g., the promotion committee.
Though working full-time at the present, I plan to retire fully in about
three to four years, but still work in an outpatient nephrology clinic for
one morning per week. Once again, thanks for asking about my present
activities.”
Alfred Lawton wrote: “As my 90th birthday approaches I remain proud
to have been a Physiologist. It is true that we are ‘fearfully and
wonderfully’ made.
“The last of my teachings was a course in Exercise Physiology but even that
was almost six years ago. Mostly now it is my medical training that is put
to use.
“My writings have all been published, lost, or destroyed. That is good for
the passing years cause one to fall behind. It’s a long road from smoked
drum tracings to computer print outs. Retirement clears away the road for
youth to make continued progress in understanding our scientific
discipline.”
Ben Libet writes: “Thank you for your greeting from the Physiological
Society on my forthcoming 90th birthday, April 12. I am still academically
active to some degree. I have recently written and sent off an article
(titled ‘Reflections on the problem of brain mind interaction’) to the
journal Progress in Neurobiology. This journal is collecting articles
by former colleagues of the late Sir John Eccles, the great
neurophysiologist of the 20th century. Two large issues of this journal will
be published in 2006.
“I also wrote a book (Mind Time) on my experimental work on brain and
consciousness, published in 2004 by Harvard University Press. A paperback
edition followed in 2005. There are now published translations in German,
Japanese and Italian. I started this work, with awake human subjects, in
1958, with the experimental neurosurgeon, Dr. Bertram Feinstein. (He was
married to Dianne Feinstein, the current US Senator from California.)
“Also, I carried out a long series of animal experiments on sympathetic
ganglia, in which we discovered and analyzed synaptic responses with
durations ranging from 10 msec. through 100s of msec. and up to 30 minutes!
“As for advice to our younger colleagues, I encourage them to sustain their
creative activities in research, into and beyond their retirement date. I
thought I would never retire from the researches I was progressing with. The
latest experiments I carried out were in a series on the time factor for
brain production of a conscious experience, done when I was 70-75 years old.
This important, difficult result was published in Brain in 1991. Of course,
one loses the lab facilities and energy to continue with experiments. I
would note that I am one of the older generation who does not have or use a
computer (I don’t boast about that)!
“Thanks again for your interest and best wishes to all the physiologists,
especially those who may remember me or be aware of my works.”
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