Dr. Howard Morgan: Winfield, USA
Dr. Howard Morgan was born in Bloomington, Illinois, and began his college education there with one year at the Illinois Wesleyan University (1944-45). He then moved directly into medical school at Johns Hopkins University, where he received his M.D. degree in 1949. His original intention was to become an obstetrician-gynecologist, a career he began on the house staff of the hospital of Vanderbilt University (1949-53). The following year (1953-54) he was instructor in these disciplines. He then became for a year a fellow in medical research in the unit of the Howard Hughes Medical Institute established in the Department of Physiology at Vanderbilt (1954-55). But the following year he was back in obstetrics and gynecology as assistant chief of that service on active duty in the U.S. Army Station Hospital at Fort Campbell, Kentucky. He then returned to Vanderbilt, and for the next ten years (1957-67) he was an investigator in the Hughes Institute, with faculty rank that progressed from assistant professor (1959-62), to associate professor (1962-66), and professor (1966-67). Morgan then became the first professor and chairman of the Department of Physiology in the Milton S. Hershey Medical Center of the Pennsylvania State University in Hershey, Pennsylvania. From 1973 he has been also Associate Dean for Research, and in 1974 was honored by designation as the Evan Pugh Professor of Physiology. In 1982 he was further honored by appointment as a scholar of the Howard Hughes Medical Institute. Morgan wrote briefly of his training:
“Because I entered physiological research after eight years of clinical training, research, and practice in obstetrics and gynecology, my training was entirely as a postdoctoral fellow. Charles R. Park served as my preceptor and guided me into studies of the effects of insulin on glucose uptake and sugar transport. With a solid background obtained in Park’s laboratory, I later was able to undertake the new areas of investigation that have characterized the remainder of my career.”
Dr. Morgan was been a member of the Executive Committee of the American Section of the International Society for Heart Research (1976-79; president, 1979-82). From this office he became president elect of the International Society (1980-83) and served as president (1983-86).
In 1996, Dr. Morgan was elected to be the Founding President of the International Academy of cardiovascular Sciences. He served to early development of IACS until 2005 and made an indelible mark of the creation and future of the organization.
In addition to the honors from the Howard Hughes Medical Institute and from his own university, Morgan has received an Award of Merit from AHA (1979), the Carl J. Wiggers Award from the Cardiovascular Section of APS (1984), and an honorary fellowship in the American College of Cardiology (1985). He was elected to APS Council in 1983 and became president elect the following year.
In areas related to cardiology, Morgan has as a member of the Physiological Chemistry Research Study Group of AHA (1973-75; chairman 1976-79) and of the AHA Research Committee (1974-79 and 1980-81). In 1977-78 he was vice-president for research, chair- man of the Research Committee, a member of the Board of Directors of AHA and AHA President (1987-88). NIH has called on him for membership in the Metabolism Study Section (1967-71), on an ad hoc committee for the National Heart Center Program (1973), on a Cardiology Advisory Committee (1975-78), and on the Advisory Council of the National Heart, Lung and Blood Institute (1979-83). In 1982 Morgan was asked to be chairman of a special panel appointed by this latter institute “to review allege misconduct at Brigham and Women’s Hospital/Harvard Medical School.”
Another important feature of Morgan’s career is his association with scientific journals. Beginning with the Editorial Board of the American Journal of Physiology (1967-73), he became editor of Physiological Reviews (1973-78), associate editor of the American Journal of Physiology: Endocrinology and Metabolism (1979-81), and editor of the American Journal of Physiology: Cell Physiology (1981- 84). For much of this time he served on the Publications Committee (1979-85; chairman, 1981-85). Other journals for which he has provided editorial assistance include Circulation Research (1971-76 and 1982-), the Journal of Biological Chemistry (1973-78 and 1980-85), the Journal of Cardiovascular Pharmacology (1977-82), and the Journal of Molecular and Cellular Cardiology (1974-; associate editor, 1979-83). Of this listing, his influence was perhaps the greatest on Physiological Reviews. During his tenure as editor it grew significantly in international reputation and influence.
Morgan’s research interest was the physiological regulation of intermediary metabolism. For many of his studies he used the isolated and perfused rat heart. He has described his work as follows: “Initial studies dealt with the mechanism of action of insulin on glucose uptake and the nature of glucose transport. Insulin was found to accelerate glucose transport, a stereospecific, saturable process in the cell mem- brane. A kinetic model of sugar transport was proposed, based on studies in rabbit erythrocytes. This model and its mathematical description have been used by many other investigators in characterizing transport phenomena. Experiments measuring the rate of glycogen utilization led to investigation of the allosteric control of phosphorylase a and b and to the discovery that phosphorylase b activity was increased by 5’-AMP [adenosine 5’-monophosphate] and inhibited by ATP [adenosine triphosphate] and G-6-P [glucose 6-phosphate]. This mechanism of allosteric control accounted for the differential effects of anoxia and glucagon and for acceleration of glycogen utilization in working hearts.”
“My interest in the effects of heart work on cardiac metabolism led to development of the isolated perfused working rat heart that has been used extensively both in our laboratory and elsewhere for study of the effects of mechanical performance on carbohydrate, fat, and protein metabolism. In this model, perfusion medium is introduced into the left atrium over a range of atrial filling pressures and is pumped against a variable outflow resistance. With this model, myocardial oxygen consumption was found to depend on the aortic pressure to which the heart was exposed; greater oxygen consumption was accompanied by faster utilization of oxidative substrates.”
During the next phase of my research career, my interest shifted to identification of factors that control growth of the heart and that can lead to cardiac hypertrophy. Initiation of peptide chains on myocardial ribosomes was found to become a rate controlling step during in vitro perfusion and to be accelerated by insulin, fatty acids, and other non- carbohydrate substrates, leucine, increased cardiac work, and exposure to higher aortic pressure. A rigorous method for estimation of rates of protein synthesis was developed that depended on measurements of the specific activities of phenylalanyl-tRNA. Protein degradation also was identified as a site of control of protein turnover that is affected by insulin, diabetes, energy availability, noncarbohydrate substrates, leucine, cardiac work, and increased aortic pressure. The factor that links cardiac work to faster rates of protein synthesis and slower proteolysis appears to be stretch of the ventricular wall, because these effects could be observed in hearts arrested with tetrodotoxin and containing a ventricular drain. In these preparations, an increase in aortic pressure stretched the ventricular wall, accelerated protein synthesis, and inhibited proteolysis. These events appear to represent early changes in the hypertrophy process.”
“After longer periods of exposure to pressure overload or to thyrotoxicosis in vivo, we found that content of cardiac RNA increased and accounted for much of the increment in protein synthesis. since ribosomal RNA constitutes about eighty-five percent of cardiac RNA, these changes indicated that net ribosome production was increased, either by acceleration of rRNA transcription or processing or by inhibition of rRNA degradation. These events are the focus of my current research.”