David Francis Bohr
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51st APS President (1978-1979)
David Francis Bohr
1915-2008

As president elect of APS, in the fall of 1977 Bohr visited medical schools and especially departments of physiology in Cuba (11). He reported that under Communist management the national rate of illiteracy has been reduced from twenty-five percent to three percent; that the 3,000 physicians who left Cuba after the revolution have been replaced threefold, resulting in a current physician-to-population ratio higher than in the United States; and that medical education is not only of good quality, but also is free, with students receiving in addition an allowance for living expenses. He found physiology to be an active profession in both teaching and research. The president of the Cuban Physiological Society, F. R. Dorticos, seemed interested in the possibility of joint meetings of his society and APS, possibly in cooperation with the Mexican Physiological Society or with the Latin American Society of Physiological Sciences. As a result of Bohr's initiative, the Latin American society was invited to take part in the APS Fall Meeting in San Diego in October 1982. There the president of the Latin American society, Cesar Tim-Iaria of Sao Paulo, Brazil, met with Council to discuss ways to foster better communication between the Americas.

Although for more than fifty years Bohr's career has been identified with the University of Michigan, he was born in Zurich, Switzerland, lived for five years as a boy in Cuba, and received most of his primary school education in the southernmost part of California. In 1933 he entered the University of Michigan, matriculated in 1936 in its medical school, and graduated in 1942 after having spent two years as a teaching and research assistant in the Department of Physiology where Robert Gesell was chairman. Bohr interned at Henry Ford Hospital for a year before he was assigned by the U.S. Army to a Dutch hospital ship for three years of duty as laboratory officer and detachment commander (1943-46). He then spent two years (1946-48) as a research fellow at the University of California in San Francisco before returning permanently to the University of Michigan. In 1957 he was promoted to the rank of professor.

On two occasions Bohr has served as visiting professor, first in 1955-56 at the Department of Pharmacology at the University of California at San Francisco and again in 1961-62 at the Physiologische Institut at Heidelberg. Michigan chose him for a Distinguished Faculty Achievement Award in 1973 and for the Distinguished Faculty Lectureship in Biological Research in 1983. In 1977 he gave the Wiggers Lecture for APS, and in 1984 he received the Ciba Award for Hypertension Research. He is a member of the International Society of Hypertension, the InterAmerican Hypertension Society, and the Council for High Blood Pressure Research of AHA (1968-; chairman, 1978-80). For five years (1969-74) he was a member of the Research Advisory Committee of AHA and also chairman of one of its cardiovascular study committees.

As a member of the Physiology Study Section, Bohr began association with NIH advisory groups in 1960-64. He served with the NIH Hypertension Task Force (1978-79) and on the Study Section B of the Heart, Lung and Blood Institute (1981-86). He has been a member of the Committee on Physiology of the National Board of Medical Examiners (1965-68) and also of the Cardiovascular Review Panel for the Space Science Board of NAS (1968-72). Most of his editorial responsibilities have similarly involved the circulatory system. He served the Society on the Editorial Board of its journals in 1966-69, in 1969-75 as coeditor of the circulation section of the American Journal of Physiology, and in 1983-86 as associate editor of the American Journal of Physiology: Heart and Circulatory Physiology. He also served as editor of the Handbook of Physiology, Vascular Smooth Muscle. He was a member of the editorial boards of Circulation Research (1960-65 and 1968-74), Proceedings of the Society for Experimental Biology and Medicine (1978-81), Blood Vessels (1974-), and Hypertension (1979-81).

Bohr joined APS in 1949. His earliest committee responsibility was with the Membership Committee (1966-69; chairman, 1967-69). for a year (1969-70) he was chairman of the Subcommittee on Undergraduate Education in Physiology and then joined the Education Committee (1970-73). In 1970-73 he was a member of the Steering Committee of the Circulation Group of the Society. From 1974-1977 he served with the Perkins Memorial Fund Committee, after his election to Council in 1973. He became president elect in 1977. Regarding his presidential years, Bohr has written:

"There are two things for which I feel some satisfaction during my tenure at the helm. One was the institution of the Standing Committee on Career Opportunities in Physiology. Walter Randall agreed to serve as first chairman of the committee, and at least half of the members are to be under the age of forty years. Anything we can do to help those who are getting launched in our field will be of value to our profession and will be much appreciated by those we are helping. The other memorable event was the Society's support of my visit to Cuba (11). It initiated a regrettably abortive relationship with physiologists in Cuba, which I certainly would like to see rekindled. It will not be easy, but I would be glad to help."

A third important event was a meeting Bohr encouraged between members of the APS Animal Care Committee and representatives of animal welfare groups. In February 1980, Helene Cecil, chairwoman of the APS committee, met with Leon Bernstein and Christine Stevens and others of the Animal Welfare Institute for discussion of the use of animals and alternatives to such use in research and teaching. Christine Stevens is the daughter of Bohr's mentor, Robert Gesell. The meeting was reported briefly in The Physiologist [23(3): 16, 1980].

In regard to his research interests, training, and publications, Bohr wrote:

"[At first] I worked with John Bean in the Department of Physiology on oxygen toxicity (1). It was obvious then and still is that you can get major rewards in physiology from problem solving by using physical and chemical tools plus common sense. . . . I then began to be interested primarily in the contractile machinery of vascular smooth muscle, which made me want to know what causes the pressure to go up in hypertension. I have been working at these two problems for the last thirty years."

"It is an interesting coincidence that both of my favorite publications appeared in Science. The first (2) demonstrated that calcium not only causes contraction of vascular smooth muscle but also in higher concentrations decreases excitability. The second, published two years later (3), quantified the calcium requirement for contractile activity of vascular smooth muscle and skeletal muscle and showed that the contractile apparatus of the two machines has identical calcium dependency. Recently, I have been trying to understand those changes in contractile machinery of resistance in hypertension. . . . Here are thumbnail sketches of later papers."

Reference 4. Small coronary arteries from the dog have little or no alpha-adrenergic activity but respond to catecholamines with relaxation resulting from activation of beta-adrenergic receptors. Large coronary arteries have both alpha- and beta-adrenergic activity. The beta-receptors of coronary vessels appear to differ from those in vessels supplying skeletal muscle.

Reference 5. There is an as yet unidentified vasoactor in plasma that causes contraction of isolated vascular smooth muscle. This factor may play a role in the maintenance of normal vascular tone.

Reference 6. Sensitivity of vascular smooth muscle to constrictor agonists was found to be elevated in deoxycorticosterone acetate, renal, and spontaneously hypertensive rats. This increase in sensitivity reflects a lessening of calcium binding to the cell membrane in vascular smooth muscle from rats with these types of hypertension.

Reference 7. The increase in sensitivity of vascular smooth muscle from hypertensive rats was demonstrated to be primary. It occurred in the hindlimb vasculature that was protected from the hypertension by ligation of the iliac artery.

Reference 8. Vascular smooth muscle made to contract in a potassium-free medium undergoes a relaxation when potassium is added back to the muscle bath. This relaxation was demonstrated to be due to membrane hyperpolarization resulting from activation of the electrogenic sodium pump. this phenomenon was subsequently used extensively to evaluate sodium pump activity in isolated vascular smooth muscle.

Reference 9. Pressor responses to intravenous infusions of norepinephrine or of angiotensin were elevated as early as two days after the beginning of treatment of the pig with deoxycorticosterone acetate.

Reference 10. Blood pressure elevation in the pig began two days following deoxycorticosterone acetate treatment and reached a plateau three weeks later. The pressure elevation was caused in some pigs by an elevation in cardiac output and in others by an elevation in total peripheral resistance, but in most animals it was caused by an elevation in both of these determinants of arterial pressure.

Reference 13. Evidence is presented to support a hypothesis that the primary fault in the pathophysiology of hypertension is a defect in the calcium binding of the plasma membrane of the cells of a pressure-regulating center in the hypothalamus.

Reference 14: Basilar arteries from spontaneously hypertensive rats (but not from normotensive controls) were characterized by spontaneous contraction which resulted form a membrane leak of extracelluar calcium.

Reference 15. Administration of deoxycorticosterone to the sheep results in hypertension, polydipsia, hypokalemia, and the development of a "salt appetite."

Reference 16. Treatment of isolated vascular smooth muscle with serotonin results in the following sequence of events that causes an attenuation of the response resulting from subsequent stimulation of the muscle with norepinephrine: 1) increased membrane permeability to sodium, 2) elevated intracellular sodium, 3) stimulation of the sodium efflux pump, 4) membrane hyperpolarization, and 5) depressed calcium influx via the norepinephrine-operated receptor.

One of the themes that occurs and recurs in past-presidential addresses is the responsibility of physiologists in the overall enterprise of medical education and perhaps in what is know as "delivery" of health care. Bohr (12) pointed out that problems in medical practice have two parts: 1) economy or finances and 2) attitude. After summarizing how medical costs have become so high, he spoke of the contrast between what has happened in the United States and what he observed in Cuba. There health care is available to all without charge. Yet even though Cuban education and health care have moved forward rapidly, any visitor can see that "the economy is clearly an unsurmounted hurdle. Housing is poor, manufactured items are in scarce supply, clothing is rationed, and very few people have their own automobiles" (11). Later he added, "and besides, there is virtually nothing to buy" (12).

Bohr ended his remarks with a few words about improving attitudes of physicians and how medical education might be modified to preserve throughout their training the sensitive, ethical dedication students bring to medical school. "Sensitivity and feeling add nothing to the cost of health care." As physiologists working within medical schools, because "we train future clinical doctors, nurses, and dentists, we hold a measure of responsibility for the caliber, the quality, and the integrity of health care in America that we cannot disown."

Selected Publications

1. Bean, J. W., and D. F. Bohr.. High oxygen effects on isolated striated muscle. Am. J. Physiol. 126: 188-195, 1939.

2. Bohr, D. F. Vascular smooth muscle: dual effect of calcium. Science Wash. DC 139: 597-599, 1963.

3. Filo, R. S., D. F. Bohr, and J. C. Ruegg. Glycerinated skeletal and smooth muscle: calcium and magnesium dependence. Science Wash. DC 147: 1581-1583, 1965.

4. Bohr, D. F. Adrenergic receptors in coronary arteries. Ann. NY Acad. Sci. 139: 799-807, 1967.

5. Bohr, D. F., and J. Sobieski. A vasoactive factor in plasma. Federation Proc. 27: 1396-1398, 1968.

6. Holloway, E. T., and D. F. Bohr. Reactivity of vascular smooth muscle in hypertensive rats. Circ. Res. 33: 678-685, 1973.

7. Hansen, T. R., and D. F. Bohr. Hypertension, transmural pressure, and vascular smooth muscle response in rats. Circ. Res. 36: 590-598, 1975.

8. Bonaccorsi, A., K. Hermsmeyer, O. Aprigliano, C. B. Smith, and D. F. Bohr. Mechanism of potassium relaxation of arterial muscle. Blood Vessels 14: 261-276, 1977.

9. Berecek, K. H., and D. F. Bohr. Whole body vascular reactivity during the development of deoxycorticosterone acetate hypertension in the pig. Circ. Res. 42: 764-771, 1978.

10. Miller, A. W., D. F. Bohr, A. M. Schork, and J. M. Terris. Hemodynamic responses to DOCA in young pigs. Hypertension Dallas 1: 591-597, 1979.

11. Bohr, D. F. President-elect's tour. Changes in Cuba. Physiologist 22(1): 9-11, 1979.

12. Bohr, D. F. Past-president's address. The health market and physiologists. Physiologist 22(6): 15-17, 1979.

13. Bohr, D. F. What makes the pressure go up? A hypothesis. Hypertension Dallas 3, Suppl. II: 160-165, 1981.

14. Winquist, R. J., and D. F. Bohr. Structural and functional changes in cerebral arteries from spontaneously hypertensive rats. Hypertension Dallas 5, Suppl. III: 292-297, 1983.

15. MItchell, J., W. D. Ling, and D. F. Bohr. Deoxycorticosterone acetate hypertension in sheep. J. Hypertension 2: 473-478, 1984.

16. Moreland, R. S., C. van Breemen, and D. F. Bohr. Mechanism by which serotonin attenuates contractile response of canine mesenteric arterial smooth muscle. J. Pharmacol. Exp. Ther. 232: 322-329, 1985.

 

 
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