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Frank Byrom was elected to fellowship of the College on 6 September 1940 because of his distinction in medical research and the importance to clinical medicine of his research on hypertension. Three other distinguished medical practitioners were made Fellows on the same day, Dr Neil Hamilton Fairley (qv 1), Professor Horace Smirk and Professor RD Wright (qv). Earlier that year Byrom had taken a joint appointment as director in postgraduate pathology at Prince Henry Hospital Sydney and lecturer in postgraduate pathology of the University of Sydney. This was a new post in the postgraduate unit which had been established at Prince Henry Hospital by the University in 1938, with SA Smith (qv 1) as director of medicine and Hugh Poate director of surgery, both first-class clinicians. Byrom's appointment gave a strong research component to the unit. He had already achieved a reputation as an able investigator and he continued his outstandingly successful work in Sydney for the next seventeen years.
Research and scientific method could be said to be in his blood, for his father, Thomas Henry Byrom, was an industrial and research chemist in Wigan, Lancashire where Frank was born. After studying medicine at the London Hospital and graduating with honours in 1924 he filled various medical posts over the next six years at the London, from house physician to first assistant. During the latter part of that period he was also a demonstrator in physiology and he engaged in physiological research. Subsequently he had further research experience at the university of Chicago on a Rockefeller Scholarship before returning to the London Hospital on a research fellowship awarded by the Beit Memorial Trust.
It was when he joined forces with Clifford Wilson at the London Hospital in 1935 that his interest became focused on experimental hypertension, the field on which he continued to work with such success throughout his life. Wilson was intrigued by the work of Goldblatt who had produced severe hypertension in dogs by excising one kidney and later causing ischaemia in the other by clamping the renal artery. Wilson and Byrom carried Goldblatt's work much further. They used rats, aided by a tail plethysmograph which Byrom devised, working on an idea proposed by Wilson. Byrom had a great gift for mechanical invention. He also displayed the intellectual ability to define clearly the problem to be solved, to design a simple research project to provide the answer and to carry it through to fruition. Though his earlier work on hypertension was a joint effort with Wilson, much of his later research was done with minimal support and was made possible by a combination off his mechanical skills and his problem-solving ability.
Wilson and Byrom initially set about studying the effect of experimentally produced hypertension on the unclamped, and therefore unprotected, kidney. They were fortunate in discovering that in rats, as was later shown to be the case in humans, chronic hypertension usually developed when one renal artery was constricted by a clamp, with the opposite kidney and its blood supply left intact. In these rats the unclamped kidney soon developed necrotizing arteritis with glomerular and tubular lesions similar to those found in human malignant hypertension. The clamped kidney, being protected from the hypertension, did not develop these changes. They therefore concluded that the renal lesions of malignant hypertension were the result of hypertension and not its cause. They were also able to demonstrate that when the rats were kept alive and hypertensive for long periods, the unclamped kidney developed the characteristic changes seen in longstanding hypertension in man, thus proving that these lesions too were secondary to the hypertension. Furthermore they found that, in the rats with chronic hypertension, removal of the clamped kidney did not always reverse the hypertension and, in those animals which remained hypertensive, the lesions in the unprotected kidney were severe. This gave rise to the concept of a vicious cycle and threw new light on the age-old problem of the relationship between Bright's diseases and hypertension.
The war years caused a great loss of staff from civilian hospitals to military units and the postgraduate unit at Prince Henry Hospital which Byrom joined in 1940 soon had to restrict its activities. Byrom gave his attention to devising and developing a facility for freeze-drying plasma in large quantities for use by United States and Australian military forces and in 1942 he was seconded to the University of Sydney for this purpose. Later he was given facilities to continue his research on hypertension at St Vincent's Hospital.
Working initially with LF Dobson, a young medical graduate embarking on a research career, he set out to test whether, in chronic hypertension initiated by renal ischaemia, any extrarenal mechanism developed which might be responsible for the permanency of the hypertension following removal of the clamped kidney. Working on rats with one kidney removed and the remaining kidney rendered ischaemic by a clamp (like Goldblatt's dogs) Byrom and Dobson showed that, even after as long as thirty-two weeks of hypertension, the blood pressure returned to normal after nephrectomy. In addition, the generalised vascular lesions normally found in these hypertensive animals healed, and the left ventricular hypertrophy diminished. This work showed clearly that in these animals there was no secondary extrarenal factor causing the hypertension to persist. Byrom and Dobson therefore concluded that the persistence of hypertension after excision of the clamped kidney, previously noted by Wilson and Byrom, was due to secondary changes in the unprotected kidney. Their elegant experiment had clarified the mechanism of the vicious cycle and placed it on a solid foundation. It also provided a stimulus for more aggressive attempts to control long-standing hypertension in humans by demonstrating the reversibility of the changes in peripheral arteries once the blood pressure was lowered. Byrom did further work on the cerebral arterial circulation, showing that cerebral arteries, contrary to prevailing opinion, were capable of spasm in hypertension; on cerebral oedema, defining its place in hypertensive encephalopathy; and on the retinal circulation. All of his work greatly influenced our understanding of hypertension and its treatment.
Byrom was a quiet, rather retiring man, who did not seek publicity, but he was a model clinical worker. In 1957 he returned to England where he continued his investigations at the Maudsley Hospital and, from 1964, at the London Hospital until his retirement. He died in 1976 survived by his wife and five children, two of whom were medical graduates.