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Hypertension. 2000;35:693

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(Hypertension. 2000;35:693.)
© 2000 American Heart Association, Inc.


Editorial

Research Means "Look Back"

Edward D. Frohlich

From Hypertension, Alton Ochsner Medical Foundation, New Orleans, La.

Correspondence to Edward D. Frohlich, MD, Editor-in-Chief, Hypertension, Alton Ochsner Medical Foundation, 1516 Jefferson Hwy, BH 514, New Orleans, LA 70121.


*    Introduction
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*Introduction
down arrowReferences
 
Anumber of concerns have been raised recently by medical editors; one issue receiving attention relates to the "myopic" or condensed view of literature review,1 aided and abetted by the use of "single" or "double" Medline searches (restricting the review of the medical literature variously to three or six years). This restricted search of the extant literature was termed "MEDLINE-Induced Blindness."1 Not only is this issue no laughing matter, but it is extremely costly because it leads to repetitive research activity of well-established lines of scientific knowledge. Furthermore, journal reviewers, it would seem, are loathe to point out this serious lapse in the appropriate manner to write a scientific paper since, perhaps, by citing unreferred references to the authors of manuscripts under review, they may disclose their identity in the review process and their loss of assured anonymity.

Recently, one report appeared in one of the most prestigious weekly medical journals indicating that angiotensin-converting enzyme inhibition therapy of patients with chronic renal failure will reduce "adrenergic hyperactivity."2 The concept apparently was deemed so novel that an accompanying editorial commentary was included in that issue of the journal.3 No references included in either communication referred to the well-known and well-established phenomenon of angiotensin II augmentation of adrenergic activity in medullary centers or in ganglionic function.4 5 Only a few weeks after this publication, yet another paper was published in a "sister journal" of the American Heart Association indicating increased sympathetic nerve activity in patients with renovascular hypertension.6 Again, no evidence was provided in the references to prior knowledge that increased angiotensin II augments adrenergic outflow from brain or in the paravertebral ganglia. By no means is this experience restricted to the foregoing cited work; it is rampant throughout the literature. And, not infrequently, it is aided and abetted by published statements in these papers stating that "this is the first report" a remark that frequently raises deep concern by one of my co-editors. This, of course, is based on the entire body of extant scientific research preceding any scientific communication. Clearly, any report of new knowledge is founded on a background of well-conceived and carefully documented scientific study.

This practice of a less than thorough review of the literature at best shows inadequate awareness of existing scientific knowledge by authors publishing in major scientific journals and at the worst does not serve science well. It belittles past contributions of other scientists and colleagues, demeans prior authoritative and respected peer-reviewed journal and published scientific knowledge, and it diminishes the authoritative status of the authors, reviewers, and editors of those journals that have published this work. Furthermore, it also obscures the context in which a truly new observation must be interpreted. If we are to expect others to respect and follow tried and tested scientific method and, if we expect that our journals should publish that which is new and exciting in a rapid fashion, let us begin with ourselves. Let us respect and honor our past colleagues and their work. On the other hand, this editorial statement is not a plea for an exhaustive recantation of the extant literature but a careful search for primary references of general value and interest that acknowledges the major contributions of our predecessors. And let us also remember what is literally meant by "research"—it means, "look back!"


*    Footnotes
 
The opinions expressed in this editorial are not necessarily those of the editors of the American Heart Association.


*    References
up arrowTop
up arrowIntroduction
*References
 
1. Baum GL. MEDLINE-Induced Blindness. Chest. 1999;115:1224.[Free Full Text]

2. Ligtenberg G, Blankestijn PJ, Oey PL, Klein IHH, Kijkhorst-Oei L-T, Boomsma F, Wieneke GH, Van Huffelen AC, Koomans HA. Reduction of sympathetic hyperactivity by enalapril in patients with chronic renal failure. N Engl J Med. 1999;340:1321–1328.[Abstract/Free Full Text]

3. Devereux RB, Roman MJ. Sympathetic overactivity in hypertensive patients with chronic renal disease. N Engl J Med. 1999;340:1358–1359.[Free Full Text]

4. Scroop GC, Lowe RD. Efferent pathways of the cardiovascular response to vertebral artery infusions of angiotensin in man. Clin Sci. 1969;37:605–619.[Medline] [Order article via Infotrieve]

5. McCubbin JW, Page IH. Neurogenic component of chronic renal hypertension. Science. 1963;139:210–215.[Abstract/Free Full Text]

6. Johansson M, Elam M, Rundqvist B, Eisenhofer G, Herlitz H, Lambert G, Friberg P. Increased sympathetic nerve activity in renovascular hypertension. Circulation. 1999;99:2537–2542.[Abstract/Free Full Text]




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