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Editors' Notes

The journals are proud to provide a historical salute to the ATS 100-year anniversary by publishing historical reviews of the advances in clinical care (AJRCCM) and pathogenesis (AJRCMB) for major pulmonary diseases. As a coauthor of this month's review (pages 367–372), I would like to apologize in advance for undoubtedly leaving out important studies. It is impossible in the 4,000-word format to pay appropriate tribute to a field. Also, it should be noted that neither author for the COPD piece in this issue, while respectful of history, has lived half of the century—neither has PubMed. To overcome these limitations, we invite readers to submit letters of correspondence to the Journal to fill us in on important omissions.

We believe that this exercise is more than just a respectful tribute. The amount of medical knowledge is growing at an incredibly rapid pace. We will likely double our entire knowledge regarding disease pathogenesis in the next decade. While it is easier for us to forward cogent ideas on the shoulders of this knowledge base, the old literature is full of outstanding ideas that really have not been adequately refuted or proven. Application of old hypotheses with the scientific tools of today is likely to lead to great new—or is that old?—discoveries.

The invited translational review by Drs. Robinson and Lancaster (Hemoglobin-mediated, hypoxia-induced vasodilatation via nitric oxide: mechanism(s) and physiologic versus pathophysiologic relevance; AJRCMB 2005;32:257–261) discussed clearly and succinctly the controversies in this area of research. Because of the importance of this area of research, the editors invited two distinguished scientists, Drs. Mark T. Gladwin and Andrew Gow, who have written extensively on this topic, to submit two editorials addressing the following questions:

1. How does NO generated by endothelial cells escape hemoglobin capture?
   
2. Does oxygen act as an allosteric modulator for the loading and unloading of NO by hemoglobin during normal metabolism? If so, does release of NO from hemoglobin during passage of red blood cells through the microvasculature contribute to vasodilatation during basal conditions?
   
3. Does release of NO by hemoglobin contribute to vasodilatation during hypoxia, sepsis, NO breathing, exercise, etc.? Is the vasoconstriction observed during hyperoxia due to the inability of hemoglobin to release NO?
   
4. Which mechanisms account for the loading and unloading of NO from hemoglobin? Is there reversible transport binding of NO between heme and ß93 cysteines or does deoxyhemoglobin reduce nitrite to NO?
   
5. What type of experiments needs to be done to reconcile existing controversies?
   

Dr. Gladwin's editorial, in support of nitrite reduction, appears below, and Dr. Gow's editorial, supporting the formation of nitrosohemoglobin, will appear in the June issue of AJRCMB. A synopsis of the original review and the two editorials will appear in the July issue of the Journal.

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