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Research Article Free access | 10.1172/JCI105684
Department of Medicine, University of Utah College of Medicine, Salt Lake City, Utah
‡Faculty Research Associated of the American Cancer Society; present address: Department of Medicine, Rutgers Medical School, New Brunswick, N. J.
Address requests for reprints to Dr. John C. Marsh, Departments of Internal Medicine and Pharmacology, Yale University School of Medicine, 333 Cedar Street, New Haven, Conn. 06510.
*Received for publication 16 June 1967 and in revised form 2 August 1967.
Supported by a research grant (AM-04489) and a graduate training grant (AM-5098) from the National Institute of Arthritis and Metabolic Diseases, Bethesda, Md. Presented in part at the Ninth Annual Meeting of the American Society of Hematology, 6 December 1966.
Find articles by Marsh, J. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Utah College of Medicine, Salt Lake City, Utah
‡Faculty Research Associated of the American Cancer Society; present address: Department of Medicine, Rutgers Medical School, New Brunswick, N. J.
Address requests for reprints to Dr. John C. Marsh, Departments of Internal Medicine and Pharmacology, Yale University School of Medicine, 333 Cedar Street, New Haven, Conn. 06510.
*Received for publication 16 June 1967 and in revised form 2 August 1967.
Supported by a research grant (AM-04489) and a graduate training grant (AM-5098) from the National Institute of Arthritis and Metabolic Diseases, Bethesda, Md. Presented in part at the Ninth Annual Meeting of the American Society of Hematology, 6 December 1966.
Find articles by Boggs, D. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Utah College of Medicine, Salt Lake City, Utah
‡Faculty Research Associated of the American Cancer Society; present address: Department of Medicine, Rutgers Medical School, New Brunswick, N. J.
Address requests for reprints to Dr. John C. Marsh, Departments of Internal Medicine and Pharmacology, Yale University School of Medicine, 333 Cedar Street, New Haven, Conn. 06510.
*Received for publication 16 June 1967 and in revised form 2 August 1967.
Supported by a research grant (AM-04489) and a graduate training grant (AM-5098) from the National Institute of Arthritis and Metabolic Diseases, Bethesda, Md. Presented in part at the Ninth Annual Meeting of the American Society of Hematology, 6 December 1966.
Find articles by Cartwright, G. in: JCI | PubMed | Google Scholar
Department of Medicine, University of Utah College of Medicine, Salt Lake City, Utah
‡Faculty Research Associated of the American Cancer Society; present address: Department of Medicine, Rutgers Medical School, New Brunswick, N. J.
Address requests for reprints to Dr. John C. Marsh, Departments of Internal Medicine and Pharmacology, Yale University School of Medicine, 333 Cedar Street, New Haven, Conn. 06510.
*Received for publication 16 June 1967 and in revised form 2 August 1967.
Supported by a research grant (AM-04489) and a graduate training grant (AM-5098) from the National Institute of Arthritis and Metabolic Diseases, Bethesda, Md. Presented in part at the Ninth Annual Meeting of the American Society of Hematology, 6 December 1966.
Find articles by Wintrobe, M. in: JCI | PubMed | Google Scholar
Published December 1, 1967 - More info
Neutrophil kinetics of acute experimental infection were studied with diisopropylfluorophosphate-32P labeling in 31 dogs inoculated intrabronchially with pneumococci. In vitro neutrophil labeling indicated a rapid transit time through the blood in early infections, with an elevated marginal granulocyte pool sometimes preceding an elevation of the circulating granulocyte pool. 13 hr after infection, the circulating and total blood granulocyte pools were increased but the rate of neutrophil transit through the blood was normal. During the recovery from infection there was a marked prolongation of neutrophil blood transit time, suggesting virtually complete cessation of bone marrow release of neutrophils into the blood. Labeling of neutrophils in vivo indicated an increased rate of emptying of the bone marrow storage pool proportional to the severity of infection as measured by the fever index. The change in the blood ratio of nonsegmented to segmented neutrophils was a much more accurate index of the severity of infection than the blood granulocyte concentration, correlating significantly with the fever index.