HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Leddy, J. P. Articles by Lauf, P. K. Search for Related Content PubMed Articles by Leddy, J. P. Articles by Lauf, P. K.

Immune Hemolysis

II. Studies on the Mechanism of Enhanced Lysis of Sheep Red Cells in a High K⁺ Medium¹

Department of Medicine and Division of Immunology, University of Rochester School of Medicine and Dentistry, Rochester, New York and the Department of Physiology, Duke University Medical Center, Durham, North Carolina

Abstract

Enhancement of immune lysis of HK (MM) and LK (LM) sheep red cells by a high K⁺ medium did not require that the K⁺ be present during the action of rabbit hemolysin and complement on the cells. Preliminary exposure of these red cells to a high K⁺ buffer sufficed, and the K⁺ effect withstood vigorous washing of the treated cells. Enhancement of immune lysis by a high K⁺ medium was time, temperature and concentration dependent. It was also 80 to 90% inhibited by 10^-4 M ouabain and much less effectively by equimolar G-strophanthidin, the aglycone of ouabain. The transition step from E* to ghost was not demonstrably affected by a high K⁺ medium. The ability of high concentrations of Rb⁺ or Li⁺ to enhance immune lysis was confirmed. Washing experiments suggested that these cations have lesser affinity for relevant sites on the red cell than K⁺, in the order K⁺ ; Rb⁺ ; Li⁺. The Rb⁺ and Li⁺ effects on lysis were also antagonized by ouabain.

Although these phenomena suggest certain similarities to the stimulation of the traditional red cell Na⁺-K⁺ pump, several important differences exist. It is suggested that the K⁺-induced increment in immune lysis is not directly related to pump activity but possibly to conformational changes in the cell membrane influencing the effectiveness of complement.

Footnotes

¹ This research was supported by United States Public Health Service Grants AM-09810, HE-06241 and AM-15148.

² Work begun during the tenure of a Senior Investigator Award of The Arthritis Foundation.

³ Canadian Medical Research Council Fellow, Hematology Unit, University of Rochester. Present address: Institut Pathologie de Cellulaire, Hôpital Bicetre, Kremlin-Bicetre, France.

⁴ Recipient, Research Career Development Award, United States Public Health Service 1-K4-GM-50, 194-01.