|
|
||||||||
AJP - Regulatory, Integrative and Comparative Physiology, Vol 261, Issue 2 351-R357, Copyright © 1991 by American Physiological Society
ARTICLES |
D. R. Meldrum, A. Ayala, P. Wang, W. Ertel and I. H. Chaudry
Department of Surgery, Michigan State University, East Lansing 48824.
Although it is known that decreased ATP levels in liver and kidney contribute to organ dysfunction after shock, it remains unknown whether there is any association between decreased splenocyte ATP levels and splenic immune functions. Moreover, although studies have shown that ATP-MgCl2 treatment after shock improves hepatic and renal ATP levels and organ function, it remains unknown whether splenocyte ATP levels and immune functions are similarly affected by this agent. To study this, C3H/HeN mice were bled to a mean blood pressure of 35 mmHg, maintained at that pressure for 60 min, resuscitated with shed blood and Ringer lactate, and treated with ATP-MgCl2 (80 mumol/kg) or vehicle (saline). Splenocytes (SPL) were harvested at various intervals after hemorrhage, ATP levels were assessed by 31P nuclear magnetic resonance spectrometry, and functions were determined by measuring proliferative capacity and interleukin (IL)-2, and IL-3 synthesis. Hemorrhage depleted SPL ATP levels to 1.7 +/- 0.8% of control levels. However, there was a significant increase in ATP levels of ATP-MgCl2-treated mice (77 +/- 11%, P less than 0.05) compared with vehicle-treated animals (13 +/- 4.1%) at 1 h after resuscitation. SPL ATP levels returned to control by 2 h after resuscitation in the ATP-MgCl2 group, whereas ATP levels of the vehicle-treated mice remained significantly depressed (P less than 0.05) for up to 12 h after resuscitation. At 1 h after resuscitation, SPL proliferative capacity and IL-2 and IL-3 synthesis were all profoundly depressed in the vehicle-treated group (P less than 0.05 vs. control).(ABSTRACT TRUNCATED AT 250 WORDS)
This article has been cited by other articles:
![]() |
T. S. A. Samy, R. Zheng, T. Matsutani, L. W. Rue III, K. I. Bland, and I. H. Chaudry Mechanism for normal splenic T lymphocyte functions in proestrus females after trauma: enhanced local synthesis of 17{beta}-estradiol Am J Physiol Cell Physiol, July 1, 2003; 285(1): C139 - C149. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. K. Meldrum, D. R. Meldrum, K. L. Hile, E. B. Yerkes, A. Ayala, M. P. Cain, R. C. Rink, A. J. Casale, and M. A. Kaefer p38 MAPK mediates renal tubular cell TNF-{alpha} production and TNF-{alpha}-dependent apoptosis during simulated ischemia Am J Physiol Cell Physiol, August 1, 2001; 281(2): C563 - C570. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. K. Donnahoo, X. Meng, A. Ayala, M. P. Cain, A. H. Harken, and D. R. Meldrum Early kidney TNF-alpha expression mediates neutrophil infiltration and injury after renal ischemia-reperfusion Am J Physiol Regulatory Integrative Comp Physiol, September 1, 1999; 277(3): R922 - R929. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. R. Meldrum Tumor necrosis factor in the heart Am J Physiol Regulatory Integrative Comp Physiol, March 1, 1998; 274(3): R577 - R595. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |