![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
R Kraemer and KM Mullane
Department of Pharmacology, New York Medical College, Valhalla.
A postischemic contractile dysfunction termed myocardial stunning has been described in vivo and is attributed, in part, to the generation of oxygen-derived free radicals and the presence of neutrophils. An analogous contractile derangement occurs in the posthypoxic heart in vitro. This study determined the role of neutrophils in hypoxia/reoxygenation-induced cardiac dysfunction in the isolated buffer-perfused rabbit heart utilizing a recirculating system with or without neutrophils present. In control hearts perfused with a neutrophil-free buffer, reoxygenation after 20 min of hypoxia was associated with a slow recovery of contractility which returned to prehypoxic values by 30 to 45 min. Although perfusion with buffer- containing neutrophils did not affect the hypoxia-induced decrease in myocardial contractility, the recovery of contractile function during subsequent reoxygenation was significantly diminished (P less than .01 vs. control), remaining depressed by 30 to 35% at 45 min. The myocardial neutrophil content increased approximately 2-fold in response to hypoxia and reoxygenation, as assessed using 51Cr-labeled neutrophils. The deleterious effects of neutrophil perfusion on cardiac function could not be attributed to neutrophil-mediated plugging of coronary vessels or enhanced myocellular damage. These results support the concept that neutrophils contribute to the cardiac dysfunction described in this model.
This article has been cited by other articles:
|
|
 |
|
  J. Zhu, Y. Qiu, Q. Wang, Y. Zhu, S. Hu, L. Zheng, L. Wang, and Y. Zhang Low dose cyclophosphamide rescues myocardial function from ischemia-reperfusion in rats Eur. J. Cardiothorac. Surg., September 1, 2008; 34(3): 661 - 666. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G Matheis, M Scholz, J Gerber, U Abdel-Rahman, G Wimmer-Greinecker, and A Moritz Leukocyte filtration in the early reperfusion phase on cardiopulmonary bypass reduces myocardial injury Perfusion, January 1, 2001; 16(1): 43 - 49. [Abstract] [PDF]
|
|
|
|
|
|
B. S Allen and M. N Ilbawi Hypoxia, reoxygenation and the role of systemic leukodepletion in pediatric heart surgery Perfusion, January 1, 2001; 16(1_suppl): 19 - 29. [Abstract] [PDF]
|
|
|
|
|
|
G Matheis, M Scholz, A Simon, D Henrich, G Wimmer-Greinecker, and A Moritz Timing of leukocyte filtration during cardiopulmonary bypass Perfusion, January 1, 2001; 16(1_suppl): 31 - 37. [Abstract] [PDF]
|
|
|
|
 |
|
 M. T. Kronon, B. S. Allen, A. Halldorsson, S. Rahman, T. Wang, and M. Ilbawi L-ARGININE, PROSTAGLANDIN, AND WHITE CELL FILTRATION EQUALLY IMPROVE MYOCARDIAL PROTECTION IN STRESSED NEONATAL HEARTS J. Thorac. Cardiovasc. Surg., October 1, 1999; 118(4): 665 - 673. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Kupatt, H. Habazettl, S. Zahler, C. Weber, B. F Becker, K. Messmer, and E. Gerlach ACE-inhibition prevents postischemic coronary leukocyte adhesion and leukocyte-dependent reperfusion injury Cardiovasc Res, December 1, 1997; 36(3): 386 - 395. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. S. Bolling, A. Halldorsson, B. S. Allen, S. Rahman, T. Wang, M. Kronon, and H. Feinberg PREVENTION OF THE HYPOXIC REOXYGENATION INJURY WITH THE USE OF A LEUKOCYTE-DEPLETING FILTER J. Thorac. Cardiovasc. Surg., June 1, 1997; 113(6): 1081 - 1090. [Abstract] [Full Text]
|
|
|
|
 |
|
 H. Weisman, T Bartow, M. Leppo, H. Marsh Jr, G. Carson, M. Concino, M. Boyle, K. Roux, M. Weisfeldt, and D. Fearon Soluble human complement receptor type 1: in vivo inhibitor of complement suppressing post-ischemic myocardial inflammation and necrosis Science, July 13, 1990; 249(4965): 146 - 151. [Abstract] [PDF]
|
|
 |
 |
 |
|
 |
 |
 |
