Diminished basal nitric oxide release after myocardial ischemia and reperfusion promotes neutrophil adherence to coronary endothelium.

@article{Ma1993DiminishedBN,
  title={Diminished basal nitric oxide release after myocardial ischemia and reperfusion promotes neutrophil adherence to coronary endothelium.},
  author={X. L. Ma and Andrew S. Weyrich and David J. Lefer and Allan M. Lefer},
  journal={Circulation research},
  year={1993},
  volume={72 2},
  pages={
          403-12
        }
}
We measured changes in basal release of nitric oxide and its effect on polymorphonuclear leukocyte (PMN) adherence to endothelial cells (ECs) in a feline model of myocardial ischemia (90 minutes) and reperfusion. Basal release of nitric oxide from the left anterior descending coronary artery (LAD) after myocardial ischemia/reperfusion and from the control left circumflex coronary artery (LCX) was assessed by NG-nitro L-arginine methyl ester (L-NAME)-induced vasocontraction. L-NAME induced a… Expand
L-arginine reduces endothelial inflammation and myocardial stunning during ischemia/reperfusion.
TLDR
An excessive endothelial injury/inflammatory response after regional ischemia/reperfusion that can be ameliorated through augmented nitric oxide is supported. Expand
L-Arginine inhibits neutrophil adherence and coronary artery dysfunction.
TLDR
This study tested the hypothesis that the endogenous NO precursor L-arginine (L-Arg) would reduce PMN-induced coronary artery dysfunction by attenuating O2- production and neutrophil adherence by inhibition of adherence via the L- arginine-NO pathway. Expand
Modulation of ischemia/reperfusion-induced microvascular dysfunction by nitric oxide.
TLDR
The results of this study indicate that I/R-induced microvascular dysfunction (albumin leakage) is attenuated by NO and that the protective effect of NO donors may be related to their ability to reduce leukocyte-endothelial cell and leukocytes-platelet interactions and/or mast cell degranulation. Expand
Nitric Oxide and the Vascular Endothelium in Myocardial Ischemia‐Reperfusion Injury a
Abstract: The normal coronary vascular endothelium (VE) tonically releases nitric oxide (NO) by converting L‐arginine to citrulline by a constitutive NO synthase. Reperfusion after myocardialExpand
Supplement of nitric oxide attenuates neutrophil-mediated reperfusion injury.
TLDR
This study demonstrated directly the decrease in NO production during reperfusion and showed that supplement of NO with NO donor attenuated the injury in which PMNs were involved. Expand
Attenuation of myocardial ischemia-reperfusion injury with nitric oxide replacement therapy.
  • A. Lefer
  • Medicine
  • The Annals of thoracic surgery
  • 1995
TLDR
The cardioprotective potential of NO offers a new therapeutic approach to the reduction of ischemia-reperfusion injury after coronary artery occlusion and reperfusion and the mechanism or mechanisms involve preservation of endothelial function and inhibition of neutrophil accumulation in ischemic- reperfused tissue. Expand
Inhibition of inducible nitric oxide synthase after myocardial ischemia increases coronary flow.
TLDR
High selective inhibition of inducible nitric oxide synthase results in increased coronary flow after ischemia but not after continuous perfusion, with decreased neutrophil accumulation and a trend toward increased contractility without elevation of cyclic guanosine monophosphate levels. Expand
Basal nitric oxide expresses endogenous cardioprotection during reperfusion by inhibition of neutrophil-mediated damage after surgical revascularization.
TLDR
It is concluded that blockade of endogenous nitric oxide augments postischemic injury mediated by polymorphonuclear neutrophils, and this damage is expressed primarily during the reperfusion phase. Expand
NO produced by endothelial NO synthase is a mediator of delayed preconditioning-induced endothelial protection.
TLDR
The abolition of preconditioning by l-NAME, but not by selective nNOS or iNOS inhibition, suggests that NO produced by eNOS is a mediator of delayed endothelium-dependent relaxations to acetylcholine. Expand
Nitric oxide attenuates neutrophil-mediated myocardial contractile dysfunction after ischemia and reperfusion.
TLDR
PMN-mediated myocardial contractile dysfunction is attenuated by NO and exacerbated by blockade of NO synthesis, as evidence by a 93% reduction in LVDP at 45 minutes of reperfusion and a 91% reduce in PRP. Expand
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 54 REFERENCES
Time course of endothelial dysfunction and myocardial injury during myocardial ischemia and reperfusion in the cat.
Myocardial ischemia and reperfusion have been shown to impair coronary vasorelaxation to endothelium-dependent vasodilators. To examine the time course of this dysfunction, occlusion of the leftExpand
Neutrophil-mediated vasoconstriction and endothelial dysfunction in low-flow perfusion-reperfused cat coronary artery.
TLDR
Results indicate that activated PMNs produce significant vasoconstriction and endothelial dysfunction in coronary arteries isolated from low-flow perfusion-reperfused hearts. Expand
Attenuated coronary relaxation after reperfusion: effects of superoxide dismutase and TxA2 inhibitor U 63557A.
TLDR
Cor coronary occlusion followed by reperfusion attenuates the relaxation of canine coronary artery rings in response to LTD4 as well as acetylcholine (ACh), suggesting loss of endothelium-dependent coronary reactivity. Expand
Reperfusion after acute coronary occlusion in dogs impairs endothelium-dependent relaxation to acetylcholine and augments contractile reactivity in vitro.
TLDR
The hypothesis that reperfusion of ischemic myocardium augments reactivity to vasoconstrictor agents by causing endothelial cell damage, excessive calcium influx, and loss of modulating vasodilator function is supported. Expand
Contribution of nitric oxide to dilation of resistance coronary vessels in conscious dogs.
Endothelium-dependent relaxation of conductance coronary vessels involves nitric oxide formation from L-arginine. The present study examines whether a similar mechanism intervenes in the vasomotorExpand
Time course and mechanism of endothelial dysfunction in isolated ischemic- and hypoxic-perfused rat hearts.
TLDR
It is suggested that endothelial dysfunction resulting in decreased release of endothelium-derived relaxing factor occurs very early after reperfusion or reoxygenation and may be due to the action of superoxide free radicals. Expand
Nitric oxide modulates microvascular permeability.
TLDR
The results suggest that inhibition of NO production by vascular endothelium leads to a reversible increase in microvascular protein efflux that is mediated by both leukocyte-dependent and -independent mechanisms. Expand
Antibody to CD-18 exerts endothelial and cardiac protective effects in myocardial ischemia and reperfusion.
TLDR
Inhibition of neutrophil adherence to the endothelium exerts significant protective effects in this model of reperfusion injury and induces significant myocardial injury and endothelial dysfunction in the cat involving a CD18-dependent neutrophIL adherence mechanism. Expand
Coronary blood flow in rats is dependent on the release of vascular nitric oxide.
  • L. Jones, M. Brody
  • Medicine
  • The Journal of pharmacology and experimental therapeutics
  • 1992
TLDR
The present study evaluated the role of nitric oxide in determining basal coronary vascular tone and the mechanism by which NO regulates coronary blood flow and the effect of LNAME on CBF, which resulted in an increase in coronary vascular resistance. Expand
Polymorphonuclear leukocytes induced vasoconstriction in isolated canine coronary arteries.
TLDR
Findings indicate that PMNs induce the contraction of coronary arterial rings in the presence of intact endothelial cells through the release of vasoconstrictive substances by metabolic interaction between PMNs and endothelium cells. Expand
...
1
2
3
4
5
...