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Lipoteichoic acid induces delayed protection in the rat heart: A comparison with endotoxin.
Arterioscler Thromb Vasc Biol. 2000 Jun; 20(6):1521-8.AT

Abstract

Classic ischemic preconditioning transiently (30 to 120 minutes) protects the myocardium against subsequent lethal ischemia/reperfusion injury. After dissipation of this acute protection, a second window of protection (SWOP) appears 12 to 24 hours later; this SWOP lasts up to 3 days. Several triggers induce a SWOP, including brief repetitive cycles of coronary artery occlusion, rapid ventricular pacing, stimulation of adenosine A(1) receptors, and administration of wall fragments of Gram-negative bacteria, such as lipopolysaccharide (LPS). The aim of this study was to investigate whether lipoteichoic acid (LTA), a cell wall fragment of Gram-positive bacteria, can induce a SWOP in a rat model of left anterior descending coronary artery (LAD) occlusion (25 minutes) and reperfusion (2 hours). Thus, 166 male Wistar rats were pretreated (2 to 24 hours) with saline, LTA (1 mg/kg IP), or LPS (1 mg/kg IP) and subjected to LAD occlusion/reperfusion. Pretreatment with LTA or LPS for 16 hours led to a substantial, approximately 65%, reduction in infarct size and a reduction in the release of cardiac troponin T into the plasma. The dose of LTA used had no toxic effect (on any of the parameters studied), whereas the same dose of LPS caused a time-dependent activation of the coagulation system and liver injury. By use of RNase protection assays, it was determined that LPS caused a time-dependent induction of tumor necrosis factor-alpha, interleukin-1beta, and manganese superoxide dismutase mRNA content in the heart, whereas LTA failed to induce manganese superoxide dismutase. LPS also caused an upregulation of the expression of intercellular adhesion molecule-1 and P-selectin, whereas LTA downregulated these molecules and attenuated the accumulation of polymorphonuclear granulocytes caused by myocardial ischemia/reperfusion. This study demonstrates for the first time that pretreatment with LTA at 8 to 24 hours before myocardial ischemia significantly reduces (1) infarct size, (2) cardiac troponin T, and (3) the histological signs of tissue injury in rats subjected to LAD occlusion and reperfusion. The mechanism(s) underlying the observed cardioprotective effects of LTA warrants further investigation but is likely to be related to its ability to inhibit the interactions between the coronary vascular endothelium and polymorphonuclear granulocytes. Therefore, LTA represents a novel and promising agent capable of enhancing myocardial tolerance to ischemia/reperfusion injury.

Authors+Show Affiliations

William Harvey Research Institute, St. Bartholomew's and The Royal London School of Medicine and Dentistry, London, UK. k.zacharowski@mds.qmw.ac.ukNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

10845867

Citation

Zacharowski, K, et al. "Lipoteichoic Acid Induces Delayed Protection in the Rat Heart: a Comparison With Endotoxin." Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 20, no. 6, 2000, pp. 1521-8.
Zacharowski K, Frank S, Otto M, et al. Lipoteichoic acid induces delayed protection in the rat heart: A comparison with endotoxin. Arterioscler Thromb Vasc Biol. 2000;20(6):1521-8.
Zacharowski, K., Frank, S., Otto, M., Chatterjee, P. K., Cuzzocrea, S., Hafner, G., Pfeilschifter, J., & Thiemermann, C. (2000). Lipoteichoic acid induces delayed protection in the rat heart: A comparison with endotoxin. Arteriosclerosis, Thrombosis, and Vascular Biology, 20(6), 1521-8.
Zacharowski K, et al. Lipoteichoic Acid Induces Delayed Protection in the Rat Heart: a Comparison With Endotoxin. Arterioscler Thromb Vasc Biol. 2000;20(6):1521-8. PubMed PMID: 10845867.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Lipoteichoic acid induces delayed protection in the rat heart: A comparison with endotoxin. AU - Zacharowski,K, AU - Frank,S, AU - Otto,M, AU - Chatterjee,P K, AU - Cuzzocrea,S, AU - Hafner,G, AU - Pfeilschifter,J, AU - Thiemermann,C, PY - 2000/6/10/pubmed PY - 2000/7/6/medline PY - 2000/6/10/entrez SP - 1521 EP - 8 JF - Arteriosclerosis, thrombosis, and vascular biology JO - Arterioscler Thromb Vasc Biol VL - 20 IS - 6 N2 - Classic ischemic preconditioning transiently (30 to 120 minutes) protects the myocardium against subsequent lethal ischemia/reperfusion injury. After dissipation of this acute protection, a second window of protection (SWOP) appears 12 to 24 hours later; this SWOP lasts up to 3 days. Several triggers induce a SWOP, including brief repetitive cycles of coronary artery occlusion, rapid ventricular pacing, stimulation of adenosine A(1) receptors, and administration of wall fragments of Gram-negative bacteria, such as lipopolysaccharide (LPS). The aim of this study was to investigate whether lipoteichoic acid (LTA), a cell wall fragment of Gram-positive bacteria, can induce a SWOP in a rat model of left anterior descending coronary artery (LAD) occlusion (25 minutes) and reperfusion (2 hours). Thus, 166 male Wistar rats were pretreated (2 to 24 hours) with saline, LTA (1 mg/kg IP), or LPS (1 mg/kg IP) and subjected to LAD occlusion/reperfusion. Pretreatment with LTA or LPS for 16 hours led to a substantial, approximately 65%, reduction in infarct size and a reduction in the release of cardiac troponin T into the plasma. The dose of LTA used had no toxic effect (on any of the parameters studied), whereas the same dose of LPS caused a time-dependent activation of the coagulation system and liver injury. By use of RNase protection assays, it was determined that LPS caused a time-dependent induction of tumor necrosis factor-alpha, interleukin-1beta, and manganese superoxide dismutase mRNA content in the heart, whereas LTA failed to induce manganese superoxide dismutase. LPS also caused an upregulation of the expression of intercellular adhesion molecule-1 and P-selectin, whereas LTA downregulated these molecules and attenuated the accumulation of polymorphonuclear granulocytes caused by myocardial ischemia/reperfusion. This study demonstrates for the first time that pretreatment with LTA at 8 to 24 hours before myocardial ischemia significantly reduces (1) infarct size, (2) cardiac troponin T, and (3) the histological signs of tissue injury in rats subjected to LAD occlusion and reperfusion. The mechanism(s) underlying the observed cardioprotective effects of LTA warrants further investigation but is likely to be related to its ability to inhibit the interactions between the coronary vascular endothelium and polymorphonuclear granulocytes. Therefore, LTA represents a novel and promising agent capable of enhancing myocardial tolerance to ischemia/reperfusion injury. SN - 1079-5642 UR - https://www.unboundmedicine.com/medline/citation/10845867/Lipoteichoic_acid_induces_delayed_protection_in_the_rat_heart:_A_comparison_with_endotoxin_ L2 - https://www.ahajournals.org/doi/10.1161/01.atv.20.6.1521?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -