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Endotoxin induces a second window of protection in the rat heart as determined by using p-nitro-blue tetrazolium staining, cardiac troponin T release, and histology.
Arterioscler Thromb Vasc Biol. 1999 Sep; 19(9):2276-80.AT

Abstract

Pretreatment of rats with small doses of lipopolysaccharide (LPS), eg, for 24 hours, attenuates the cardiac dysfunction caused by subsequent period of myocardial ischemia. This phenomenon of enhanced tolerance to an ischemic insult has been termed "second window of protection." Although the cardioprotective effects of LPS were first reported in 1989, it is still unclear whether the observed attenuation by LPS of the ischemia-induced cardiac dysfunction is indeed secondary to the protection of cardiac myocytes against ischemic cell injury and death. This study was designed to investigate the effects of "preconditioning" with LPS on cell injury caused by regional myocardial ischemia and reperfusion in the anesthetized rat. Thirty-five Wistar rats were subjected to 25 minutes occlusion of the left anterior descending coronary artery followed by 2 hours of reperfusion. Hemodynamic parameters were continuously recorded, and at the end of the experiments, infarct size (using p-nitro-blue tetrazolium staining), cardiac troponin T release, and histological markers of cell injury and death were determined. In rats pretreated with a bolus of saline (vehicle for LPS) 2 or 24 hours before left anterior descending coronary artery occlusion and reperfusion, the infarct size was 59+/-4% (2 hours saline-control, n=6) and 61+/-3% (24 hours saline-control, n=6), respectively. Pretreatment of animals with a bolus of LPS (1 mg/kg IP) 24 hours before the onset of myocardial ischemia and reperfusion reduced both infarct size (to 18+/-7%; P<0.05, n=6) as well as histological signs of cell injury. Pretreatment (24 hours, as above) of rats with LPS also reduced the release of cardiac troponin T from 58+/-13 ng/mL (saline-control) to 16+/-9 ng/mL. In contrast, pretreatment of rats with LPS (2 hours, as above) did not affect infarct size (56+/-8%, n=6), cardiac troponin T release, or the histological parameters of cell injury. These data provide the first conclusive evidence that pretreatment of rats with a bolus of LPS 24 hours before intervention reduces the cell injury and death caused by a subsequent period of myocardial ischemia and reperfusion.

Authors+Show Affiliations

William Harvey Research Institute, London, UK. k.zacharowski@mds.qmw.ac.ukNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

10479673

Citation

Zacharowski, K, et al. "Endotoxin Induces a Second Window of Protection in the Rat Heart as Determined By Using P-nitro-blue Tetrazolium Staining, Cardiac Troponin T Release, and Histology." Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 19, no. 9, 1999, pp. 2276-80.
Zacharowski K, Otto M, Hafner G, et al. Endotoxin induces a second window of protection in the rat heart as determined by using p-nitro-blue tetrazolium staining, cardiac troponin T release, and histology. Arterioscler Thromb Vasc Biol. 1999;19(9):2276-80.
Zacharowski, K., Otto, M., Hafner, G., Chatterjee, P. K., & Thiemermann, C. (1999). Endotoxin induces a second window of protection in the rat heart as determined by using p-nitro-blue tetrazolium staining, cardiac troponin T release, and histology. Arteriosclerosis, Thrombosis, and Vascular Biology, 19(9), 2276-80.
Zacharowski K, et al. Endotoxin Induces a Second Window of Protection in the Rat Heart as Determined By Using P-nitro-blue Tetrazolium Staining, Cardiac Troponin T Release, and Histology. Arterioscler Thromb Vasc Biol. 1999;19(9):2276-80. PubMed PMID: 10479673.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Endotoxin induces a second window of protection in the rat heart as determined by using p-nitro-blue tetrazolium staining, cardiac troponin T release, and histology. AU - Zacharowski,K, AU - Otto,M, AU - Hafner,G, AU - Chatterjee,P K, AU - Thiemermann,C, PY - 1999/9/10/pubmed PY - 1999/9/10/medline PY - 1999/9/10/entrez SP - 2276 EP - 80 JF - Arteriosclerosis, thrombosis, and vascular biology JO - Arterioscler Thromb Vasc Biol VL - 19 IS - 9 N2 - Pretreatment of rats with small doses of lipopolysaccharide (LPS), eg, for 24 hours, attenuates the cardiac dysfunction caused by subsequent period of myocardial ischemia. This phenomenon of enhanced tolerance to an ischemic insult has been termed "second window of protection." Although the cardioprotective effects of LPS were first reported in 1989, it is still unclear whether the observed attenuation by LPS of the ischemia-induced cardiac dysfunction is indeed secondary to the protection of cardiac myocytes against ischemic cell injury and death. This study was designed to investigate the effects of "preconditioning" with LPS on cell injury caused by regional myocardial ischemia and reperfusion in the anesthetized rat. Thirty-five Wistar rats were subjected to 25 minutes occlusion of the left anterior descending coronary artery followed by 2 hours of reperfusion. Hemodynamic parameters were continuously recorded, and at the end of the experiments, infarct size (using p-nitro-blue tetrazolium staining), cardiac troponin T release, and histological markers of cell injury and death were determined. In rats pretreated with a bolus of saline (vehicle for LPS) 2 or 24 hours before left anterior descending coronary artery occlusion and reperfusion, the infarct size was 59+/-4% (2 hours saline-control, n=6) and 61+/-3% (24 hours saline-control, n=6), respectively. Pretreatment of animals with a bolus of LPS (1 mg/kg IP) 24 hours before the onset of myocardial ischemia and reperfusion reduced both infarct size (to 18+/-7%; P<0.05, n=6) as well as histological signs of cell injury. Pretreatment (24 hours, as above) of rats with LPS also reduced the release of cardiac troponin T from 58+/-13 ng/mL (saline-control) to 16+/-9 ng/mL. In contrast, pretreatment of rats with LPS (2 hours, as above) did not affect infarct size (56+/-8%, n=6), cardiac troponin T release, or the histological parameters of cell injury. These data provide the first conclusive evidence that pretreatment of rats with a bolus of LPS 24 hours before intervention reduces the cell injury and death caused by a subsequent period of myocardial ischemia and reperfusion. SN - 1079-5642 UR - https://www.unboundmedicine.com/medline/citation/10479673/Endotoxin_induces_a_second_window_of_protection_in_the_rat_heart_as_determined_by_using_p_nitro_blue_tetrazolium_staining_cardiac_troponin_T_release_and_histology_ DB - PRIME DP - Unbound Medicine ER -