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The role of endogenous nitric oxide in inhibition of ischemia/reperfusion-induced cardiomyocyte apoptosis.
Folia Histochem Cytobiol. 2001; 39(2):179-80.FH

Abstract

The effect of nitric oxide (NO) synthase inhibition on apoptosis of cardiomyocytes during ischemia/reperfusion was investigated. Isolated perfused guinea-pig hearts were subjected to 35 min ischemia (I) followed by 30 min reperfusion (IR) in the presence or absence of NO synthase inhibitors, L-NAME or L-NMMA or a superoxide scavenger, SOD. Apoptosis was assessed by immunohistochemistry (TUNEL assay, Bax protein staining), by spectrophotometric measurement of cytochrome oxidase activity (COX), and by ultrastructural analysis. Inhibition of NOS significantly increased apoptosis with activation of Bax protein and decrease of COX. SOD infusion had a protective effect on these apoptotic markers. The results suggest that endogenous NO synthesis during I/R protects the heart against apoptotic cell death.

Authors+Show Affiliations

Department of Pathology, The Children's Memorial Health Institute, Warsaw, Poland. czar@czd.waw.plNo 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

11374814

Citation

Czarnowska, E, et al. "The Role of Endogenous Nitric Oxide in Inhibition of Ischemia/reperfusion-induced Cardiomyocyte Apoptosis." Folia Histochemica Et Cytobiologica, vol. 39, no. 2, 2001, pp. 179-80.
Czarnowska E, Kurzelewski M, Beresewicz A, et al. The role of endogenous nitric oxide in inhibition of ischemia/reperfusion-induced cardiomyocyte apoptosis. Folia Histochem Cytobiol. 2001;39(2):179-80.
Czarnowska, E., Kurzelewski, M., Beresewicz, A., & Karczmarewicz, E. (2001). The role of endogenous nitric oxide in inhibition of ischemia/reperfusion-induced cardiomyocyte apoptosis. Folia Histochemica Et Cytobiologica, 39(2), 179-80.
Czarnowska E, et al. The Role of Endogenous Nitric Oxide in Inhibition of Ischemia/reperfusion-induced Cardiomyocyte Apoptosis. Folia Histochem Cytobiol. 2001;39(2):179-80. PubMed PMID: 11374814.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The role of endogenous nitric oxide in inhibition of ischemia/reperfusion-induced cardiomyocyte apoptosis. AU - Czarnowska,E, AU - Kurzelewski,M, AU - Beresewicz,A, AU - Karczmarewicz,E, PY - 2001/5/26/pubmed PY - 2001/10/12/medline PY - 2001/5/26/entrez SP - 179 EP - 80 JF - Folia histochemica et cytobiologica JO - Folia Histochem. Cytobiol. VL - 39 IS - 2 N2 - The effect of nitric oxide (NO) synthase inhibition on apoptosis of cardiomyocytes during ischemia/reperfusion was investigated. Isolated perfused guinea-pig hearts were subjected to 35 min ischemia (I) followed by 30 min reperfusion (IR) in the presence or absence of NO synthase inhibitors, L-NAME or L-NMMA or a superoxide scavenger, SOD. Apoptosis was assessed by immunohistochemistry (TUNEL assay, Bax protein staining), by spectrophotometric measurement of cytochrome oxidase activity (COX), and by ultrastructural analysis. Inhibition of NOS significantly increased apoptosis with activation of Bax protein and decrease of COX. SOD infusion had a protective effect on these apoptotic markers. The results suggest that endogenous NO synthesis during I/R protects the heart against apoptotic cell death. SN - 0239-8508 UR - https://www.unboundmedicine.com/medline/citation/11374814/The_role_of_endogenous_nitric_oxide_in_inhibition_of_ischemia/reperfusion_induced_cardiomyocyte_apoptosis_ DB - PRIME DP - Unbound Medicine ER -