Tags

Type your tag names separated by a space and hit enter

Cardioprotective activity of endogenous and exogenous nitric oxide on ischaemia reperfusion injury in isolated guinea pig hearts.
Inflamm Res. 1999 Nov; 48(11):561-8.IR

Abstract

BACKGROUND

We evaluated the contribution of endogenous and exogenous nitric oxide (NO) in ischaemia reperfusion (IR) injury and histamine release in the isolated guinea pig heart.

METHODS

Ischaemia reperfusion was performed in isolated Langendorff perfused guinea pig heart throughout the ligature of the left anterior descending coronary (LAD) artery for 20 min, and following the release of the ligature for a further 20 min.

RESULTS

IR promoted a linear release of lactate dehydrogenase (LDH) and a preferential release of histamine in the reperfusion phase. The amount of nitrite (NO2-, one of the breakdown products of NO) released during IR was significantly lower than in the control hearts. These effects were accompanied by an increase in calcium levels and malonyl-dialdehyde (MDA) production in the left ventricle and by a decrease in cardiac mast cell metachromasia. Perfusion of the hearts with two inhibitors of the nitric oxide synthase pathway, namely N(G)-monomethyl-L-arginine (L-NMMA, 10(-4) M) or nitroarginine methylester (L-NAME, 10(-5) M) significantly enhanced histamine and LDH release; these effects were attenuated by co-infusion with L-arginine (10(-4) M) but not D-arginine (10(-4) M), while L-arginine (10(-4) M) alone had no effect. Perfusion of the heart with sodium nitroprusside (SNP), 3-morpholinosydnonimine (SIN-1), glyceryl trinitrate (GTN), all at 10(-5) M, reduced histamine release, LDH release, calcium overload and MDA production induced by IR. These effects were amplified by concomitant perfusion with superoxide dismutase (SOD, 50 IU/ml).

CONCLUSION

The endogenous production of NO provides significant myocardial protection from IR injury and histamine release. These effects were mimicked by various NO donors.

Authors+Show Affiliations

Department of Preclinical and Clinical Pharmacology, Florence, Italy. masini@server1.pharm.unifi.itNo affiliation info availableNo affiliation info availableNo affiliation info availableNo 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

10598011

Citation

Masini, E, et al. "Cardioprotective Activity of Endogenous and Exogenous Nitric Oxide On Ischaemia Reperfusion Injury in Isolated Guinea Pig Hearts." Inflammation Research : Official Journal of the European Histamine Research Society ... [et Al.], vol. 48, no. 11, 1999, pp. 561-8.
Masini E, Salvemini D, Ndisang JF, et al. Cardioprotective activity of endogenous and exogenous nitric oxide on ischaemia reperfusion injury in isolated guinea pig hearts. Inflamm Res. 1999;48(11):561-8.
Masini, E., Salvemini, D., Ndisang, J. F., Gai, P., Berni, L., Moncini, M., Bianchi, S., & Mannaioni, P. F. (1999). Cardioprotective activity of endogenous and exogenous nitric oxide on ischaemia reperfusion injury in isolated guinea pig hearts. Inflammation Research : Official Journal of the European Histamine Research Society ... [et Al.], 48(11), 561-8.
Masini E, et al. Cardioprotective Activity of Endogenous and Exogenous Nitric Oxide On Ischaemia Reperfusion Injury in Isolated Guinea Pig Hearts. Inflamm Res. 1999;48(11):561-8. PubMed PMID: 10598011.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cardioprotective activity of endogenous and exogenous nitric oxide on ischaemia reperfusion injury in isolated guinea pig hearts. AU - Masini,E, AU - Salvemini,D, AU - Ndisang,J F, AU - Gai,P, AU - Berni,L, AU - Moncini,M, AU - Bianchi,S, AU - Mannaioni,P F, PY - 1999/12/22/pubmed PY - 1999/12/22/medline PY - 1999/12/22/entrez SP - 561 EP - 8 JF - Inflammation research : official journal of the European Histamine Research Society ... [et al.] JO - Inflamm. Res. VL - 48 IS - 11 N2 - BACKGROUND: We evaluated the contribution of endogenous and exogenous nitric oxide (NO) in ischaemia reperfusion (IR) injury and histamine release in the isolated guinea pig heart. METHODS: Ischaemia reperfusion was performed in isolated Langendorff perfused guinea pig heart throughout the ligature of the left anterior descending coronary (LAD) artery for 20 min, and following the release of the ligature for a further 20 min. RESULTS: IR promoted a linear release of lactate dehydrogenase (LDH) and a preferential release of histamine in the reperfusion phase. The amount of nitrite (NO2-, one of the breakdown products of NO) released during IR was significantly lower than in the control hearts. These effects were accompanied by an increase in calcium levels and malonyl-dialdehyde (MDA) production in the left ventricle and by a decrease in cardiac mast cell metachromasia. Perfusion of the hearts with two inhibitors of the nitric oxide synthase pathway, namely N(G)-monomethyl-L-arginine (L-NMMA, 10(-4) M) or nitroarginine methylester (L-NAME, 10(-5) M) significantly enhanced histamine and LDH release; these effects were attenuated by co-infusion with L-arginine (10(-4) M) but not D-arginine (10(-4) M), while L-arginine (10(-4) M) alone had no effect. Perfusion of the heart with sodium nitroprusside (SNP), 3-morpholinosydnonimine (SIN-1), glyceryl trinitrate (GTN), all at 10(-5) M, reduced histamine release, LDH release, calcium overload and MDA production induced by IR. These effects were amplified by concomitant perfusion with superoxide dismutase (SOD, 50 IU/ml). CONCLUSION: The endogenous production of NO provides significant myocardial protection from IR injury and histamine release. These effects were mimicked by various NO donors. SN - 1023-3830 UR - https://www.unboundmedicine.com/medline/citation/10598011/Cardioprotective_activity_of_endogenous_and_exogenous_nitric_oxide_on_ischaemia_reperfusion_injury_in_isolated_guinea_pig_hearts_ L2 - https://dx.doi.org/10.1007/s000110050504 DB - PRIME DP - Unbound Medicine ER -