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[Ischemic preconditioning and exogenous L-arginine reduce infarct size in rabbit heart].
Sheng Li Xue Bao. 1996 Dec; 48(6):564-70.SL

Abstract

The effects of NO donor--L-arginine (L-arg) and ischemic preconditioning (IP) on the hemodynamics and myocardial infarct size were examined in the anesthetized rabbit subjected to myocardial ischemia-repefusion to define whether exogenous L-arg could exert a beneficial effect in this pathological model, and whether the L-arg-NO pathway was involved in the cardioprotection provided by IP. The results obtained were as follows: (1) During the course of ischemia (30 min)-reperfusion (180 min), blood pressure, heart rate and myocardial oxygen consumption decreased progressively, and the myocardial infarct size occupied 33.9 +/- 2.4% of the whole left ventricle. (2) The myocardial infarct size could be reduced to 20.1 +/- 2.2% (P < 0.01) by pretreatment with L-arg (300 mg/kg). This myocardial protective effect of L-arg was abolished by NO synthesis inhibitor--Nitro-L-arginine (L-NNA), thereby indicating the involvement of L-arg-NO pathway. (3) IP significantly reduced the infarct size to 21.9 +/- 2.1% (P < 0.01), indicating the prominent cardioprotective effect of such an intervention. Since L-NNA showed no effect on the cardioprotection afforded by IP, it was implied that the L-arg-NO pathway was not involved in the cardioprotective mechanism of IP. (4) Exogenous L-arg might markedly augment cardioprotection provided by IP. The above results strongly suggested that the cardioprotective effect of L-arg on ischemia-reperfused myocardium was mediated by L-arg-NO pathway, which, however, was not involved in the cardioprotection provided by IP.

Authors+Show Affiliations

Department of Physiology, Hebei Medical University, Shijiazhuang.No affiliation info availableNo affiliation info available

Pub Type(s)

English Abstract
Journal Article

Language

chi

PubMed ID

9389155

Citation

Ding, Y F., et al. "[Ischemic Preconditioning and Exogenous L-arginine Reduce Infarct Size in Rabbit Heart]." Sheng Li Xue Bao : [Acta Physiologica Sinica], vol. 48, no. 6, 1996, pp. 564-70.
Ding YF, Li YL, Ho SY. [Ischemic preconditioning and exogenous L-arginine reduce infarct size in rabbit heart]. Sheng Li Xue Bao. 1996;48(6):564-70.
Ding, Y. F., Li, Y. L., & Ho, S. Y. (1996). [Ischemic preconditioning and exogenous L-arginine reduce infarct size in rabbit heart]. Sheng Li Xue Bao : [Acta Physiologica Sinica], 48(6), 564-70.
Ding YF, Li YL, Ho SY. [Ischemic Preconditioning and Exogenous L-arginine Reduce Infarct Size in Rabbit Heart]. Sheng Li Xue Bao. 1996;48(6):564-70. PubMed PMID: 9389155.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Ischemic preconditioning and exogenous L-arginine reduce infarct size in rabbit heart]. AU - Ding,Y F, AU - Li,Y L, AU - Ho,S Y, PY - 1996/12/1/pubmed PY - 1997/12/6/medline PY - 1996/12/1/entrez SP - 564 EP - 70 JF - Sheng li xue bao : [Acta physiologica Sinica] JO - Sheng Li Xue Bao VL - 48 IS - 6 N2 - The effects of NO donor--L-arginine (L-arg) and ischemic preconditioning (IP) on the hemodynamics and myocardial infarct size were examined in the anesthetized rabbit subjected to myocardial ischemia-repefusion to define whether exogenous L-arg could exert a beneficial effect in this pathological model, and whether the L-arg-NO pathway was involved in the cardioprotection provided by IP. The results obtained were as follows: (1) During the course of ischemia (30 min)-reperfusion (180 min), blood pressure, heart rate and myocardial oxygen consumption decreased progressively, and the myocardial infarct size occupied 33.9 +/- 2.4% of the whole left ventricle. (2) The myocardial infarct size could be reduced to 20.1 +/- 2.2% (P < 0.01) by pretreatment with L-arg (300 mg/kg). This myocardial protective effect of L-arg was abolished by NO synthesis inhibitor--Nitro-L-arginine (L-NNA), thereby indicating the involvement of L-arg-NO pathway. (3) IP significantly reduced the infarct size to 21.9 +/- 2.1% (P < 0.01), indicating the prominent cardioprotective effect of such an intervention. Since L-NNA showed no effect on the cardioprotection afforded by IP, it was implied that the L-arg-NO pathway was not involved in the cardioprotective mechanism of IP. (4) Exogenous L-arg might markedly augment cardioprotection provided by IP. The above results strongly suggested that the cardioprotective effect of L-arg on ischemia-reperfused myocardium was mediated by L-arg-NO pathway, which, however, was not involved in the cardioprotection provided by IP. SN - 0371-0874 UR - https://www.unboundmedicine.com/medline/citation/9389155/[Ischemic_preconditioning_and_exogenous_L_arginine_reduce_infarct_size_in_rabbit_heart]_ L2 - https://medlineplus.gov/heartattack.html DB - PRIME DP - Unbound Medicine ER -