Nitric oxide triggers late preconditioning against myocardial infarction in conscious rabbits

Y. Qiu, A. Rizvi, X. L. Tang, S. Manchikalapudi, H. Takano, A. K. Jadoon, W. J. Wu, R. Bolli

Research output: Contribution to journalArticle

Abstract

We tested the hypothesis that late preconditioning (PC) against myocardial infarction is triggered by the formation of nitric oxide (NO). Conscious rabbits underwent a 30-min coronary occlusion followed by 3 days of reperfusion. In group I (control group, n = 10), rabbits were not preconditioned, whereas in group H (n = 10), they were preconditioned 24 h earlier with a sequence of six 4-min occlusion/4-min reperfusion cycles. Myocardial infarct size (tetrazolium staining) was reduced by 50% by PC (28.6 ± 3.2% of the risk region ingroup II vs. 56.9 ± 5.9% in controls, P <0.05). This reduction in cell death was associated with improved recovery of myocardial function [systolic thickening fraction (by sonomicrometry) at 3 days: 2.0 ± 11.0% of baseline in group II vs. -20.0 ± 2.8% ingroup I, P <0.05]. Group III rabbits (n = 11) underwent the same protocol as group H except that the rabbits received the NO synthase inhibitor N(ω)-nitro-L- arginine (L-NNA, 13 mg/kg) before the PC ischemia. In these animals, infarct size did not differ significantly from that observed in control rabbits, indicating that L-NNA completely blocked the development of late PC against myocardial infarction. In group/V (n = 9), rabbits received L-NNA as in group III, but without the six occlusion-reperfusion cycles, and were subjected to the 30-min occlusion 24 h later. In this group, infarct size did not differ from that observed in controls, demonstrating that pretreatment with L-NNA, in itself, did not affect the extent of cell death. Taken together, these results indicate that, in the conscious rabbit, the development of late PC against myocardial infarction is triggered by the generation of NO during the PC ischemia. It is proposed that NO plays a key role in the delayed myocardial adaptation to ischemic stress.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume273
Issue number6 42-6
StatePublished - 1997
Externally publishedYes

Fingerprint

Nitric Oxide
Myocardial Infarction
Rabbits
Reperfusion
Cell Death
Ischemia
Coronary Occlusion
Recovery of Function
Nitric Oxide Synthase
Arginine
Staining and Labeling
Control Groups

Keywords

  • L-arginine
  • Myocardial ischemia-reperfusion
  • Nitric oxide synthase
  • Nitrogen radicals
  • Oxygen radicals

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Qiu, Y., Rizvi, A., Tang, X. L., Manchikalapudi, S., Takano, H., Jadoon, A. K., ... Bolli, R. (1997). Nitric oxide triggers late preconditioning against myocardial infarction in conscious rabbits. American Journal of Physiology - Heart and Circulatory Physiology, 273(6 42-6).

Nitric oxide triggers late preconditioning against myocardial infarction in conscious rabbits. / Qiu, Y.; Rizvi, A.; Tang, X. L.; Manchikalapudi, S.; Takano, H.; Jadoon, A. K.; Wu, W. J.; Bolli, R.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 273, No. 6 42-6, 1997.

Research output: Contribution to journalArticle

Qiu, Y, Rizvi, A, Tang, XL, Manchikalapudi, S, Takano, H, Jadoon, AK, Wu, WJ & Bolli, R 1997, 'Nitric oxide triggers late preconditioning against myocardial infarction in conscious rabbits', American Journal of Physiology - Heart and Circulatory Physiology, vol. 273, no. 6 42-6.
Qiu, Y. ; Rizvi, A. ; Tang, X. L. ; Manchikalapudi, S. ; Takano, H. ; Jadoon, A. K. ; Wu, W. J. ; Bolli, R. / Nitric oxide triggers late preconditioning against myocardial infarction in conscious rabbits. In: American Journal of Physiology - Heart and Circulatory Physiology. 1997 ; Vol. 273, No. 6 42-6.
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AU - Qiu, Y.

AU - Rizvi, A.

AU - Tang, X. L.

AU - Manchikalapudi, S.

AU - Takano, H.

AU - Jadoon, A. K.

AU - Wu, W. J.

AU - Bolli, R.

PY - 1997

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N2 - We tested the hypothesis that late preconditioning (PC) against myocardial infarction is triggered by the formation of nitric oxide (NO). Conscious rabbits underwent a 30-min coronary occlusion followed by 3 days of reperfusion. In group I (control group, n = 10), rabbits were not preconditioned, whereas in group H (n = 10), they were preconditioned 24 h earlier with a sequence of six 4-min occlusion/4-min reperfusion cycles. Myocardial infarct size (tetrazolium staining) was reduced by 50% by PC (28.6 ± 3.2% of the risk region ingroup II vs. 56.9 ± 5.9% in controls, P <0.05). This reduction in cell death was associated with improved recovery of myocardial function [systolic thickening fraction (by sonomicrometry) at 3 days: 2.0 ± 11.0% of baseline in group II vs. -20.0 ± 2.8% ingroup I, P <0.05]. Group III rabbits (n = 11) underwent the same protocol as group H except that the rabbits received the NO synthase inhibitor N(ω)-nitro-L- arginine (L-NNA, 13 mg/kg) before the PC ischemia. In these animals, infarct size did not differ significantly from that observed in control rabbits, indicating that L-NNA completely blocked the development of late PC against myocardial infarction. In group/V (n = 9), rabbits received L-NNA as in group III, but without the six occlusion-reperfusion cycles, and were subjected to the 30-min occlusion 24 h later. In this group, infarct size did not differ from that observed in controls, demonstrating that pretreatment with L-NNA, in itself, did not affect the extent of cell death. Taken together, these results indicate that, in the conscious rabbit, the development of late PC against myocardial infarction is triggered by the generation of NO during the PC ischemia. It is proposed that NO plays a key role in the delayed myocardial adaptation to ischemic stress.

AB - We tested the hypothesis that late preconditioning (PC) against myocardial infarction is triggered by the formation of nitric oxide (NO). Conscious rabbits underwent a 30-min coronary occlusion followed by 3 days of reperfusion. In group I (control group, n = 10), rabbits were not preconditioned, whereas in group H (n = 10), they were preconditioned 24 h earlier with a sequence of six 4-min occlusion/4-min reperfusion cycles. Myocardial infarct size (tetrazolium staining) was reduced by 50% by PC (28.6 ± 3.2% of the risk region ingroup II vs. 56.9 ± 5.9% in controls, P <0.05). This reduction in cell death was associated with improved recovery of myocardial function [systolic thickening fraction (by sonomicrometry) at 3 days: 2.0 ± 11.0% of baseline in group II vs. -20.0 ± 2.8% ingroup I, P <0.05]. Group III rabbits (n = 11) underwent the same protocol as group H except that the rabbits received the NO synthase inhibitor N(ω)-nitro-L- arginine (L-NNA, 13 mg/kg) before the PC ischemia. In these animals, infarct size did not differ significantly from that observed in control rabbits, indicating that L-NNA completely blocked the development of late PC against myocardial infarction. In group/V (n = 9), rabbits received L-NNA as in group III, but without the six occlusion-reperfusion cycles, and were subjected to the 30-min occlusion 24 h later. In this group, infarct size did not differ from that observed in controls, demonstrating that pretreatment with L-NNA, in itself, did not affect the extent of cell death. Taken together, these results indicate that, in the conscious rabbit, the development of late PC against myocardial infarction is triggered by the generation of NO during the PC ischemia. It is proposed that NO plays a key role in the delayed myocardial adaptation to ischemic stress.

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