Inducible and endothelial nitric oxide synthase expression in repetitive myocardial stunning

C. S R Baker, O. Rimoldi, P. G. Camici, E. Barnes, D. O. Haskard, J. M. Polak, R. J C Hall

Research output: Contribution to journalArticlepeer-review


Inducible nitric oxide synthase (iNOS) may mediate the late window of ischaemic preconditioning (IP) and endothelial NOS (eNOS), the delayed, enhanced vasodilation seen following myocardial stunning (MS). To study NOS expression after MS, 6 open chested swine (34-39Kg) underwent ten 2-minute episodes of circumflex artery occlusion. Four sham operated animals acted as external controls (EC). Regional myocardial function was measured using segment shortening. Nitric oxide (NO) was assayed from the aorta and local coronary vein draining the ischaemic segment at baseline and up to 6 hrs post reperfusion by chemiluminesence. iNOS, eNOS and CD31 expression was quantitated by Western blotting and localisation of iNOS and eNOS expression was performed on ischaemic, non-ischaemia (internal control, IC) and EC tissues by immunocytochemistry. Results: Myocardial function fell to 53 +/- 8% (mean +/- SEM) of baseline 30 min post reperfusion, recovering to 92 +/- 8.7% by 6 hrs (indicating MS). Function remained stable in controls. No rise in serum CK-MB was seen during the study. NO production increased significantly from baseline in the stunned group at 6 hrs (15.1 +/- 5.7% vs. -6 +/- 3.75%, p

Original languageEnglish
Issue numberSUPPL. 1
Publication statusPublished - May 1999

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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