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editorial
. 2002 Jun;87(6):507–509. doi: 10.1136/heart.87.6.507

Table 1.

Proposed beneficial and adverse effects of nitric oxide (NO) on myocardial function in sepsis

Potential cardiodepressant effects of NO
    (1) Alterations in protein kinase activity and then L type calcium channel
    (2) Decrease in the myofibril response to calcium
    (3) Decreased cAMP via phosphodiesterase
    (4) Direct inhibition of mitochondrial respiration and therefore adenosine triphosphate production within the myocardium
    (5) Stimulation of cellular damage following binding with reactive oxygen species to form peroxynitrite
    (6) Triggering of apoptosis in cardiomyocytes
Potential cardioprotective effects of NO
    (1) Increased myocardial perfusion due to vasodilatory effect
    (2) Free radical scavenger reducing ischaemia reperfusion injury via:
        –inhibition of platelet aggregation
        –inhibition of leucocyte adhesion to endothelial cells
        –stabilisation of cell membranes
    (3) Mediation of ventricular dilatation allowing utilisation of Frank-Starling mechanism
    (4) Antiarrhythmic properties of NO
    (5) Macrophage activation leading to bacterial lysis