Key result
Magnesium and diltiazem reduced plasma fibronectin release during reperfusion after acute myocardial infarction in swine, whereas Mac-1 inhibition increased fibronectin levels during ischemia.
Why the study?
Does administration of magnesium, diltiazem, or a Mac-1 inhibitor modulate plasma fibronectin levels during myocardial ischemia-reperfusion in a swine model?
Does administration of magnesium, diltiazem, or a Mac-1 inhibitor modulate plasma fibronectin levels during myocardial ischemia-reperfusion in a swine model?
Magnesium and diltiazem attenuate the release of plasma fibronectin during myocardial ischemia-reperfusion in swine, suggesting potential modulatory effects of these agents in coronary artery disease.
Should not change MI management; leaves open fibronectin modulation as a hypothesis-generating target in reperfusion injury.
The important role of fibronectin (Fn) has been recognized in patients with ischemic heart disease. However, serial changes of Fn during both brief and prolonged ischemia-reperfusion are poorly known. Plasma Fn was measured during acute myocardial infarction (AMI) and myocardial stunning (MS), and in the absence of myocardial injury. The effects of magnesium (Mg), diltiazem, and a Mac-1 inhibitor on the level of Fn were elucidated. Forty-nine swine underwent prolonged (50 min) or brief (8 min) coronary artery occlusion followed by reperfusion, while six control animals were free of ischemia. During the AMI experiments, plasma Fn underwent a significant progressive increase. Mg or diltiazem similarly affects the plasma Fn, reducing its release during the entire reperfusion period, and did not influence the plasma Fn in the absence of myocardial injury. Contrarily, Mac-1 inhibition resulted in the Fn elevation in controls, and during the occlusion phase, with no significant effect during reperfusion. There were no changes in the plasma Fn during MS, while inhibition of Mac-1 was associated with the significant increase of Fn during ischemia-reperfusion. Ability of Mg, diltiazem, and leumedins to modulate plasma Fn level may have direct clinical implications for the use of these agents in patients with coronary artery disease.
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Serebruany et al. (1998) studied Myocardial ischemia-reperfusion (n=55). Magnesium, diltiazem, and a Mac-1 inhibitor vs. Control animals free of ischemia was evaluated on Plasma fibronectin levels. Magnesium and diltiazem reduced plasma fibronectin release during reperfusion after acute myocardial infarction in swine, whereas Mac-1 inhibition increased fibronectin levels during ischemia.
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