Release of 4-hydroxynonenal, an aldehydic mediator of inflammation, during postischaemic reperfusion of the myocardium.

For the first time it was demonstrated that 4-hydroxynonenal (HNE) is formed by the myocardium. 1 to 2 pmol HNE/min/mg protein were released from isolated perfused hearts of 18-month-old WKY rats during a normoxic period of perfusion. During the first minutes of reperfusion following 30 min of ischaemia, the mean value of HNE release increased in comparison to pre-ischaemic HNE release (pre-ischaemic control). However, the alterations were significant only in the second minute of reperfusion. HNE liberation significantly intensified during the early reperfusion period of hearts of 18-month-old spontaneously hypertensive rats (SHR, with cardiac hypertrophy and congestive heart failure) in comparison with the pre-ischaemic control period. Furthermore, HNE liberation from those hearts was higher than from hearts of normotensive control animals (WKY rats). Maximum quantities were observed 2 min after ischaemia, with 6 to 10 pmol HNE/min/mg protein. The results suggest that the formation of chemotactic products of radical-induced lipid peroxidation, such as HNE, is markedly increased in reperfused hypertrophic and failing myocardium, and emphasize the role of HNE as a possible chemotactic agent during postischaemic reoxygenation.