4-HYDROXYRMONENAL, A NOVEL INDICATOR OF LIPID-PEROXIDATION FOR REPERFUSION INJURY OF THE MYOCARDIUM

4-Hydroxynonenal (KNE) has been proposed as an important marker of rad ical-induced lipid peroxidation (LPO) during postischemic reperfusion injury of the myocardium. Therefore, the liberation of HNE into the ef fluent of isolated perfused rat hearts was investigated. For the first time, the formation of the aldehyde is demonstrated in myocardium. Du ring control perfusion, 1.28 +/- 0.33 pmol HNE . min(-1). mg protein(- 1) were formed by the hearts of 18-mo-old Wistar-Kyoto (WKY) rats and 2.74 +/- 1.12 pmol . min(-1). mg protein(-1) by those of 18-mo-old spo ntaneously hypertensive (SHR) rats, respectively. In the WKY group, HN E release increased to 3.35 +/- 1.13 pmol . min(-1). mg protein(-1) 2 min after the onset of reperfusion following 30 min of total and globa l ischemia compared with the preischemic control period (P < 0.05). In the SHR group, HNE liberation was higher during reperfusion (8.66 +/- 1.33 pmol . min(-1). mg protein(-1), maximum at 2 min reperfusion) co mpared with both the respective preischemic control and the respective reperfusion interval of the WKY group (P < 0.05 each). The SHR rats s howed signs of congestive cardiac failure of a decompensated hypertrop hy in comparison to the normotensive WKY rats. Moreover, the SHR rat h earts exhibited a lower release of adenine nucleotide degradation prod ucts (adenine, inosine, hypoxanthine plus uric acid: 48.1 +/- 10.2 nmo l . 30 min(-1). mg protein(-1); P < 0.05) and a diminished functional recovery (left ventricular developed pressure, 32 +/- 16 mmHg; P < 0.0 5) during 30 min of reperfusion compared with the WKY group (77.9 +/- 14.4 nmol 30 min-1 . mg protein(-1); 90 +/- 21 mmHg). The results sugg est that products of radical-induced LPO are generated and released fr om the reperfusion-injured failing myocardium in relation to the degre e of functional deterioration. To evaluate this injury, HNE is a poten t indicator.