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 radical-induced lipid peroxidation (LPO) during postischemic reperfusion injury of the myocardium. Therefore, the liberation of HNE into the effluent of isolated perfused rat hearts was investigated. For the first time, the formation of the aldehyde is demonstrated in myocardium. During 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 spontaneously hypertensive (SHR) rats, respectively. In the WKY group, HNE 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 global 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) compared with both the respective preischemic control and the respective reperfusion interval of the WKY group (P < 0.05 each). The SHR rats showed signs of congestive cardiac failure of a decompensated hypertrophy in comparison to the normotensive WKY rats. Moreover, the SHR rat hearts exhibited a lower release of adenine nucleotide degradation products (adenine, inosine, hypoxanthine plus uric acid: 48.1 +/- 10.2 nmol . 30 min(-1). mg protein(-1); P < 0.05) and a diminished functional recovery (left ventricular developed pressure, 32 +/- 16 mmHg; P < 0.05) 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 suggest that products of radical-induced LPO are generated and released from the reperfusion-injured failing myocardium in relation to the degree of functional deterioration. To evaluate this injury, HNE is a potent indicator.