Reduced 4-hydroxynonenal degradation in hearts of spontaneously hypertensive rats during normoxia and postischemic reperfusion.

4-Hydroxynonenal (HNE) degradation was investigated in isolated perfused rat hearts of the WKY and SHR strains before and after ischemia. HNE (10 mumoles l-1) were infused and the concentration of HNE in the effluent was determined. The rate of initial consumption was about 50 nmoles min-1 g-1 wet weight in hearts of both the WKY and SHR rats. In the WKY rat hearts, this rate of HNE degradation did not change during several minutes of HNE infusion and also remained constant during postischemic reperfusion. In the hearts of the SHR rats the HNE degradation rate declined within 5 min to 25 nmoles min-1 g-1 wet weight. Also during postischemic reperfusion, there was a lower HNE degradation rate in the SHR rat hearts than in the WKY rat hearts. The influence of hypertrophy on the rate of HNE degradation is discussed. It is suggested that the low degradation of the cytotoxic lipid peroxidation product, HNE, in hypertrophic hearts may contribute to reduced antioxidant defence in those hearts.