Ventricular homogenates and isolated heart mitochondria from rats made uremic by 5/6 nephrectomy were used to assess the effects of chronic uremia (25±3 days) on the intrinsic ability of the heart to transport and oxidize long-chain fatty acids. Control animals underwent sham operations and were pair-fed daily with the uremic rats. Chronically uremic animals had significantly elevated systolic blood pressures (205±15 mm Hg vs. 150±10 for controls), and their heart weights were increased 30% when compared to pair-fed controls with similar body weights. Myocardial levels of neutral lipid were similar in the chronically uremic and control animals. There was a consistent decrease in the content of free, acetyl-, and acyl-carnitines in hearts from the chronically uremic rats (total carnitine 866±148 nmol/gm wet wt. vs. 1239±270 for controls, p<0.01). Myocardial carnitine content was not reduced in rats made acutely uremic (2 days) by bilateral nephrectomy or in nonuremic rats with cardiac hypertrophy due to chronic (28 days) renovascular hypertension. Palmitylcarnitine acyltransferase activity of isolated heart mitochondrial was not diminished in the chronically uremic animals (13.9±1.1 nmol/min/mg of protein vs. 12.8±0.9 for controls). Rates of mitochondrial oxidation of palmitylcarnitine and values for respiratory control ratio, measured polarographically, were similar in chronically uremic and control rats. In this controlled model of chronic uremia, isolated subcellular components of heart retain the enzymatic ability both to transport and to oxidize long-chain fatty acid normally. However, the myocardial content of carnitine, required for the oxidation of long-chain fatty acid, was significantly reduced after 25 days of uremia.
|Original language||English (US)|
|Number of pages||8|
|Journal||Journal of Laboratory and Clinical Medicine|
|State||Published - Dec 1 1978|
ASJC Scopus subject areas
- Pathology and Forensic Medicine