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OBJECTIVE Cigarette smoking may exert its atherogenic effect by delaying the plasma clearance of dietary fat and cholesterol, allowing more time for their interaction with the artery wall. To study the effects of smoke on chylomicron metabolism in rats, we examined the metabolic effects of smoke on both whole animals and chylomicron particles in vitro. METHODS Carbon 14- and hydrogen 3-labeled chylomicrons were injected intravenously into smoke-treated rats and control rats that were not exposed to smoke (sham smoked). Plasma clearance, hepatic uptake, and heart binding were measured. In a second set of experiments, chylomicron particles were exposed to cigarette smoke in vitro by either: (1) passing smoke through chylomicrons suspended in saline solution (SCM) or (2) passing smoke through saline solution alone, then mixing the saline solution with chylomicrons (CM + SS). Normal (non-smoke exposed) rats were infused with either SCM, CM + SS, or control chylomicrons (CCM). Plasma clearance, hepatic uptake, and heart binding were again measured. RESULTS The initial plasma clearance time of labeled chylomicrons did not differ between smoke-treated and control animals. However, hepatic uptake of chylomicron cholesterol was slower in smoke-treated animals (46.1% +/- 0.9% of injected dose) than in controls (61.5% +/- 2.1%, p < 0.001). In contrast, more labeled chylomicrons remained in the heart of smoke-treated rats than controls (0.89% +/- 0.18% vs 0.45% +/- 0.05%, p < 0.05). Disappearance of 14C-labeled cholesterol from blood was delayed in rats injected with SCM (half-life = 9.0 +/- 0.4 minutes) and CM + SS (half-life = 8.0 +/- 0.4 minutes), compared with the time in rats injected with CCM (6.6 +/- 0.3 minutes, p < 0.05). Hepatic uptake of SCM (40.6% +/- 1.9% of injected dose) and CM + SS (45.0% +/- 1.9%) was less than that of CCM (60.7% +/- 4.4%, p < 0.05). In addition, the binding to the heart increased from 0.97% +/- 0.29% (CCM) to 2.45% +/- 0.30% with the infusion of SCM (p < 0.05). The binding in the heart of CM + SS (0.95% +/- 0.04%) was not different from that of CCM. CONCLUSIONS These data demonstrate for the first time that cigarette smoke exposure prolongs chylomicron residence time in tissues (heart) and delays hepatic uptake of chylomicron cholesterol in rats. The effect is present when either the animal or the chylomicron particle is exposed to smoke. We hypothesize that prolonged binding of relatively cholesterol-rich chylomicron remnants to endothelial surfaces could create a more atherogenic postprandial milieu.
X M Pan, and
I Staprans, and
T E Read, and
J H Rapp
August 1994,
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