Lipoprotein regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity in rat liver cell cultures.

A primary cell culture technique was used to study the effects of lipoproteins on rat hepatocyte 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase activity. In this system, lipoproteins prepared from normocholesterolemic rat and human plasma, including low density lipoproteins, did not inhibit hepatocyte HMG-CoA reductase activity whereas very low density lipoproteins and high density lipoproteins isolated from the same sources were stimulatory. A lipoprotein was isolated from the plasma of cholesterol-fed rats that did inhibit hepatocyte HMG-CoA reductase activity.

Failure of certain antiplatelet drugs to affect myointimal thickening following arterial endothelial injury in the rat.

The effect of aspirin, reserpine, and flurbiprofen on in vivo platelet function and intimal smooth muscle cell hyperplasia in rat carotid arteries subjected to endothelial injury was investigated and related to the effect of these drugs on in vitro platelet aggregation. Endothelial injury was achieved by infusing air briefly into a segment of right common carotid artery. Beginning before or after surgery, experimental animals were given sufficient drug to suppress platelet aggregation in vitro in response to collagen, adenosine diphosphate, or thrombin.

Regression of myointimal thickening following carotid endothelial injury and development of aortic foam cell lesions in long term hypercholesterolemic rats.

In an earlier report (Clowes AW, Ryan GB, Breslow JL, Karnovsky MJ: Lab Invest 35:6, 1976) we demonstrated that cholesterol feeding of rats led to hypercholesterolemia but no increase in smooth muscle cell (SMC) proliferation in right carotid arteries subjected to a standard endothelial injury when compared with normolipemic control animals. We have now examined these plaques at 6 months and 1 year after injury. In control animals, the carotid initimal thickening regressed to a relatively small, acellular, fibrous scar; there was no evidence of renewed endothelial injury and secondary SMC proliferation.

Absence of enhanced intimal thickening in the response of the carotid arterial wall to endothelial injury in hypercholesterolemic rats.

Young male Sprague-Dawley rats fed a high cholesterol, thyroid-suppressive diet were subjected to drying injury of carotid artery endothelium; animals were sacrificed at various times up to 3 months after injury, and the vessels were examined by light, scanning, and transmission electron microscopy. The diet induced marked elevation of serum cholesterol mainly present in lipoproteins of density less than 1.063.