Smooth muscle cell (SMC) proliferation is known to be an important factor for the development of restenosis after percutaneous transluminal coronary angioplasty. To determine the time course of intimal and medial SMC proliferation and morphological changes after experimental angioplasty, an intimal atheroma was produced with repeated weak electrical stimulations in the right carotid artery of 45 male New Zealand White rabbits. Angioplasty was subsequently performed in 35 rabbits, and the proliferative responses were analyzed with histomorphological and immunohistological criteria at 3, 7, 14, 21, 28, and 42 days after intervention. A hemodynamic relevant stenosis after angioplasty was found in eight (23%) of 35 dilated arteries. In five rabbits the stenosis was due to a mural thrombus, and in three animals restenosis was caused by intimal SMC proliferation. In all dilated arteries the intimal wall thickness increased from 13 +/- 5 intimal cell layers (after electrical stimulation) to 33 +/- 14 cell layers during 28 days after angioplasty (p less than 0.05). Later than 4 weeks after angioplasty, no additional increase of intimal thickening occurred. Application of bromodeoxyuridine 18 and 12 hours before excision of the vessels allowed determination of the percent of cells undergoing DNA synthesis in the intima and media using monoclonal antibody against bromodeoxyuridine. SMCs were identified by alpha-actin staining. Immunohistological quantification of intimal SMC proliferation showed a maximum of cells undergoing DNA synthesis within the first 7 days after angioplasty (p less than 0.01). In contrast, medial proliferation of SMCs was delayed and showed a small but significant increase 21 days after dilatation (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

The purpose of our study was to evaluate the cytotoxicity of incubation solutions used in heart surgery to endothelial cells. The endothelial layer of human saphenous veins (HSV) and bovine internal mammary arteries (BMA) and veins (BMV) were studied after a two-hour storage interval and compared with control vessel segments prepared immediately after harvesting. To visualize the endothelial cell damage, specimens were stained with a silver nitrate technique. The surface covered by light-microscopically intact endothelial cells was computed in percent. In the control HSV segments 70.8 +/- 4.6% of the endothelium were found to be morphologically intact. The results for stored HSV segments were 50.0 +/- 4.2% (Bretschneider's solution), 14.8 +/- 4.5% (physiological saline), 0.45 +/- 0.1% (physiological saline with heparin), 16.7 +/- 4.7% (Ringer's lactate) and 37.2 +/- 5.3% (heparinized blood). Comparable values obtained with BMA specimens were 98.3 +/- 0.7% (controls), 78.1 +/- 4.7% (Bretschneider's solution), 39.2 +/- 3.3% (physiological saline), 8.4 +/- 2.0% (physiological saline with heparin), 11.3 +/- 1.7% (Ringer's lactate) and 67.8 +/- 6.2% (heparinized blood). A similar trend was found with BMV segments: 85.2 +/- 4.7% (controls), 75.6 +/- 6.0% (Bretschneider's solution), 49.5 +/- 8.9% (physiological saline), 5.95 +/- 0.7% (physiological saline with heparin), 6.2 +/- 0.7% (Ringer's lactate) and 54.3 +/- 5.1% (heparinized blood). In conclusion, Bretschneider's solution proved to be superior for storage of bypass grafts in comparison to all other tested solutions in this series.

To study the effect of nicotine, cholesterol feeding, and their combination on endothelial and smooth muscle cells in vascular wall plaques an experimental method was established which allows the immunohistochemical detection and quantification of the fractions of endothelial and smooth muscle cells in DNA synthesis under the effect of these stimuli. For this purpose standardized fibromuscular plaques were produced by electrostimulation in the common carotid arteries of rabbits. The animals received either nicotine via implanted osmotic minipumps or a cholesterol diet or both. Plaque size was determined at the end of the experiments after 7 or 14 days as well as the fraction of endothelial and smooth muscle cells in DNA synthesis during exposure to bromodeoxyuridine (BrdU). The BrdU labeling index of endothelial cells clearly increased under chronic nicotine administration for either 7 days or 14 days compared to controls. The combination of nicotine and cholesterol diet led to a more significant increase. In contrast, the BrdU labeling index of smooth muscle cells was not increased under nicotine delivery. The combination of nicotine and cholesterol, however, led to a significant increase of the BrdU labeling index of smooth muscle cells in the plaques compared to cholesterol feeding. Measurement of the plaque size revealed no difference between controls and nicotine-treated animals after 14 days of nicotine delivery, whereas the combination of cholesterol and nicotine produced increased plaque formation compared to a group of animals which received a cholesterol diet alone.

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