title: Endothelial dysfunction in human atherosclerotic coronary arteries.
abstract: Human coronary arteries were taken from heart transplant patients. Arteriosclerotic arteries were more depolarized and constricted over the whole PO2 range between 535 and 0 mmHg. During oxygen deficiency, control preparations showed a maximal hyperpolarization of delta V = 10.9 mV and a maximal relaxation of delta T = 0.466 g. Arteriosclerotic arteries, however, became hyperpolarized by merely delta V = 7.1 mV and relaxed by delta T = 0.258 g. In normal coronary arteries, indomethacin reduced the hypoxic hyperpolarization and dilatation at 30 mmHg PO2 by about 51%. The reduction was 27% in arteriosclerotic vessels. The complete removal of the endothelium caused a 49% (73% in arteriosclerotic coronaries) restriction of dilatory vascular reactivity. The relationship was quite similar for a carbogen Krebs solution. The hyperpolarizing and dilatory contribution of prostacyclin was 32% in normal and 12% in arteriosclerotic coronary arteries. The remainder could be attributed to the basal release of endothelium-derived hyperpolarizing factor (EDHF). Thus, it may be concluded that in arteriosclerotic blood vessels, prostacyclin (PGI2) synthesis and release are predominantly diminished. Finally, we found that the ratio PGI2/EDHF in the voltage and tension changes strongly shifted to the PGI2 side with a declining oxygen concentration. This is true for normal and arteriosclerotic vessels. In addition, a disturbed transmembrane cation distribution in the arteriosclerotic coronary vessels may be an additional explanation for the depolarized membrane potential and increased muscle tone. [Na+]i of normal arteries amounted to 16.6, of arteriosclerotic arteries to 60.9 mmol.l-1; [K+]i values were 134.6 in normal and 95.0 mmol.l-1 in arteriosclerotic coronaries, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Institute of Physiology, Free University of Berlin, Germany.
authors.forename: G
authors.initials: G
authors.lastname: Siegel
authors.forename: K
authors.initials: K
authors.lastname: Rückborn
authors.forename: F
authors.initials: F
authors.lastname: Schnalke
authors.forename: J
authors.initials: J
authors.lastname: Müller
mesh_terms: D003324:Coronary Artery Disease / Q000503:physiopathology*; D003331:Coronary Vessels / Q000502:physiology*; D004730:Endothelium, Vascular / Q000737:chemistry / Q000502:physiology* / Q000503:physiopathology; D011464:Epoprostenol / Q000032:analysis; D006801:Humans; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000502:physiology / Q000503:physiopathology; D009569:Nitric Oxide / Q000032:analysis; D010100:Oxygen / Q000097:blood; D011188:Potassium / Q000032:analysis; D012964:Sodium / Q000032:analysis
chemical_list: D009569:Nitric Oxide; D012964:Sodium; D011464:Epoprostenol; D011188:Potassium; D010100:Oxygen