[Early changes in experimental carotid artery sclerosis].
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Biomedical subjects
Publications and source records attributed to E Betz.
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In rabbit carotid arteries intimal smooth muscle cell proliferations were induced by repeated local electrical stimulation of the artery wall. Oxygen uptake and lactate production of the proliferating tissue were determined in vitro and compared with the results obtained from nonstimulated arterial wall segments. Under the incubation conditions employed, oxygen consumption and lactate production of the proliferating tissue were 91.3 and 62.5 nmol x min-1 x mg-1 DNA, compared with the control values of 70.8 and 41.6 nmol x min-1 x mg-1 DNA. The DNA content of the proliferates and normal arterial wall tissue amounted to 9.6 and 12.0 microgram DNA x mg-1 dry weight. The results show that in proliferates obtained with the described procedure there is an increased capacity for ATP regenerating systems, respiration and glycolysis, indicating a modified function of the proliferating smooth muscle cells.
Local transmural electrical stimulation by chronically implanted electrodes of a carotid artery in rabbits was daily repeated. The area in direct contact to the electrodes covered 0.5 x 5 mm of adventitia. The carotid walls received DC impulses (10 ms/imp, 10 Hz, 100 microA) 2 x 1/2 h daily. Within 4 weeks a proliferate of smooth muscle cells develops in the intima at the spot where the anode contacts the outside of the artery. If the animals were fed 2% cholesterol in normal food the proliferate developed to a typical atheroma. The other parts of the arterial system did not develop plaques within this time. At the luminal side of the plaques no significant adhesions of platelets could be seen. Addition of 300 mg 2-ethyl-3-[-4-hydroxybenzoyl]-benzofuran (benzarone, Fragivix) to 100 g of animal food (containing 2% cholesterol) caused a less pronounced increase of serum cholesterol than in the controls which received cholesterol-containing food without benzarone. The development of plaques could not be prevented by benzarone, however, the growth of the atheromatous plaque was inhibited and the incorporation of lipids into the plaques was less pronounced than in those animals which received a diet with cholesterol but without benzarone. In those animals which received benzarone more lipid-laden foam cells were seen moving through the endothelium out of the plaque into the lumen of the stimulated artery. These foam cells were of mononuclear origin.
Common carotid arteries of rabbits were locally stimulated every day by chronically repeated electrical impulses for periods up to 4 weeks. Morphological observations revealed that, primarily at the anodal site of the stimulated segment, smooth muscle cells penetrated from the media through the internal elastic membrane and proliferated in the subendothelial space below a morphologically unchanged endothelium. When the plasma cholesterol was raised by cholesterol feeding, typical atheromatous plaques were formed. Biochemical studies showed an increased metabolic activity of the proliferating cells; in comparison with normal intima-media, the tissue content of DNA, protein, and lactate was increased, whereas that of glucose and glycogen was decreased in the proliferates. Furthermore, during in vitro incubation, the uptake of oxygen and glucose and the production of lactate was enhanced. The increased energy consumption of the proliferates indicates a modified metabolic function of these cells.
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In addition to outlining what to teach patients, the Staff Manual for Teaching Patients with Diabetes and the Staff Manual for Teaching Patients with Hypertension outline how patient and family learning can be promoted. A chapter specifically on the teaching-learning process is included in each manual with concrete examples relevant to the disease process being discussed. Each manual also includes a brief chapter on how to organize and set up patient education in a hospital setting using a team approach.
The effect of glucose withdrawal upon mechanical activity and the redox level of pyridine nucleotides and flavoproteins was investigated in isolated rat portal veins under aerobic conditions. A decrease of extracellular glucose concentration correlated with contractile activity. During acetylcholine-induced tetanic contractions. NADH and flavoproteins were oxydized only in vessels supplied with glucose. The myogenic activity was restituted when glucose was added after withdrawal parallel with a reduction of NAD and flavoproteins. The results suggest that glucose, besides its effect on the energy metabolism, has an influence on the excitability of smooth muscle cells of rat portal veins.
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In cats the perivascular space of small pial arteries was perfused with mock CSF by means of micropipettes. Variations of K+, H+ and Ca++ activities in the perfusate cause changes of the diameters of the affected vessels. Increases of H+ and moderate increases of K+ lead to dilatations, Ca++ -increases elicit constrictions. The ions interact in such a way that perivascular Ca++ inhibits the K+ or H+ induced dilator response of the pial arteries. Alkalosis intensifies the constrictor action of Ca++. Perivascular microperfusion with Ca++ -free mock CSF causes dilatation which can be augmented by additional acidosis (pH 6.5). However, an increase of K+ to 10.8-10(-3) mol.1(-1) (4 times normal) does not change the diameters of the vessels already dilated, thus indicating differences in the action of K+ and H+ upon the membranes of the pial vascular smooth muscle cells. Small vessels (less than 80 micron diameter) respond with a significantly stronger dilatation when Ca++ is complexed with EGTA as compared with vessels of more than 80 micron diameter.
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By means of perivascular perfusion of thin sections of pial arteries with differently composed cerebrospinal fluid (CSF) the vessel diameters can be influenced. In cats, anesthetized with pentobarbital, addition of serotonin, norepinephrine or calcium to an artificial CSF which was infused through micropipettes into the perivascular space of the pial arteries, caused constrictions of the arteries contacting the modified CSF. Hyperventilation or perivascular perfusion of alkaline CSF also caused reduction of the pial arterial diameters. 2-Ethyl-3-(-hydroxy-benzoyl)-benzofuran (benzarone) inhibited or abolished the constrictions elicited by the above mentioned stimuli. The effect was dose-dependent. High doses of benzarone caused pial arterial dilations: The inhibition of the calcium induced constriction especially, seems worth mentioning since this ion plays a central role in the contraction mechanisms of the vascular smooth muscle cells.
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