Coronary arteries of cardiac patients are hyperreactive and contain stores of amines: a mechanism for coronary spasm.

Coronary arteries from hearts of cardiac patients contain significantly higher concentrations of histamine than do those from noncardiac patients. The coronary vessels of cardiac patients are also hyperresponsive to histamine and serotonin. These differences between groups of patients suggest an explanation for coronary artery spasm in heart disease.

Neuropeptide-Y. A peptide found in human coronary arteries constricts primarily small coronary arteries to produce myocardial ischemia in dogs.

Neuropeptide-Y (NPY), a brain peptide, is located in the walls of human coronary arteries. This study assessed the effects of NPY on the coronary circulation in 40 chloralose-anesthetized, open-chest dogs. Intracoronary NPY (42 nmol over 5.2 min) caused a 39% reduction in coronary blood flow without changing heart rate or aortic pressure. To determine whether this vasoconstriction could produce ischemia, intramyocardial pH was measured in seven dogs (group I) and decreased from 7.45 +/- 0.06 to 7.37 +/- 0.06 pH units after NPY in the subendocardium (P less than 0.0002), and from 7.45 +/- 0.06 to 7.40 +/- 0.05 pH units (P less than 0.04) in the subepicardium of the infused zone. Left ventricular ejection fraction (LVEF), measured by radionuclide angiography, decreased from 0.52 +/- 0.08 to 0.42 +/- 0.12 U (n = 5, P less than 0.01) during NPY. NPY-induced vasoconstriction was also associated with ST-T wave changes on the electrocardiogram (ECG) in eight of nine other animals (group V). In another group of six dogs (group IV), the change in small vessel resistance accounted for 94% of the increase in total resistance, so that the primary vasoconstrictor effect of NPY was exerted on small coronary arteries. Thus, NPY, a peptide found in human coronary arteries, caused constriction of primarily small coronary arteries that was severe enough to produce myocardial ischemia as determined by ECG ST-T wave changes, and decreases in intramyocardial pH and LVEF in dogs.

Effects of a new nonionic and a conventional ionic contrast agent on coronary sinus ionized calcium and left ventricular hemodynamics in dogs.

Transient myocardial depression associated with intracoronary injections of contrast medium has been attributed to hypertonicity and to calcium binding. To further assess the importance of calcium binding, a new technique for continuous monitoring of coronary sinus ionized calcium with an intravascular calcium-selective electrode was used. With this calcium-selective electrode the effects of intracoronary injection in dogs of a conventional ionic contrast agent, sodium meglumine diatrizoate (Renografin-76), and a new nonionic agent, iohexol, were assessed and compared. Left ventricular pressure was measured with a micromanometer catheter. After bolus injection of 0.2 ml/kg body weight of Renografin-76 (n = 10), coronary sinus pCa increased by 0.27 from 2.98 +/- 0.02 to 3.25 +/- 0.03, indicating a decrease in ionized calcium from 2.0 to 1.1 mEq/liter. With iohexol (n = 9), pCa increased by only 0.05 +/- 0.01 (p less than 0.001), indicating a decrease in ionized calcium from 2.0 to 1.8 mEq/liter. Peak changes occurred approximately 6 seconds after injection. Renografin-76 caused a marked decrease in left ventricular systolic pressure (140 +/- 7 to 106 +/- 8 mm Hg) and in heart rate (122 +/- 7 to 101 +/- 5 beats/min) with an increase in end-diastolic pressure (5 +/- 1 to 12 +/- 1 mm Hg), whereas iohexol did not significantly alter these variables. Using Renografin-76 with calcium added to achieve an ionized calcium level of 2 (n = 4), 4 (n = 4) or 6 (n = 4) mEq/liter, the changes in coronary sinus pCa were abolished and the hemodynamic changes attenuated. These findings indicate that Renografin-76 results in greater myocardial depression than the new nonionic agent iohexol.(ABSTRACT TRUNCATED AT 250 WORDS)

Action and localization of vasoactive intestinal peptide in the coronary circulation: evidence for nonadrenergic, noncholinergic coronary regulation.

Vasoactive intestinal polypeptide, a neurotransmitter peptide detected in animal and human hearts, has been found in nerves of coronary arteries. To determine the amount and distribution of vasoactive intestinal polypeptide in the large coronary vessels and its possible participation in coronary vasoregulation, two groups of animals were studied. In the first group, 11 anesthetized dogs were sacrificed to collect three (1 cm) segments along the circumflex and left anterior descending coronary arteries. These segments represented proximal (I), middle (II) and distal (III) portions of the two arteries. Concentrations (ng/g) of vasoactive intestinal polypeptide-like immunoreactive substance were determined by radioimmunoassay. Vasoactive intestinal polypeptide-like immunoreactivity was present in the left anterior descending (I = 7.28 +/- 1.65, II = 3.74 +/- 0.57, III = 2.29 +/- 0.53) and circumflex (I = 4.16 +/- 1.52, II = 4.58 +/- 1.13, III = 4.00 +/- 0.81) coronary arteries. The difference in vasoactive intestinal polypeptide-like immunoreactivity among epicardial segments of the anterior descending artery was significant, but there was no significant difference among segments of the circumflex coronary artery. In the second group (eight closed chest anesthetized dogs), the effects of vasoactive intestinal polypeptide intracoronary infusion on epicardial coronary constriction were examined at rest and with the artery constricted by serotonin. Left anterior descending (segments I, II and III) artery responses (% area change) to vasoactive intestinal polypeptide and vasoactive intestinal polypeptide plus serotonin were examined using quantitative coronary angiography. Vasoactive intestinal polypeptide infusion resulted in significant vasodilation in all the segments (I, II and III) of the left anterior descending artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Differential binding of the lectins Griffonia simplicifolia I and Lycopersicon esculentum to microvascular endothelium: organ-specific localization and partial glycoprotein characterization.

The lectins Griffonia simplicifolia I and Lycopersicon esculentum were used to assess the presence of endothelium-specific glycoproteins in the microvasculature of the rat myocardium, diaphragm and superficial cerebral cortex. Organs fixed by intravascular perfusion were processed to obtain semithin (0.5 micron) and thin (less than 0.1 micron) frozen sections that were reacted with biotinylated lectin followed by streptavidin conjugated to Texas Red, for semithin sections, or by streptavidin conjugated to 5-nm colloidal gold particles, for thin sections. Lycopersicon esculentum lectin exclusively labeled the endothelium of all small vessels in all three microvascular beds; it did not bind to components of either the parenchyma or the extracellular matrix. Griffonia simplicifolia I lectin exclusively labeled the endothelium of the entire microvasculature in the myocardium and diaphragm, but marked primarily pericytes in the cerebral microvasculature. It did not label any parenchymal or interstitial organ component. At the electron microscope level, the lectin Griffonia simplicifolia I labeling was associated with the plasmalemma proper and especially with plasmalemmal vesicles and their introits, and Lycopersicon esculentum lectin bound primarily to the luminal plasmalemma in the microvascular beds of the myocardium and diaphragm. In the cerebral cortex, labeling of the microvasculature was clearly different: Griffonia simplicifolia I bound primarily to pericytes and vascular smooth muscle cells whereas Lycopersicon esculentum labeled only the microvascular endothelium. Lysates prepared from the myocardium, diaphragm and cerebral cortex were processed through Griffonia simplicifolia I lectin affinity separation followed by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) analysis of the fraction obtained. A number of putative endothelium-specific glycoproteins was detected and found to differ qualitatively and quantitatively from organ to organ. The most prominent polypeptide, approximately 97 kDa, was present in substantial amounts in the myocardium and diaphragm, but in considerably lower concentration in the cerebral cortex. The reverse applied for a approximately 55 kDa protein. The preferential distribution of the approximately 97 kDa protein parallels differences in Griffonia simplicifolia I lectin binding by fluorescence and electron microscopy on sections of the corresponding organs. The results provide further evidence for the existence of endothelial glycoproteins specific for different microvascular beds and possibly connected with local functional differentiations.

Quantitative HPLC analysis of human plaque proteins in coronary and thoracic aorta arteries.

Quantitative HPLC analysis of saline-soluble proteins obtained from human coronary and thoracic aorta plaque and from whole internal mammary artery were performed. Protein extracts were characterized by anion exchange and reverse-phase HPLC and the integrated chromatographs revealed significant differences in both peak retention times and areas for protein species from coronary artery compared to thoracic aorta artery plaque. Coronary artery plaque proteins possessed a high degree of cationic charge and polarity compared to those present in thoracic aorta plaque and normal mammary artery. This suggests that specific protein markers may be expressed in plaque of different anatomical origin, and that the processing of protein may be distinct to plaque sites. In contrast, characterization of molecular weight by gel electrophoresis resolved no major differences between plaque types. These findings indicate that proteins in human plaque lesions of different anatomical origin can be resolved by HPLC methodology and that they exhibit different charge and polarity. Such an HPLC approach may prove useful in the quantitative identification and ultimate isolation of specific protein markers present in plaque during atherogenesis, and in the study of mechanisms of protein involvement in plaque formation.

Comparison of different ways of presenting the results of biochemical analyses of human coronary arteries.

Three methods of expressing the results of biochemical analyses of normal and atherosclerotic human coronary intima-medias were compared by calculating the results per unit area of vessel surface to obtain the content, per unit weight of dry defatted tissue (d.t.) to obtain the concentration, and per unit weight of organic d.t. to obtain the inorganic salt-corrected concentration. The content reflects the amount of a substance in an anatomically defined portion of the arterial wall, whereas the concentration gives the amount of the substance relative to a defined mass of arterial tissue. Since calcium salts form a sizable portion of fibrous plaques, concentrations become overcorrected in the oldest age groups. For example, there was an unexpected age-related decrease of collagen concentration in fibrous plaques-containing coronary arteries while its content and inorganic salt-corrected concentration increased. In studies involving arterial biochemical analyses it is appropriate to calculate the results in terms of both the content and the concentration. If severely affected specimens are studied, it is recommendable also to use the inorganic salt-corrected concentration, especially when different age groups are compared with one another.

Effect of post-mortem time on the biochemical composition of coronary arteries.

The effects of post-mortem autolysis on the biochemical composition of coronary intima-medias were studied by keeping the coronary arteries of 25 slaughterhouse pigs at +4 degrees C for periods up to 7 days. The samples were analysed for DNA, total protein, collagen, glycosaminoglycans (GAGs), free and esterified cholesterol, triglycerides, phospholipid fractions, and fatty acid composition in various lipid classes. The content of sulphated GAGs decreased steadily, whereas that of hyaluronic acid remained unchanged. These alterations led to a significant decrease in the content of total GAGs and to an increase in the percentage of hyaluronic acid in total GAGs. The results indicate a continuous post-mortem degradation of arterial proteoglycans. After 7 days storage, there was a significant increase in the content of free fatty acids, and the composition of this fraction was changed by increases in the relative amounts of oleic and linoleic acids. These changes were accompanied by an increase in lysolecithin and a decrease in lecithin, which suggests a post-mortem action of arterial phospholipases.

Arteriosclerosis in the African elephant: Part 2. Medial sclerosis.

SUMMARY: A type of spontaneous arteriosclerosis, described as medial sclerosis and quite distinct from atherosclerosis, was found in the aortas, coronary arteries and aortic branch arteries of free-living elephants (Loxodonta africana) in Uganda and Kenya. The lesions took the form of calcified fibrotic plaques in the inner tunica media. The calcification appeared to commence in the internal elastic lamina and was associated with atrophy of medial smooth muscle fibres and their replacement by fibrous tissue. In the aorta, medial sclerosis was found to be associated with aortic dilatation, decreased wall thickness and decreased extensibility. These changes were shown to result in substantial increases in the tangential stresses carried by the tissues of the aorta and coronary arteries. As with atherosclerosis, medial sclerosis increased progressively with age; and the approximate involvement of the aorta at different ages could be predicted from linear regression equations. There was no difference in the severity of lesions between male and female animals. Biochemically, the lesions of medial sclerosis were associated with decreased amounts of elastin and increased amounts of collagen in arterial walls. Arterial tissue showing medial calcification always contained less than 30% elastin by weight. In addition, the severity of medial sclerosis in individual elephants was found to be positively correlated with the concentration of calcium in their sera. The pathogenesis of these lesions is discussed and it is suggested that mechanical stress, medial anoxia and high serum calcium levels all contribute to the aetiology of medial sclerosis.

Histochemical detection of esterified cholesterol within human atherosclerotic lesions using the fluorescent probe filipin.

The fluorescent cholesterol probe filipin has been used in this study to histochemically examine the morphology and cholesterol composition of intra- and extracellular Sudanophilic lipid deposits which accumulate in human atherosclerotic lesions. Because filipin reacts with unesterified but not esterified cholesterol, detection of cholesteryl esters was carried out by first extracting native unesterified cholesterol with ethanol, and then enzymatically converting esterified to unesterified cholesterol before filipin staining. The size and structure of particles comprising extracellular cholesteryl ester-rich lipid deposits was different in regions of necrosis as detected using filipin compared with the Sudan lipid-soluble dye oil red 0. Whereas oil red 0 staining often indicated that extracellular cholesteryl ester in these regions occurred in amorphous and spherical particles of varying sizes, filipin staining revealed that extracellular cholesteryl ester occurred in spherical particles more uniform in size than indicated by oil red 0 staining. Also, the majority of extracellular cholesteryl ester-rich particles in necrotic regions were smaller than intracellular cholesteryl ester-containing lipid droplets. In addition, the use of filipin to detect intracellular cholesteryl ester allowed distinction of 2 subpopulations of oil red 0-stained cells which did and did not contain detectable cholesteryl ester.

Acidic glycosaminoglycan, lipid and water contents in human coronary arterial branches.

The acidic glycosaminoglycans (AGAG) of the human coronary arterial tree (the main left and right branches and their distal portions) were analyzed by enzymatic methods employing chondroitinases, hyaluronidase and heparitinase. The AGAG content of human coronary arteries was highest in the left branch, intermediate in the right branch and lowest in the distal portions. Some compositional differences in AGAG were found in these three parts. The amount of AGAG in the coronary arterial tree decreased with increasing severity of atherosclerosis. The main AGAG were heparan sulfate (HS) and chondroitin 6-sulfate (C-6S), constituting 33-38% and 24-36% of the total AGAG, respectively. Dermatan sulfate (DS) and chondroitin 4-sulfate (C-4S) each comprised 1/5-1/10 of the total AGAG. Hyaluronic acid (HA) and oversulfated DS comprised smaller proportions of the total AGAG. A small amount of heparin was occasionally detected in the coronary arterial tree, particularly in the distal portions. The lipid content of the main branches was increased in mildly atherosclerotic parts but diminished in severely affected parts. The water content was relatively higher in the main branches and decreased with severity of atherosclerosis. A possible function of these AGAG in atherosclerosis is discussed with respect to the compositional changes.

Atherosclerosis and biochemical composition of coronary arteries in Finnish men. Comparison of two populations with different incidences of coronary heart disease.

Men in Eastern Finland show a substantially higher rate of coronary heart disease (CHD) than men in the Western part of the country. To study possible differences in the biochemical composition and atherosclerotic involvement of coronary arteries between these two populations, we analyzed major lipid and non-lipid components of coronary arteries from 15- to 60-year-old Finnish men after accidental death. The material consisted of 59 age-matched pairs from East and West Finland, respectively, collected at successive autopsies during 1979-1983. The coronary arteries from East Finland contained significantly more esterified cholesterol and a higher percentage of oleate in cholesteryl esters. The findings were most conspicuous under the age of 40 years, and imply a higher degree of atherosclerosis together with an increased rate of intracellular cholesterol esterification in coronary arteries in Eastern as compared with Western Finland. The vessels from East Finland also tended to contain more free cholesterol and raised lesions, but the differences were not statistically significant. No major regional differences were seen in total phospholipids, phospholipid subfractions, DNA, calcium, collagen, total protein, or glycosaminoglycans.

Immunohistochemical localization of apolipoprotein E in atherosclerotic lesions of the aorta and coronary arteries.

The distribution of apolipoprotein E (apo E) immunoreactive substances (IRS) in atherosclerotic lesions and lesion-free areas of the aorta and coronary arteries obtained from 17 autopsied cases was studied using a specific anti-apo E serum and the unlabeled peroxidase-antiperoxidase (PAP) method. In fatty streak lesions of the aorta, many cells containing apo E-IRS were found in the deeper layer of the intima and diffuse staining of apo E in the extracellular spaces was also noted. In more advanced lesions apo E-positive cells could not be found. Immunohistochemical findings of coronary arteries differed distinctly from those of the aorta in that the apo-E-positive cells were absent in the deeper layer of the intima. The endothelial cells of coronary arteries, but not those of the aorta, showed positive staining for apo E.

Experimental atherosclerosis in hypercholesterolemic mini-pigs. Regression of cholesterol ester accumulation in aorta and coronary arteries after treatment with clofibrate, beta-pyridylcarbinol or a normo-lipidemic diet.

Studies have been performed on groups of mini-pigs 21-23 months of age, which after 18 months of hypercholesterolemia (approximately 10 mmol) had developed raised atherosclerotic lesions with high levels of cholesterol esters, especially in the abdominal aorta and the coronary arteries. If the hypercholesterolemia was continued for 18 months, no significant change in the cholesterol ester content in the aorta occurred; in the coronary arteries there was a significant decrease in these older pigs. If the hypercholesterolemic pigs also were treated with beta-pyridylcarbinol the findings were very similar to the first. When hypercholesterolemic pigs were treated with clofibrate, or when the hypercholesterolemic diet was replaced with the basal food for 18 months, the plasma cholesterol level was normalized (approximately 2 mmol) within 1-2 months. The cholesterol ester content in the thoracic aorta was reduced in both groups but not that in the abdominal aorta. Clofibrate decreased the cholesterol ester level in the coronary arteries when compared to the hypercholesterolemic group; the drug also reduced the free cholesterol level when compared to the basal group. We suggest that an increased plasma cholesterol level initiated the development of the atherosclerotic lesions; their later development was only partly dependent on the plasma cholesterol level.

Changes in the connective tissue proteins, glycosaminoglycans and calcium in the arteries of the cynomolgus monkey during atherosclerotic induction and regression.

The chemical composition of the aorta, carotid, coronary and cerebral arteries of the cynomolgus monkey was determined during the induction and 'regression' of atherosclerosis. The feeding of a 2% cholesterol and 10% butter diet for 6 months resulted in extensive and severe atherosclerosis involving the aorta, carotid and coronary arteries. The involvement of these vessels was reflected by increases in arterial weight and chemical content of cholesterol, collagen, elastin, glycosaminoglycans (GAGs) and calcium. The cerebral arteries, which showed no atherosclerotic involvement, likewise showed no significant changes in weight and composition. During the 12-month regression period marked changes in the chemical composition of the involved arteries occurred and these included further increases in the collagen, GAG and calcium content of the vessels and decreases in the free and esterified cholesterol content. These changes were consistent with the gross and microscopic findings which revealed that during regression the pre-established lesions had not decreased in size but had become more fibrotic and calcified while the number of foam cells and amount of lipid contained in the lesion had decreased. During induction and regression, much of the cholesterol contained in the involved vessels appeared to be present in a crystalline form as indicated by the appearance of cholesterol clefts in the lesions. Aortic collagen was not altered with respect to amino acid composition and behavior in acrylamide gels throughout the study. However, elastin prepared by hot alkali treatment from diseased vessels, showed minor changes in amino acids during induction and marked changes during regression presumably due to the binding of glycoproteins to the elastin. The GAG composition of the involved arteries did not change during induction, whereas during regression the percent dermatan sulfate increased while the percent of heparan sulfate decreased. The over-all findings are consistent with the concept that the interaction of the connective tissue proteins with the GAGs, lipoproteins and calcium of the artery plays an important role in the development and regression of advanced atherosclerotic disease.

The effect of sex hormones on glycosaminoglycan content of canine aorta and coronary arteries.

Hyaluronate (HA), heparan sulfate (HS), dermatan sulfate (DS) and isomeric chondroitin sulfates (CS) were measured in vascular walls of 9-10 months old normal and hypophysectomized female beagles treated with sex hormones. Following hypophysectomy the animals were maintained for 8 weeks without any hormonal replacement therapy and then they were exposed for 3 weeks to parenteral treatment with sex hormones. One group received twice weekly 25 mg testosterone, another group was given the same amount of progesterone, and a third group received on day 1 and day 14, estrogens in 2 injections, consisting of a mixture of 10 mg short-acting estradiol-17-phenylpropionate and 2.5 mg long-acting estradiol benzoate. After 11 weeks all animals were sacrificed, coronary arteries and aortas were immediately removed and the latter were divided into three segments: arch, thoracic and abdominal. Removal of the pituitary led to a reduction of the HA content in the aortic arch and thoracic segment, but coronary arteries and abdominal aorta were not affected. The main consequence of hypophysectomy both in the entire aorta and in coronary arteries was a sharp reduction of the sulfated glycosaminoglycan (GAG) content. All three hormones produced a modest rise in the HS content of coronary arteries. A more definite response was seen in the thoracic aorta where each of the three hormones raised the low DS content to normal levels. Concerning the effect of sex hromones on aortic GAG other than DS, TESTOSTERONE RAISED THE CS content towards normal in thoracic and abdominal segments, while estrogen by doubling the normal HA concentration was particularly potent in the abdominal aorta. It is conceivable that the different sensitivity of various segments of aorta and coronary arteries to sex (and other) hormones in terms of regulating GAG metabolism may prove to be of relevance to the uneven distribution of lesions in degenerative vascular disease.

Spontaneous coronary artery dissection and eosinophilic inflammation: a cause and effect relationship?

Spontaneous coronary artery dissection is described in eight patients 26 to 47 years of age. Six died suddenly, and two died after the onset of chest pain. All had normal heart weights and all had dissection of left anterior descending coronary artery, which occurred mainly in the outer one third of the media. The adventitial of the dissected artery contained inflammatory infiltrates which were predominantly eosinophilic granulocytes. Forty-six cases previously published in 32 reports are reviewed. It is suggested that adventitial eosinophilic infiltrate may be responsible for spontaneous coronary artery dissection.

Dog coronary artery adenosine receptor: structure of the N6-aryl subregion.

Previous structure-coronary vasoactivity correlations of the N6-alkyladenosine analogues of N6-[(R)-1-phenyl-2-propyl]adenosine, 1, support the hypothesis that the coronary artery A2 adenosine receptor contains an N6 region of specialized structure. The part of this receptor region that binds the 2-propyl moiety of 1 determines stereoselectivity and contributes to coronary vasoactivity. The present study uses 92 adenosine analogues containing an aryl group in the N6 substituent to test the hypothesis that the N6 receptor region contains an aryl subregion that binds the phenyl moiety of 1 and thereby contributes to its coronary vasoactivity. N6-Aralkyladenosines are often more potent than their alkyl congeners. Two methylene residues seem to provide optimum separation of the aryl group from N6. Among adenosines with semirigid N6 substituents, N6-[(1R,2S)-trans-2-phenylcyclohexyl]adenosine was uniquely active, evidence that when 1 occupies the receptor, the axis of the propyl C-1 to phenyl C-1 bond is nearly in the plane described by N6 and propyl C-1 and C-2. The torsion angle around this bond is unknown. Replacing the phenyl group of N6-2-phenethyladenosine with a thienyl or a 3-pyridyl group raises activity. The structure-activity relationships of the N6-(arylethyl)-, the N6-(arylmethyl)-, and the N6-phenyladenosines differ strinkingly from each other. Taken together, such results support the idea that the N6 region of the dog coronary artery A2 adenosine receptor includes an aryl subregion.

Alpha-smooth muscle actin, a differentiation marker of smooth muscle cells, is present in microfilamentous bundles of pericytes.

alpha-Smooth muscle (alpha-sm) actin, an isoform typical of smooth muscle cells (SMC) and present in high amounts in vascular SMC, was demonstrated in the cytoplasm of pericytes of various rat and human organs by means of immunocytochemistry at the electron microscopic level. In SMC and pericytes, alpha-sm actin was localized in microfilament bundles, strengthening the assumption that it is the functional isoform in these cell types and supporting the assumption that pericytes exert contractile functions.

The plasminogen activator of the arterial wall.

The plasminogen activator in 645 specimens of various human arteries--thoracic, abdominal aorta, carotic, pulmonary, renal, basilar, coronary - was studied using Todd's histochemical method. 92 cadavers were used, 1--18 hours post mortem from subjects aged from 272 days to 83 years. 45 specimens of pulmonary, renal and splenic arteries were obtained during surgery. The greatest fibrinolytic activity was within the adventitia. Intima occasionally showed very little fibrinolytic activity, or none at all. No statistically significant differences in plasminogen activator activity were found between the various arteries examined. A statistically significant increase in fibrinolysis in adventitia of atherosclerotic arteries was established. No correlation was found between the fibrinolytic activity of the arteries and their alkaline phosphatase content. Some properties of the plasminogen activator of the arterial vessel wall were evaluated. Influence of storage, inactivation with epsilonaminocaproic acid and extracted with potassium thiocyanate was studied.