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The cholesterol metabolism of homogeneous populations of mouse peritoneal macrophages was evaluated under in vitro conditions. Macrophages are rich in free cholesterol and maintain a constant cholesterol to protein ratio (12 microg cholesterol/mg protein). No detectable cholesterol ester was present within the cell. More than 95% of total cholesterol was membrane associated and the majority was present in subcellular fractions containing lysosomes and plasma membrane. Less than 0.1% of cell cholesterol was synthesized from acetate-1-(14)C. During in vitro cultivation, macrophages rapidly exchanged their membrane cholesterol with that of lipoproteins of calf serum. About 30% of the cell cholesterol was exchanged per hour in 20% serum medium, and exchange was nearly complete by 5 hr. Exchange proceeded in a rapid exponential phase followed by a slower phase. Calculations based on a two compartment model indicated that the rapidly exchanging cholesterol compartment represented 60-70% of the total cell cholesterol, and the slowly exchanging compartment accounted for 30-40%. The relationship between serum lipoprotein concentration and exchange rate exhibited first-order kinetics. The rate was determined by thermal energy, in keeping with a Q(10) of 2, and an activation energy of 12 kcal/mole. Exchange was independent of bulk transport of lipoproteins by pinocytosis and phagocytosis, and was not linked to energy metabolism. The alpha-lipoproteins were the major class of proteins of calf serum participating in exchange.

The coronary arteries were studied by electron microscopy in normal rats weighing 65 to 535 gm; fixation was accomplished by perfusion for 20 min at 110-130 mm Hg. In rats of all ages (but especially in the oldest) the arterial wall contained deposits of abnormal intercellular material, consisting of granules, vesicles, myelin figures and other debris. These deposits were present in the intima and media, but rare in the adventitia; there was suggestive evidence that medial cells phagocytized some of the material. The adventitia was characterized by 1-4 layers of cells with extremely thin protoplasmic expansions wrapped around the vessel ('veil cells') and containing lysosome-like bodies as well as phagosomes. These findings, taken as a whole, suggest the following sequence of events. During normal life, the media produces cellular debris, by cell death as well as by fragmentation of cellular processes; part of these debris are phagocytized by smooth muscle cells, part diffuse outward to the adventitia where they are taken up by specialized cells (the 'veil cells'). However, due to relative inadequacy of phagocytosis in the media, the debris continue to accumulate and form intercellular deposits that increase with age. It is possible that this natural phenomenon may by itself set a maximal limit to the life-span of the arterial wall. [ABSTRACT FROM AUTHOR]

Focuses on the panel discussion regarding human arterial atherosclerosis. Indication of endothelial cell damage; Investigation on the reactions of the components of the vessel wall in intima; Selection of the different types of damaging agents.

It appears from the biochemical, histochemical and morphological analyses under discussion in this session, that the polysaccharide-protein components of the arterial ground substance, containing hexosamine, uronic acids, neuraminic acid etc. (acid and neutral proteoglycans) determine essential fundamental processes of atherosclerosis as well as every physiological and pathological metabolism in the vessel wall. So we have to understand (and further to investigate) arterial injuries and repair. The changes in the arterial fibre components depend on the chromotropic ground substance and its particular changes. We have discussed the special role of endothelia and of the dominating arterial cell, the smooth muscle cell. Our results (papers, discussions and references) further show summarizing, that atherosclerosis starts and developes with an increase of anabolism and catabolism. The particular findings of the disturbed metabolism of the intima and media in certain stages of injured arteries, especially in atherosclerosis, are demonstrated in details. The early increased anabolism and catabolism decrease under the normal level in the later atherosclerotic stages, the catabolic processes more and earlier than the anabolic processes. It results in the atherosclerotic insufficiency of the vessel wall metabolism with the well-known disorganisation, transformation and destruction, with lipid and calcium depositions in arteries. As has been stated, however, in spite of the numerous researches, aided by a diversity of methods used for the identification of the many groups of substances and components involved and their manifold interrelationships, these processes cannot yet be properly understood in detail, nor correlated with each other significantly until now. That will be the task of our further investigations on ‘Injury and Fiepair in Arterial Tissue’. [ABSTRACT FROM AUTHOR]

Presents a study on the distribution of arterio-atherosclerotic obstructive lesions in coronary arteries. Materials and method; Results and discussion.

Induction of hyperlipemia by high carbohydrate intake has been studied in 20 atherosclerotics. It appeared to be a fairly infrequent occurrence, being successful in only 25% of the patients studied. Induction was positive in 22% of the subjects with normal fasting lipid levels and in 60% of those with type IV hyperlipemia; it failed in the 6 patients with type II A or B hyperlipemia. Induction was not correlated to the degree of carbohydrate tolerance. Therefore, in patients with negative results of induction high triglyceride levels, as those found in types II B and IV, seem to be determined by genetic factors or by nutritional factors other than carbohydrates. Carbohydrate induction is quickly achieved, plasma triglycerides reaching their peak between days 3 and 5. Regression, too, starts early as a rule, sometimes even while the subject is still on the high carbohydrate diet. These findings are evidence of increased VLDL synthesis rather than reduced lipoprotein removal rate. Changes in the triglyceride/protein and triglyceride/cholesterol ratios are indicative of an increased size of both the VLDL and LDL fractions in the course of CHO-induced hyperlipemia. [ABSTRACT FROM AUTHOR]

Discusses the responsibility of pediatricians in finding children threatened by atherosclerosis in the U.S. Incidence of premature disability and death from complications of atherosclerosis in adults; Difference in opinion regarding the age of onset of the true atherosclerosis lesion in man; Conclusions of the Council of Rheumatic Fever and Congenital Heart Diseases of the American Heart Association concerning the reduction of atherosclerosis risk.

Xanthomas, in themselves, are usually harmless. However, they frequently occur in patients with atherosclerosis and abnormal lipoprotein metabolism. Therefore, studies dealing with xanthomas in experimental animals and humans, in whom hyperlipoproteinemia is present, may lead to useful information about the manner in which lipids accumulate in the foam cells of xanthonms and, more important, how the pathologic processes in the skin might mirror events occurring in the foam cells of atherosclerotic plaques. This article will review some of the current concepts of the biochemical and morphologic abnormalitites occurring in xanthomas as derived from studies of these cutaneous lesions in humans and experimental animals. This will include a discussion of the metabolism of certain lipoprotiens of importance in xanthomatosis as well as a consideration of the new hyperlipoprotein syndromes described by Fredrickson et al. (1) as they relate to various forms of xanthomas. Where possible, an attempt is made to correlate the pathologic and biochemical alterations observed in xanthomas with these occurring in atheromas. [ABSTRACT FROM AUTHOR]

Discusses the relation of coronary atherosclerosis and coronary collaterals to cardiac function. Relationship between extent of coronary artery disease and ventricular asynergy; Effect of collaterals on the prevalence of ventriculographic abnormalities; Significance of coronary collaterals.

Examines postexercise electrocardiographic response of patients with arteriographically documented coronary atherosclerosis. Materials and methods used in the study; Distribution and degree of coronary arterial stenosis; Cross-correlation between number of major coronary arteries with a significant stenosis and the degree of postexercise depression.

Considers issues important to internal medicine profession. Important changes in the publication 'Diagnostic Standards and Classification of Tuberculosis'; Effects of hypoxia and of carbon monoxide exposures on experimental atherosclerosis.

Left ventricular akinesis (localized lack of wall motion) may have a profound effect on cardiac hemodynamics. The diagnosis with angiographically proved coronary atherosclerosis and intractable congestive failure underwent resection of akinetic ventricular wall during temporary cardiopulmonary bypass. In two patients (Cases 2 and 3) thin fibrotic scars were resected; in one patient (Case 1) a full thickness area of diseased muscle was removed. All patients survived the operation and had improvement of symptoms. Cardiac catherization in one patient (Case 1) documented improved left ventricular function 9 months after surgery. Although the two other patients (Cases 2 and 3) had improvement in symptoms, they died 7 and 16 weeks after surgery. The rationale of subjection of seriously ill patients to extensive cardiac surgery is based on the idea that an area of noncontractile left ventricular wall can be identified by angiography and may be excised with improvement in left ventricular function. [ABSTRACT FROM AUTHOR]

Presents a study of young patients with known or suspected coronary atherosclerosis by a combined metabolic-angiographic protocol. Diseases associated with patients with ischemic heart disease; Methods used in the study; Results and discussion.

Discusses the interrelationship between the metabolic and genetic aspects of human atherosclerosis. Information on a laboratory method for phenotyping hyperlipidermias; Correlation between hyperlipidemias and hyperlipoproteinemias; Methods for the treatment of hypercholosterolemia.

Examines several stroke patients who had a clinical episode of cerebral infarction at age 50 years or younger. Information on atherosclerosis; Factors that accelerate the development of atherosclerosis or cerebral infarction; Correlations between the presence of hypertension, peripheral vascular disease and an elevated cholesterol level; Analysis of the relationship between blood pressure level and the presence or absence of diabetes.

Discusses some of the aspects of atherosclerosis. Frequency of familial susceptibility to atherosclerosis; Example of the effect of a single abnormal gene; Cause of the intimal thickening found in atherosclerosis; Association between blood lipid elevations and atherosclerosis.

Editorial. Comments on the diagnosis of mesenteric vascular insufficiency. Incidence of atherosclerosis in the vessels serving the bowel; Effect of splanchnic nerve stimulation on bowel blood flow; Perfusion of the superior mesenteric artery with oxygenated blood; Desensitization by the injection of bacterial endotoxin.

Editorial. Comments on cardiovascular metabolism in cardiovascular disease. Etiology of atherosclerosis; Lack of studies in the area of carbohydrate metabolism; Evidence on the association between abnormal glucose tolerance and atherosclerotic vascular disease; Connection between sucrose intake and atherosclerosis.

Discusses the correlation between mucopolysaccharides and atherosclerosis. Evidence for the influence of mucopolysaccharides on the development of atherosclerosis gained from animal studies in human pathology and from animal experiments.

Compares patterns of coronary and aortic atherosclerosis in blacks in Haiti and the United States. Description of the manner used for evaluating the subjects' hearts; Determination of how dietary factors figured in the increased risks; Analysis of diagnostic findings.

Editorial. Discusses the etiology and treatment of the atherosclerotic forms of cerebral vascular disease. Hemodynamics of reversed vertebral flow; Signs indicating the possibility of reversed vertebral flow; Surgical repair of the lesions which produces the shunt.

Examines neurologic and visual disturbances associated with carotid atherosclerosis. Pathology of distal embolization from atherosclerotic plaques; Importance of the size of embolus in determining its effect on the eye; Embolus causing the transient neurologic and monocular visual defects.

Describes a case of pronounced general atherosclerosis chiefly affecting coronary arteries associated with aneurysm, thrombosis of the left ventricle and clinical symptoms of heart failure. Thrombosis in lumbar portion of abdominal aorta; Embolism at bifurcation of aorta; Absence of arterial oscillations.

Reports on the effect of estrogens on atherosclerosis. Post-mortem comparison of the arteries of a group of men treated with estrogens for carcinoma of the prostate with those of a control group with prostatic cancer who received no hormonal therapy; Reduction of the severity of atheromatous lesions; Distribution of severity of aortic and coronary atherosclerosis; Effect of nutrition on atherosclerosis.

Reports on human population studies of atherosclerosis in the early 1960s. Clinical observations and vital statistics; Death rates for men aged 55 to 59 years; Environmental factors for 20 countries; Racial factor; Pathological approach; Roles of stress and other factors; Coronary artery disease in unselected autopsy material; Association of fat metabolism to atherogenesis.

Presents research which discussed the impact of triparanol on gastrointestinal system diseases. Contribution of the drug to prevent the endogenous biosynthesis of cholesterol in the human liver; Importance of triparanol to the treatment of hypercholesterolemia and atherosclerosis; Significance of the drug to deter vascular mural atherosclerotic plaque formation.

Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Seventy-five segments of descending thoracic aortas removed at autopsy from 40 males and 35 males were studied for severity and surface area involvement of atherosclerotic lesions, using both a qualitative grading system and a semi-quantitative planimetric technic. Since this study showed that the severity and extent of atherosclerotic lesions in the thoracic aorta may differ, it is concluded that more definitive information is obtained by simultaneous use of both methods. Five cases with diffuse pancreatic disease showed strikingly less severe atherosclerosis than 13 others in the same age group without pancreatic involvement. The possible etiological significance of a negative association between these two diseases merits further study. The greater surface area involvement and severity of atherosclerosis found in all cases in the posterior surface of the thoracic aorta at the sites of branching, emphasizes the influence of local factors on the initiation and progression of atheroma in man. [ABSTRACT FROM AUTHOR]

Studies the pathogenic factors in atherosclerosis by researchers from Piscataway, New Jersey. Description of the morphological characteristics of atherosclerosis; Acceptance of the widely held views that fatty flecks and streaks are small, uncomplicated lesions of atherosclerosis; Observation on the high variability of the characteristic lesions of atherosclerosis; Elucidation on the significant role played by structural characteristics of the arterial wall during atherogenesis.

Intravenous glucose tolerance and fasting non-esterified fatty acids, cholesterol, triglyceride and lipoprotein levels, together with fasting lipoprotein patterns, have been measured in a group of 50 patients with atherosclerotic peripheral arterial disease, and in a group of 20 healthy young adults. Reasons for taking healthy young adults as a control series rather than an age-matched group are discussed. The levels of each parameter have been classified into normal, borderline and abnormal ranges. 34% of patients had impaired glucose tolerance and 58% showed an elevation in fasting lipids. When borderline abnormalities are included the figures rose to 50% and 78% respectively. A definite abnormality of either glucose tolerance or fasting lipids was present in 66% of the series and the inclusion of borderline abnormalities makes this figure 88%. Only 6 patients (12%) had normal values for all parameters. When the disease group is compared with the control group, statistically significant reduction in glucose tolerance and elevation of fasting lipid levels is seen, the degree of significance being high in most instances. [ABSTRACT FROM AUTHOR]

Atherosclerosis has been thought for a long time to be proportionate to the arterial senility. And atheroselerotic changes in Caucasians, Boston, U. S. A. were ascertained by Gore, et al. to be much more severe than those in Japanese, Kyushu, Japan. The loss of arterial distensibility has also been thought to be an index of arterial senility with inseparable relation to atherosclerotic changes. It seems doubtful to us, however, that atherosclerosis is the index of arterial senility and can not be separable from the loss of arterial distensibility. We tried to clarify these relations among atherosclerosis, the loss of distensibility and aging, and found the results to be as follows: 1. The loss of human aortic distensibility progresses steadily with aging regardless of the atherosclerotic severity. 2. The severity of aortic atherosclerosis is not proportionate to the loss of aortic distensibility. The aorta which has severe atherosclerosis showed similar distensibility to the aorta with almost no atherosclerotic lesion in the same decade. 3. Contrary to the remarkable difference of atherosclerotic severity between Americans and Japanese, the loss of aortic distensibility of Americans does no seem bigger than that of the Japanese. They both show very similar distensibility in the same decades (5th and 6th decades). 4. We are impressed from these results that the atherosclerotic change should be separated pathologically from the loss of distensibility and the aortic senility would be shown by the latter. Atherosclerosis is only a disease which tends to occur in elderly person. [ABSTRACT FROM AUTHOR]

A method has been described which enables satisfactory angiograms of iliac, femoral, and popliteal arteries of rabbits to be made on three occasions, separated by one or several months. This permits observations to be made, in the same experimental animal, on the effects of various dietary and drug regimens related to the production and regression of large-artery atherosclerotic lesions in these animals. Stenosing lesions of popliteal arteries were apparent on angiograms in many of the rabbits fed 1% cholesterol in 4% cottonseed oil for two two-month periods, with an intervening month of normal diet. Severe aortic and pulmonary artery atherosclerosis also developed in all rabbits so treated. The addition of clofibrate 0.3% W/W to one group of rabbits did not significantly change the level of serum cholesterol, or large-vessel atherosclerosis. This lack of effect might be related to the high dose of dietary cholesterol fed, a situation not analogous to the usual multifactorial causation of hypercholesterolemia in humans. In rabbits rendered hypercholesterolemic by two months of cholesterol-cottonseed oil feeding and then returned to normal diet for three months, a marked decline in serum cholesterol occurred. Three of four of those having final angiograms showed normal vessels by angiography; two of four of those animals autopsied showed no significant large-vessel atherosclerosis. This suggests that regression of atherosclerosis may have occurred, since it has been shown that relatively short-term feeding (2–3 weeks) of 1% cholesterol can produce atherosclerosis in rabbits. [ABSTRACT FROM AUTHOR]

The relationship among hypercholesterolemia, atherosclerosis and hypertensive heart disease has been well established, in large epidemiologic studies. However, hypercholesterolemia should be long lasting in order to be considered as a factor in the pathogenesis of atherosclerosis. This paper deals with a case of hypercholesterolemia encountered during the first decade of life, associated with hypertension and coarctation of the abdominal aorta. The association of the three syndromes in this patient, may be of interest in studying their pathogenetic relationship. [ABSTRACT FROM AUTHOR]

Reports on a study to further investigate the previous observation that exaggerated cold-pressor response may be a manifestation of vascular sclerosis rather than hypertension. Systolic, diastolic and pulse pressure cold-pressor responses; Indication that atherosclerosis, rather than hypertension, may be responsible for the exaggerated cold-pressor response.

The influence of different venous collecting pressures on blood flow measurements by venous occlusion phethysmography in the human calf at rest and during post-ischemic reactive hyperemia, has been studied in 7 normal subjects and 32 patients with different degrees and locations of atherosclerosis obliterans. Blood flow measurements were performed by using an airfilled rubber segment plethysmograph. The reproducibility of the blood flow measurements was tested in 12 normal subjects and 13 patients with atherosclerosis obliterans. The accuracy of the method was found acceptable. The different venous collecting pressures used in normal subjects were 50, 60, 70, 80, and 90 mm Hg and in patients 30, 40, 50, 60, and 70 mm Hg. In 7 patients with arterial obliterations and in 1 normal subject intra-arterial blood pressure measurements were made in the iliac or femoral artery simultaneously with blood flow measurements at 3 different venous collecting pressures. Systemic blood pressure was measured by conventional technique on the arm. In 5 patients the intraarterial blood pressure was measured distal to the main arterial obliterations and in 2 patients proximal to the obliterations. The venous collecting cuff was placed distally to the tip of the intraarterial catheter. The blood pressure distal to an arterial stenosis was found to be lower than the systemic blood pressure even at rest. During reactive hyperemia there was a considerable pressure fall both in the normal subject and in the patients. The intraarterial blood pressure during reactive hyperemia was found to increase during the flow measurements indicating hindrance of arterial inflow by inflation of the collecting cuff. In normal subjects the highest resting flow was measured at venous collecting pressures similar to or a little higher than the diastolic arm blood pressure, while in patients no significant differences were found between the values obtained at the different pressures used. During reactive hyperemia in the calf of normal subjects the optimal venous collecting pressure was found to be 50 mm Hg in the first 40 seconds of the hyperemia. The most valid measurements of post-ischemic reactive hyperemia in patients with atherosclerosis obliterans were made by using a venous collecting pressure of only 30 mm Hg throughout the study. Higher venous collecting pressures may give too low blood flow values, artificial delay of the peak flow value, and an altered configuration of the blood flow curves. [ABSTRACT FROM AUTHOR]

The fibrinolytic activity was studied in fiftyone normal individuals and patients with atheroselerotic vascular disease after physical exertion or injections of nicotinic acid. All groups showed equal reactivity to the stimuli given, judged by acceleration of euglobnlin clot lysis, but in none of the patients tested could fibrinogeno/fibrinolytic breakdown products be demonstrated. Control experiments were made, testing blood samples with and without the addition of epsilon amino-caproic acid, and after the injection of nicotinic acid breakdown products were found in samples not containing inhibitor. An explanation of these findings is suggested. It is concluded that physical activity and nicotinic acid both are potent liberators of plasminogen activator, but that it is possible to have a significantly accelerated euglobulin clot lysis without simultaneous, manifest intravascular fibrinogeno/fibrinolysis. [ABSTRACT FROM AUTHOR]

1. It is confirmed that heparin given as a single dose is followed by a rebound lipemia. However, when given in multiple doses at 4-hr, intervals the rebound can be prevented and prolonged clearing accomplished. This was noted in patients confined to hospitals and reported previously. Multiple heparin injections, when taken by patients at 12-hr, intervals on an outpatient ambulatory basis, are followed by prolonged antilipemic effects in only those patients who show fasting hypertriglyceridomia and turbidity. This is not accomplished in normolipemic persons. These principles should be understood and evaluated when considering this treatment. The mechanisms of the rebound lipemia and prolonged clearing under various circumstances are discussed. The problems and side-effects associated with multiple injections of heparin given on a daily basis are few and can be controlled in most situations. [ABSTRACT FROM AUTHOR]

Ten rabbits were put on a control diet and the ten others were put on high-carbohydrate diet. Their biochemical and autopsy data are presented. This study showed a trend for rise in serum total lipids and triglyceride levels. Autopsy data on rabbits sacrificed after 6 months of study did not show any lipid deposits in the aorta and coronary vessels. It is suggested that a larger experimental study with a high-calorie, high-carbohydrate diet with normal protein and fat contents may be undertaken. [ABSTRACT FROM AUTHOR]

Among the more common saturated fatty acids, palmitic acid appears to be the most hyperlipemic when added to the basic high-fat diet of rats. Under these conditions, stearic and especially lauric acid seem to have much less effect on both the cholesterol and triglyceride serum levels. However, the rats fed the long-chain fatty acids, palmitic and mostly stearic acids, presented the most severe pblebothromboses, initiated in these rats by the intravenous injection of a S. typhosa endotoxin and resulting in multiple red hepatic infarcts. Fats richer in stearic acid, such as cacao butter and butter, are also much more thrombogenic than lard and corn oil, which contain less stearic acid and much more linoleic acid, probably an antithrombogenic fatty acid. Among a large number of fats fed to rats under comparable conditions, the results obtained were not as clear because butter was the most thrombogenic and olive oil and bovine tallow, despite a high content in stearic acid, the least thrombogenic. The low thrombogenicity of these latter fats, despite a marked hyperlipemic effect, is probably due to their high oleic acid content. However, the thrombogenicity of a fat is probably the result of multiple fatty acid interactions and should be further analyzed. Only with a limited number of fats could the lipemia or the plasma clotting time be utilized to predict the thrombotic tendency of the animals. But in large-scale experiments, serum cholesterol and triglycerides, as well as the plasma clotting time, could be considered merely as risk factors. In contrast to this, there was a highly significant correlation between the survival time of the endotoxin-treated animals and their serum triglyceride level. The effects of a few selected fats on the production of aortic fatty streaks in the rat seem to be related to the thrombogenic effect and also to the composition in fatty acids. Under the conditions of this study, neither the degree of saturation of a fat nor its origin (animal, vegetable) appears to be of any use for predicting its lipemic, thrombogenic or atherogenic effects. [ABSTRACT FROM AUTHOR]

Discusses changes in arterial elasticity in cases of early atherosclerosis of the lower limbs in man. Detection of early atherosclerotic changes in the lower limb; Measurement of the segmental pulse wave velocity; Implications on angiology.

Thirty patients with atherosclerosis obliterans of the peripheral arteries in both lower limbs wore examined. All the patients were found to be normal on clinical neurologic examination. The correlation between the vascular pathology and the ischemic impact on the peripheral nerves was determined by electromyography and motor nerve conduction velocity tests. The main points evolving from this study are: (1) The rate of subclinical damage to the peripheral nerves in patients with peripheral atherosclerosis obliterans is very high. (2) The test of preference to prove this damage is motor nerve conduction velocity which was found to be much more sensitive in comparison to electromyography. (3) Damage to the nerve in patients with intermittent claudication is much more pronounced than in patients with atherosclerosis obliterans but without intermittent claudication. [ABSTRACT FROM AUTHOR]

Focuses on the hematologic differences between thromobangiitis obliterans and atherosclerosis. Concentration of heparin-precipitable fractions of fibrinogen (HPF) in the plasma of patients with thromobangiitis obliterans; Correlations between HPF and total fibrinogen; Specific nature of the two conditions.

1. Morphology of the pulse wave curve from five segments of the lower limb (proximal) and distal half of the thigh, popliteal region, proximal and distal half of the calf) has been analyzed. Crest time (C.T.), index of elasticity (e) and Β angle were evaluated. 2. C.T. values at rest varied according to the place of recording. Normally, they did not exceed 200 msec, and reached their maxima at the thigh and their minima above the ankle. C.T. was identical with the inclination time; e was greater than 1.0; β angle was acute. The variability of the last two parameters was considerable. 3. The changes of C.T. during the cold pressure test were not significant. During the passive tilting to 60° from the horizontal plane, the C.T. significantly shortened in all segments under study. This shortening was quantitatively dependent on the increase of mean blood pressure (MBP). 4. A significant prolongation of C.T. after application of the pneumatic cuff occurred in the region proximal to the cuff before the reactive hyperemia (RH) test. During the RH itself no changes of C.T. were observed. A similar prolongation of C.T. in the distal part of the lower limb was also noticed after body heating (BH). 5. The e and β indices during the functional stresses of the circulation in the lower limb did not show any essential changes. The index of elasticity showed a slight decrease and the Β angle an unsubstantial increase during the pressor reactions (cold pressure test, head-up tilting test). 6. The advantages of the suggested method of measurement of arterial elasticity for diagnosis of early atherosclerosis in the extremities are pointed out. [ABSTRACT FROM AUTHOR]

The oxyhemoglobin desaturation rate during breath holding has been used to measure O2 consumption in patients after the subcutaneous injections of concentrated heparin solution. The desaturation rate decreases initially and continues to fall for 15 min., after which the rate increases. After approximately 30 min., it is greater than the pretreatment value, suggesting that heparin activity may be one of the factors influencing the basal metabolic rate. [ABSTRACT FROM AUTHOR]

A new method of segmental pulse wave velocity (SPWV) measurement is described. The method enables the determination of the velocity of pulse wave propagation by means of an electrical impedance plethysmograph in three segments of the lower limb: in the thigh (segment I ) , in the middle part of the limb (segment I I ) , and in the calf (segment III). SPWV values at rest wore 9.76 ± 1.01 m/sec. (segment I ); 9.74 ± 1.19 m/sec. (segment I I ); and 9.19 ± 1.28 m/sec. (segment III). No correlation was? found between the resting values of mean blood pressure and SPWV. During the pressure responses (cold pressure test, 60° head-up tilting test) the SPWV values significantly rose, the rise depending quantitatively on the increase of mean blood pressure. SPWV does not manifest any significant changes in the course of reactive hyperaemia (RH) after a 3-min. occlusion in comparison with the values before RH. A close application of the occlusive cuff to the thigh before the RH test reduces significantly SPWV in comparison with the resting values without the cuff being applied. Body heating docs not change the values of SPWV. The level of blood pressure is a decisive factor for determination of SPWV under steady state of measurement. The values of SPWV follow the values of casual or basal blood pressure. The significance and contribution of SPWV method for the clinical evaluation of arterial elasticity are briefly discussed. [ABSTRACT FROM AUTHOR]

Discusses the methods for the treatment of atherosclerotic insufficiency of the lower limbs. Reevaluation of the results of lumbar sympathectomy; Comparison of the efficacy of high lumbar sympathectomy with venous by-pass; Indication of lumbar sympathectomy.

Dogs maintained on a regular diet and given 200 or 250 mg/kg triton intravenously at intervals of 5 to 25 days develop a sustained hyperlipemia. The serum triglycerides are the first lipid fractions to rise. Soon thereafter there is a marked rise in the serum cholesterol, with the greater percentage in the free form, and the serum phospholipids. On the higher dose a large number of animals develop intravascular hemolysis, a rise in the serum bilirubin, hemoglobinuric nephrosis, and die within 2 weeks. Animals surviving for from 5 to 9 months develop atherosclerotic lesions in the aorta, coronary, pulmonary, and renal arteries. In one animal myocardial fibrosis and acute myocardial infarction was noted, associated with the severe coronary arterial lesions. In addition, the livers and spleens are enlarged and reveal large numbers of lipid-laden foamy histiocytes suggestive of some unusual storage disease. Similar-appearing foamy histiocytes are also seen in the lymph nodes. The kidneys reveal lipid-laden tubular epithelial cells and lipid-laden macrophages in the interstitial tissue as well as foam cell lesions of the glomeruli. The lesions seen in the present study are briefly compared with the naturally occurring and experimentally induced atherosclerosis in dogs and some of the similarities and differences are mentioned. It is suggested that this technique may serve as a useful experimental model in which to study selected stages of atherosclerosis. [ABSTRACT FROM AUTHOR]