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Apres irradiation gamma, des cellules endotheliales humaines ont une production accrue des interleukines (IL-) -6 et -8. Dans le but de reguler la production de ces cytokines pro-inflammatoires, nous avons utilise des cytokines dites anti-inflammatoires, l'IL-4 et l'IL-10. Ces agents ont ete ajoutes soit avant soit apres une irradiation de 10 Gy. Nos resultats montrent qu'il est possible de diminuer les productions radio-induites d'IL-6 et d'IL-8 par l'IL-4 et l'IL-10. Des differences dans l'intensite de la reponse ont toutefois ete observees selon que l'IL-4 ou l'IL-10 ont ete ajoutees avant ou apres irradiation ; leur efficacite anti-inflammatoire etant plus marquee lorsque les cytokines sont ajoutees apres l'irradiation.

To examine the effects of beta-cyclodextrin (BCD), a non-absorbable carbohydrate, on lipid metabolism, growing pigs were fed a 0.3% cholesterol-enriched diet for 4 weeks or this diet containing 5% or 10% BCD. Pigs fed a basal diet without added cholesterol or BCD were used as controls. The cholesterol-rich diet induced hypercholesterolemia (1.75 vs. 0.84 g/l plasma) due to increased LDL concentration, delayed the plasma clearance of vitamin A, enhanced liver cholesterol storage, lowered the hepatic activities of LDL-receptors (by 47%) and HMG-CoA reductase (by 62%), stimulated cholesterol 7alpha-hydroxylase (x3), and accelerated the fecal output of neutral sterols (x4). Addition of BCD to the cholesterol-rich diet prevented the elevation of plasma cholesterol due to dietary cholesterol excess. Moreover, BCD produced a dose-dependent effect in reducing liver cholesterol storage, stimulating hepatic cholesterogenesis, increasing the proportion of primary bile acids in bile and in feces, and the fecal loss of neutral sterols and bile acids. Pigs receiving 10% BCD thus differed markedly from controls, especially for HMG-CoA reductase and cholesterol 7alpha-hydroxylase hepatic activities (x5), and fecal output of total bile acids (x3) and hyocholic acid (x20), and their overall cholesterol synthesis was higher (+50%), despite the abundant dietary cholesterol. Owing to the property of BCD to bind cholesterol and bile acids in vitro, these results suggest that this resistant carbohydrate accelerates body cholesterol turnover by reducing cholesterol absorption, increasing cholesterol and bile acid synthesis, and altering the action of the intestinal microflora.

Anionic polypeptide fraction (APF) is a phospholipid- and calcium-binding apoprotein present in animal and human bile, predominantly associated with cholesterol-phospholipid vesicles. In bile, the protein may play a physiological role in preventing precipitation of calcium salts. APF has also been suggested to be of regulatory importance in the process of biliary lipid secretion. The aim of the present study was to investigate whether the secretion rates of APF and that of biliary lipids are coupled, which would support a physiological role of APF in biliary lipid secretion. Biliary secretion rates of bile acids, phospholipids, and cholesterol were experimentally modulated in three different rat models. Secretion rates of APF were compared with that of bile acids, lipids, and with that of two other biliary proteins, the lysosomal protein beta-glucuronidase and apolipoprotein A-I (apo A-I). Model 1: diurnal variation in bile formation during chronic bile diversion; model 2: specific inhibition of biliary phospholipid and cholesterol, but not of bile acid secretion by infusion of the organic anion, sulfated lithocholyltaurine; model 3: acute interruption of the enterohepatic circulation in unanesthetized rats. The diurnal variation in bile formation involved a parallel increase of the biliary secretion rates of bile acids (+56 +/- 7%, mean +/- SD), phospholipids (+53 +/- 29%), cholesterol (+73 +/- 54%), and APF (+72 +/- 86%) during the night phase of the cycle. Infusion of sulfated lithocholyltaurine inhibited biliary phospholipid and cholesterol secretion (-78 +/- 15%, and -54 +/- 25%, respectively), but did not affect biliary bile acid or APF secretion rate (-19 +/- 14%, and +12 +/- 107%, respectively). Within 4 hours after interruption of the enterohepatic circulation, bile secretion rates for bile acids (-92 +/- 3%), phospholipids (-74 +/- 13%), cholesterol (-64 +/- 8%), and APF (-58 +/- 24%) rapidly declined to a new steady-state level. Correlation analysis using the data from the three experimental models indicated that the biliary secretion rate of APF was independent from that of phospholipids, cholesterol, beta-glucuronidase, and, presumably, apolipoprotein A-I, and positively correlated to bile acid secretion rate and bile flow. The data from three experimental models indicate that the biliary secretion rates of APF and of phospholipids/cholesterol are not coupled and, therefore, do not support a direct physiological role of APF secretion in biliary lipid secretion. APF secretion into bile may, at least partially, be controlled by biliary bile acid secretion.

Cholesterol precipitation from supersaturated bile is the earliest and determinant step in the formation of cholesterol gallstones, which is thought to be diet-dependent. Bile composition, appearance and growth of cholesterol crystals were studied in fresh gall-bladder biles from pigs adapted to four different protein-containing diets over 3 weeks: 160 g dietary protein/kg as casein (C16; n 6), or as soyabean-protein concentrate (S16; n 6), or a mixture of both protein sources (casein-soyabean protein, 70:30, w/w) (CS16; n 6), or 320 g of the mixed protein/kg (CS32; n 6). Moreover, all four diets contained 3 g cholesterol/kg and 50 g beta-cyclodextrin/kg as modifiers of bile composition towards cholesterol pro-crystallization. Cholesterol precipitation was most active after the high-protein diet, CS32, and the casein diet, C16, and lowest after the soyabean-protein diet, S16. It was intermediate after the mixed diet, CS16, but still much lower than in the former two groups. These diet-induced variations were suggested to be mediated through modifications in the biliary profile of bile acids, whereas all other biliary constituents studied were essentially unchanged. The fasting level of plasma cholesterol was lowest in both 160 g protein/kg diets containing soyabean protein (S16 and CS16), highest for the high-protein diet CS32, and intermediate for the C16 diet. These results should encourage clinical studies on the effect of soyabean protein, or other vegetable proteins, for primary or recurrence prevention of cholelithiasis at its earliest stage.

Radiation exposure results in an inflammatory reaction with acute as well as subacute consequences. Leukocyte infiltration is one of the predominant early histological changes and involves both cytokines and adhesion molecules. Endothelial cells play a key role in this reaction. We have previously shown the increased production of interleukin 6 (IL-6) and IL-8 and the upregulation in intercellular adhesion molecule 1 (ICAM-1) expression by HUVEC following gamma ray exposure. In the present study, we used the cytokines IL-4 and IL-10 to regulate these radiation-induced manifestations. Human umbilical vascular endothelial cells (HUVEC) were treated with IL-4 and IL-10 (50 pg/ml) either before or after 10- Gy irradiation. Three and seven days after irradiation, IL-6 and IL-8 production by HUVEC (either treated or non-treated) was assessed by enzyme-linked immunosorbent assay (ELISA). Our results show that IL-4, when added after irradiation, reversed the radiation-induced increase in IL-8 production, although slightly increased IL-6 production. IL-10 decreased both IL-8 and IL-6 production when added after irradiation. ICAM-1 expression was evaluated 3 days after irradiation by flow cytometry. The radiation-induced upregulation in ICAM-1 expression remained unaffected by the use of IL-4. Altogether, our results show that radiation-induced endothelial cell activation may be ameliorated by IL-4 and/or IL-10, which is of significance in designing strategies for cytokine-mediated intervention and/or therapy of radiation damage.

beta-(2-Hydroxyethoxy)-5 alpha-cholest-8(14)-en-15-one, a synthetic inhibitor of cholesterol biosynthesis, was shown to exhibit a high affinity to oxysterol binding protein. This was proved by ultracentrifugation of the protein fraction from rabbit liver in the presence of the 3H-labeled inhibitor, 3 beta-(2-hydroxy-2-[3H]ethoxy)-5 alpha-cholest-8(14)-en-15-one, or by the substitution of the [3H]-25-hydroxycholesterol in its complex with the oxysterol binding protein. In human hepatoma Hep G2 cells, the inhibitor decreased activity of 3-hydroxy-3-methylglutaryl CoA reductase [ID50 (2.7 +/- 0.7) x 10(-5) M] and was transformed into 3 beta-[2-(9-Z-octadecenoyloxy)ethoxy]-5 alpha-cholest-8(14)-en-15-one.

The intravenous injection of 3 beta-(2-hydroxy-2-[3H]ethoxy)cholest- 5-ene into rats with the cannulated common bile duct resulted in the primary accumulation of radioactivity in liver (24%) and spleen (12%) tissues, bile (7%), and blood serum (15%) after 3 hours. The distribution of 3 beta-(2-hydroxy-2-[3H]ethoxy)cholest-5-ene throughout various tissues was close to that of [14C]cholesterol being administrated under the same conditions. The analysis of radioactive products from blood serum showed that 40-60% of 3 beta-(2-hydroxy-2-[3H]ethoxy)- cholest-5-ene was converted to the acyl derivative under experimental conditions.

Synthesis of 3 beta-(2-hydroxyethoxy)cholest-5-ene, 3 beta-(2-hydroxyethoxy)cholest-5-en-7-one, 3 beta-(2-hydroxyethoxy)-7 beta-hydroxycholest-5-ene, 3 beta-(2-hydroxyethoxy)-5 alpha, 6 alpha-epoxycholestane, and 3 beta-(2-hydroxyethoxy) -5 alpha, 6 beta-dihydroxycholestane was described. Substances obtained inhibited cholesterol biosynthesis in the rabbit hepatocyte cell culture with ID 50 from 5.5(+/-0.7) x 10(-8) to 1.3(+/-0.2) x 10(-5) M and also to a remarkable extent the cell protein biosynthesis.

Livers of Wistar rats were stored between 0 and 36 hrs. in the University of Wisconsin preservation liquid in order to determine time-related biochemical and morphological hepatic changes. Ursodeoxycholate (100 microM) was also added in the medium to test the hepatoprotective properties of the bile salt. Biochemical assays were performed on hepatic microsomes, plasma and biliary canalicular membranes. Protein and lipid composition of the microsomal and baso-lateral plasma membranes remained stable. Protein and cholesterol content of the biliary canalicular membranes decreased, phospholipid/cholesterol ratio increased between 0 and 36 hrs.; it resulted in a leak of 5'-nucleotidase and leucine amino peptidase activity of these biliary canalicular membranes, especially up to 12 hrs. Between 0 and 36 hrs., the lipid and protein content remained stable in the plasma membranes, as well as both tested enzymatic activities. Observations under electron microscopy showed alterations and underlined fragility of the bile canaliculi, particularly after 24 hrs. preservation. Ultrastructure of sinusoidal membranes showed damaged microvilli. Endoplasmic reticulum remained unchanged, in relation to the stability of the microsomal lipidic, proteic content and hydroxymethylglutaryl-coenzyme A reductase activity, except the decreased protein content after preservation for 36 hrs without ursodeoxycholate. Ursodeoxycholate by itself did not protect against the described disturbances.

We compared bile formation, and biliary and liver plasma membrane composition in guinea-pigs and rats in an attempt to explain the observation that the bile flow rate and the bile acid independent fraction of bile flow (BAIF) in guinea-pigs is about five to seven times higher than in rats. Analysis of electrolytes in bile showed that bicarbonate was significantly [acid] higher in guinea-pigs while Cl − , phosphate and Ca 2+ were markedly lower than in rats. High bile independent secretion in guinea-pigs was associated with a significantly lower concentration of total bile acid, phospholipid and cholesterol than in rats. Bile acid distribution studies showed that glycine conjugated chenodeoxycholate and ketolithocholate were the main bile acids in guinea-pigs, while taurine conjugated cholate and muricholate were the predominant bile acids in rats. Total fatty acid analysis of bile indicated that in rats the major fatty acids were palmitic acid (C16:0) and linoleic acid (C18:2, n-6). In guinea-pigs, the contribution of these fatty acids was lower than in rats and compensated with a significantly higher percentage of oleic acid (C18:1, n-9). Concentrations of anionic polypeptide fraction (APF), an acidic calcium binding apoprotein closely associated with biliary phospholipid and cholesterol secretion was also significantly lower in guinea-pigs. Canalicular plasma membrane analysis showed that as compared with rats, specific activities of Na + ,K + ATPase, and cholesterol and phospholipid content were markedly lower in guinea-pigs. Total fatty acid analysis of the membrane revealed that palmitic acid (C16:0), stearic acid (C18:0) and linoleic acid (C18:2, n-6) were the predominant fatty acids in guinea-pigs, while palmitic acid (C16:0), stearic acid (C18:0) and arachidonic acid (C20:4, n-6) were the most important in rats. Thus, high bile flow rate and BAIF in the guinea-pig may be attributed to the low bile acid concentration (below the critical micellar concentration), secretion of hypercholeretic bile acids (e.g. ketolithocholate) and high bicarbonate output.

The purpose of this work was to evaluate biliary phosphatidylcholine (PC) secretion after intravenous infusion of high density lipoprotein (HDL)-[3H]phosphatidylcholine (HDL-[3H]PC) in rats and to study the effect of infusion of dehydrocholic and cholic acids, which, respectively, inhibit and stimulate biliary secretion of PC. The data obtained in this study showed that, in the basal state, HDL-PC accounted for 38% of biliary PC. Dehydrocholic acid infusion caused only a "residual" secretion of HDL-PC in the bile; however, cholic acid infusion stimulated the secretion of HDL-PC as well as PC from intrahepatic microsomes. The low level of radioactivity of HDL-PC in intrahepatic compartments suggests that HDL-PC taken up by the liver is predestined for the bile secretion. The correlation between the kinetics of bile secretion of HDL-cholesterol and HDL-[3H]PC suggests the importance of HDL-PC in reverse transport of cholesterol to the liver and its transport to the bile. The differences between the effects of dehydrocholic acid and cholic acid infusions can be explained by the differences in bile salts binding to the surface of HDL.

The effects of increased dietary n-3 polyunsaturated fatty acids on gastric mucosal lipid metabolism were studied in rats fed for 8 weeks with different combinations of fish and corn oils. Lipid composition, ex vivo prostaglandin E2 (PGE2) production and enzymatic activities involved in phospholipid metabolism and peroxisomal oxidative catabolism of fatty acids and PGE2 were examined. With dietary n-6/n-3 compositional ratios ranging between 75 and 3.3 it was observed that: (i) the arachidonic acid-to-eicosapentaenoic acid ratio (AA/EPA) fell from infinity to 3.1 and 5.1 in phosphatidylcholines (PC) and phosphatidylethanolamines (PE), respectively; (ii) ex vivo production of PGE2 was lowered by a factor of about 2; and (iii) gastric phospholipase A2 activity was enhanced by 32%. With dietary n-6/n-3 ratio lower than 3.3, stimulation of PGE2-CoA oxidase activity was observed whilst the PGE2 level remained constant. These data suggest that the fish oil-induced decrease in ex vivo PGE2 production is more closely related to a decrease in the membrane AA level than to an enhanced oxidative catabolism of PGE2.

The nervous system is the organ with the second greatest concentration of lipids. These lipids participate directly in membrane functioning. Brain development is genetically programmed. It is therefore necessary to ensure that nerve cells receive an adequate supply of nutrients, especially of lipids, during their differentiation and multiplication, and throughout their lives. The effects of polyunsaturated fatty acid deficiency have been extensively studied; prolonged deficiency leads to death in animals. Linoleic acid is now universally recognized to be an essential nutrient. Until recently, however, alpha-linolenic acid was considered non-essential. Feeding animals with oils that have a low alpha-linolenic content results in all brain cells and organelles and various organs having reduced amounts of 22:6n-3, which is compensated for by an increase in 22:5n-6. The speed of recuperation from these anomalies is extremely slow for brain cells, organelles, and microvessels, in contrast to other organs. A decrease in alpha-linolenic series acids in the membranes results in a 40% reduction in the Na(+)-K(+)-ATPase of nerve terminals and a 20% reduction in 5'-nucleotidase. Some other enzymatic activities are not affected, although membrane fluidity is altered. A diet low in alpha-linolenic acid induces alterations in the electroretinogram which disappear with age; motor function and activity are little affected, but learning behavior is markedly altered. The presence of alpha-linolenic acid in the diet confers a greater resistance to certain neurotoxic agents (triethyl-lead). During the period of cerebral development, there is a linear relationship between brain content of n-3 acids and the n-3 content of the diet up to the point where alpha-linolenic levels reach 200 mg for 100 g of food intake. Beyond that level there is a plateau. For other organs, such as the liver, the relationship is also linear up to 200 mg/100 g, but then there is merely an abrupt change in slope and not a plateau. When dietary 18:2n-6 content was varied, it was noted that 20:4n-6 optimum values were obtained at 150 mg/100 g for all nerve structures, 300 mg for testicle and muscle, 800 mg for kidney, and 1200 mg for liver, lung and heart. A deficiency in alpha-linolenic acid and an excess of linoleic acid have the same main effect: an increase in 22:5n-6 levels.(ABSTRACT TRUNCATED AT 400 WORDS)

Oxidized low density lipoproteins (ox-LDL) are thought to accelerate atherogenesis. It was recently demonstrated that patients with coronary heart disease have defects in plasma fibrinolysis due to increased plasminogen activator inhibitor-1 (PAI-1) levels. Investigation of PAI-1 synthesis by endothelial cells may allow insight into the effect of native LDL (N-LDL) and ox-LDL on endothelial cells. In the present study, secretion of PAI-1 by human umbilical vein endothelial cells (HUVEC) in culture was evaluated after incubation with N-LDL and ox-LDL. Ox-LDL were obtained by peroxidation under ultraviolet radiation, which induced compositional changes in LDL, namely, a decrease in the levels of arachidonic acid, eicosapentaenoic acid, docosahexaenoic acid, and alpha-tocopherol and an increase in the malondialdehyde content. Ox-LDL induced a dose-dependent increase in PAI-1 secretion by HUVEC as assayed by an enzyme-linked immunosorbent assay. After a 24-hour incubation, a twofold increase in the PAI-1 content was observed with 50 micrograms/ml ox-LDL protein. Studies with inhibitors of protein synthesis and metabolic labeling with [35S]methionine confirmed that PAI-1 synthesis was stimulated by ox-LDL. N-LDL had no detectable effect on PAI-1 secretion. Binding studies with radiolabeled lipoproteins showed that the effect of ox-LDL was independent of the B/E receptor. Our experiments indicate that ox-LDL stimulate PAI-1 secretion from HUVEC and that this effect may involve a scavenger receptor.

The secretion of PAI-1 was measured in the conditioned medium of confluent cultures of Hep G2 cells and human umbilical vein endothelial cells (HUVEC) after low density lipoproteins (LDL) stimulation. LDL induced a dose-dependent increase in PAI-1 Ag synthesis by Hep G2 cells. They did not modify the basal level of PAI-1 secretion by HUVEC.

There is no controversy about the prosthetic replacement of the aortic valve in cases in which there is a disorder of function or cardiac failure, or in cases with a tight aortic stenosis, even if it appears to be well-tolerated clinically. It is especially critical in cases of aortic incompetence with marked cardiac enlargement, but the problems are not overwhelming. The indications for operation in very advanced cases with cardiac failure which is refractory, or in aged patients, are discussed.

The authors report the case of a 19 year old woman with supravalvar aortic stenosis and hypoplasia of the ascending aorta with stenosis at the origin of the innominate artery. This was a sporadic form, without mental deficiency nor facial dysmorphia. No similar case was found in the family. The patient had three attacks of bacterial endocarditis over a period of 3 years and became cured without any cardiac sequelae. In view of the onset of left ventricular failure and sequelae. In view of the onset of left ventricular failure and syncope, operation was decided. A lozange-shaped patch was placed on the aorta from the narrowed supravalvar part to the origin of the innominate artery and prolonged on the latter vessel after relief of the stenosis. This gave an excellent result.

A young girl of 15 with an aorto-pulmonary fistula was treated surgically, with a successful outcome. The clinical diagnosis could only be established at right-sided catheterisation, and especially at retrograde per-arterial aortography. The small size of the fistula explains the low level of the pulmonary arterial hypertension, and the way in which the condition was well-tolerated for some time. The association of this lesion with ventricular septal defect and pulmonary stenosis is extremely rare.

Selective intracoronary injection of microspheres labelled with radioactive substances which emit gamma rays with different energy levels (Indium 113 m and Technetium 99 m) allows us to explore by scintigraphic methods the areas of distribution of the two coronary arteries. Having been carefully calibrated, the particles are injected in limited numbers, and block the precapillary arterioles, where they gradually diminish in number. Scintigraphic examination is carried out in various projections (anteroposterior, left anterior oblique and right anterior oblique) immediately after coronary arteriography. Coronary scintigraphy allows us to establish the integrity of the distribution network of a coronary trunk which appears normal on coronary arteriography, to visualise the diminution of flow caused by a stenosed but patent trunk, and to visualise the extent of the collateral circulation and the quality of revascularisation achieved by an aorto-coronary bypass operation.

Although greater than in patients with stabilised coronary insufficiency, the risks of carrying out coronary arteriography during the period of a threatened infarction are still modest in the hands of an experienced team. In a series of 66 such investigations under these conditions over an 18 month period, there were no deaths as immediate sequelae. Three myocardial infarctions occurred, one of which was probably encouraged by ceasing the propranolol prior to arteriography. Analysis of the results confirms the frequency of lesions affecting all three trunks (47% of cases), the anterior descending branch being the most commonly affected. A collateral circulation was established in 23% of cases. Ventriculography was normal in one third of cases. The mean value for the ventricular ejection fraction was 0.57 over the entire series. In 58% of cases, all the arteriographic and ventriculographic criteria of operability were satisfied. It therefore appears that coronary arteriography is justifiable during the period of threatened infarction; it may be undertaken at an early stage if the angina does not respond to medical treatment. It is always best to carry it out several days after cessation of the pain where possible. The investigation may lead to urgent surgical intervention.

The 19 coronary patients studied were found to have a "normalised" rigidity k = dp/(dVP) identical to that of normal subjects, and a lowered instantaneous end-diast-lic compliance (dV/dP)TD. The increase in end-diastolic pressure is due to a small increase in end-diastolic volume, and brings about Starling's phenomenon to compensate for a diminution in contractility. The maximimum speed of shortening of the myocardium (VCFmax) shows up the baseline contractility, and appears to be more sensitive than the mean speed of myocardial shortening (VCF) and the ejection fraction.

Active biological systems can be divided into five phases: the aqueous polar phase, the monolayer and/or bilayer interfacial phase, the apolar or hydrophobic phase, the solid or insoluble phase and the gaseous phase. The micellar phase is a special dispersed state of an interfacial phase. Molecules are distributed among these five phases according to their physicochemical properties. Herein is proposed a standardization in strict compliance with the CGS (cm, g, s) unit system and uses the mass/volume, mole per cm3 (mol X cm-3) chemical unit. This standardization requires a new set of symbols to clearly distinguish the concentrations in the different phases. The numerous implications of this standardization are discussed with respect to the quantitative classification of lipids based upon interphase partition coefficients, a new definition of micelles, simple models for the study of lipid biodynamic behavior and sites of action of lipid metabolism enzymes as well as determination of the physicochemical parameters of circulating lipoproteins. By compartmentalization in an aqueous polar phase, an interfacial phase comprising phospholipids and free cholesterol and an apolar phase comprising triglycerides and esterified cholesterol, this standardization will greatly simplify quantitative research on the factors regulating and disturbing cholesterol homeostasis. The notion of total cholesterol must be foresaken, since the biodynamic behavior of free cholesterol and esterified cholesterol are fundamentally different. Free cholesterol shares the fate of the interfacial phase of which it is a part, this fate being hinged on enzymatic biotransformations and/or ligand--receptor interactions. The proposed standardization gives rise to a new rationale using simple calculations and its advantage will be 2-fold: first, in the design of experimental protocols; and second, in allowing immediate and unambiguous comparison of experimental data based upon strictly defined parameters.

A cine-angiographic study was carried out in eleven patients with major aortic incompetence, in two of whom there was an associated aortic stenosis. The ventricular end-diastolic volume is always greatly increased, disproportionately to the modest increase in end-diastolic pressure. The pressure-volume relationship during filling is therefore altered, and makes it possible for a normal end-diastolic compliance (dV/dP) TD to be preserved. The indices of contractility are markedly altered, despite the recent appearance of signs of poor tolerance. These findings argue in favour of a full haemodynamic investigation and of early corrective surgery.

Two methods were used to estimate the intracellular phospholipase activity in rat heart: one using exogenous radioactive substrate dispersed as unilamellar vesicles; the other using endogenous membrane hydrolysis and subsequent phospholipid and lysophospholipid separation by high-performance liquid chromatography and quantification by phosphorus determination. We found that the endogenous method provided a higher hydrolysis rate than the exogenous method and that phosphatidyl ethanolamine was a better substrate than phosphatidyl choline.

Advantage may be taken of the hyperaemic response to the iodine contained in the contrast medium injected during coronary angiography to assess the functional value of the coronary tree using radioactive microspheres. This series comprises 73 selective coronary scans performed in the resting state (113 m In marked microspheres) and during the hyperaemic phase (99 m TC marked microspheres) in 70 patients. A positive hyperaemic response distal to severe truncular stenosis indicates a good distal arteriolar bed and collateral circulation for aorto-coronary bypass grafting. After aorto-coronary bypass (23 cases), the hyperaemic response gives an indication of the functional value of the revascularised myocardium. In 71% cases, the results correlate well with the measurement of the peroperative blood flow through the graft. It is usually positive when the bypass graft is implanted with good distal arterial run off.

Aneurysms of Valvsalva sinus unruptured into a cavity, but developing into the membranous and even muscular interventricular septum are exceptional. Two cases illustrating this fact are reported. In one of them, a massive mitral incompetence by elongated chordae tendinae related to the presence of a voluminous intra-septal pouch. Atrio-ventricular and intraventricular conduction disturbances were present in both patients. The interest of supra-valvar angiography which makes it possible to advise operation before the eventual rupture is underlined.

The combination of radiocardiography with scintigraphy of the cavities of the heart allows us to calculate the effective systemic ejection fraction. The systolic volume effectively ejected into the systemic circulation is obtained from radiocardiography using Stewart-Hamilton's principle. It is correlated with the left ventricular end-diastolic volume as calculated by planimetry on the scintigraphic record of the cavities of the heart, making due allowance for the geometrical axis of the heart. The ejection fraction measured by this isotope method has been compared with the ejection fraction measured by selective left ventricular cineangiography, both measurements being carried out at an interval of less than 48 hours in 100 patients without valvular disease. The results show an excellent correlation between the two methods (r = 0.94). In the 15 cases where the haemodynamic status of the ventricule appeared to be normal, the ejection fraction meastured by the two techniques was 0.65 +/- 0.04 and 0.66 +/- 0.04 respectively. In those patients with valve disorders with incompetence, the effective systemic ejection fraction is always lower than the total ejection fraction given by cineangiography. The difference corresponds with the fraction of the blood volume which is regurgitated.

The findings at coronary arteriography and ventricular angiography in 52 patients with a restricted myocardial infarct were compared with those of 106 patients with acute coronary insufficiency and 100 with transmural infarcts. Certain features place restricted myocardial infarction in an intermediate category when compared with the two other syndromes. The percentage of coronary occlusions was significantly higher in transmural infarction (23.5%) and in restricted infarction (16.6%) than in acute coronary insufficiency 6.8%). Study of the vessel beyond a tight stenosis (greater than or equal to 75% was particularly effective in clearly separating the three groups. As a result, 63% of patients with coronary insufficiency, 40% of these with restricted infarcts, and only 23% of patients with a transmural infarct could be referred for surgery. Ventricular angiography showed a close relationship between restricted infarction and acute coronary insufficiency because ventricular function appeared normal or subnormal (localised hypokinesia) in 69% and 81% of cases respectively, compared with 4% of cases of transmural infarction. Restricted myocardial infarction appears to resemble coronary insufficiency, but shows elevation of enzymes and often more marked disease of distal vessels.

In order to evaluate the importance of the indices of ventricular rigidity and compliance (k=dP/dV.P and dV/dP), three groups of patients were studied and compared. A simplified method of calculating the diastolic compliance made use of the values of end-diastolic volume (EDV) measured by cineangiography, and of end-diastolic pressure (EDP), using the assumption that the relationship P-V is an exponential one arising from the ordinate: 0.43 mmHg. The correlation between EDP and EDV, which was positive in 19 coronary artery patients, was in fact negative in 11 patients with obstructive cardiomyopathy (OCM), and insignificant in 12 control patients. There were multiple correlations between k, EDPs and EDVs in 11 OCMs, and none in the two other groups. The ratio dV/dP decreased in end-diastole both in the OCM group and in the coronary group, and did not reflect the difference in pathology between these two groups. On the other hand k was increased in the patients with OCM, normal in the coronary patients, and represented in the former a primary modification in the relationship P-V and a primary increase in diastolic rigidity.