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Biomedical subjects

Y Edoute

Publications and source records attributed to Y Edoute.

At least 73 records · Page 4Linked to original sources

Difficult preoperative diagnosis of a patient with sclerosing splenic hemangioma.

We present a young asymptomatic woman with splenomegaly and a large isolated splenic mass demonstrated by ultrasonography, 99mTc sulfur colloid, and gallium scintigraphy studies. Computerized tomography (CT) and three-phase 99mTc-labeled red blood cell imaging suggested a malignant lesion. Repeated sonographically guided fine needle aspiration (FNA) obtained only blood, suggesting the possible vascular nature of the tumor. Splenectomy established the diagnosis of splenic hemangioma (SH) with marked sclerotic changes. We conclude from this case that 1) the sclerotic and cystic changes in the SH and the abdominal lymphadenopathy could explain why the three-phase red blood cell and CT scanning, respectively, suggested that the lesion was malignant rather than benign; 2) guided FNA of a splenic mass suspected to be hemangioma may be an additional safe and useful diagnostic procedure. Multiple aspirations yielding blood alone suggest hemangioma and may prevent an unnecessary operation. To the best of our knowledge, this is the first reported case in the literature of FNA of splenic hemangioma.

Adult

Effect of different degrees of hypoxia and reoxygenation on myocardial energetics.

We determined the effect of high-flow hypoxia and reoxygenation on myocardial function and O2 uptake. Isolated working rat hearts were subjected to a 30-min period of hypoxia (pO2 = 384, 296, 207 and 131 torr), followed by 30 min of reoxygenation (pO2 = 500 torr). Another group of normoxic hearts was exposed to 500 torr O2 for the same length of time. During hypoxia, lactate release increased, whereas O2 uptake (VO2), aortic flow (AF) and stroke volume decreased relative to the degree of hypoxia. In hearts subjected to a pO2 of 131 torr, coronary flow and VO2 declined to 40 and 15%, respectively, of the control values, without any AF. Reoxygenation of the hypoxic hearts after the hypoxia increased the depressed VO2 and AF relative to the previous degree of hypoxia. However, these values remained below those of the normoxic hearts, indicating persistent hypoxic injury. In a second series, we also measured the mechanical power (using aortic pressure) at three levels of inflow pO2: 500, 300 and 200 torr, and obtained good correlation between the mechanical power and both AF and VO2. Analysis of the O2 cost of production of AF showed a posthypoxic disengagement between VO2 and AF after exposure to O2 of 131 torr. The degree of hypoxia determines the amount of hypoxic damage and the ability of the heart to recover upon reoxygenation, and an accelerated injury occurs at severe hypoxia.

Animals

Evidence for improved myocardial oxygen delivery and function during hypoxia in the mole rat.

The high capillary density of the hypoxic adapted mole rat may provide an efficient oxygen extraction system that permits the maintenance of a normal metabolic rate during hypoxia. We compared myocardial function and energetics in the isolated working heart of the mole rat with that of the white rat during oxygenation (567 torr O2) and 3 hypoxic periods of 319, 232 and 155 torr O2, each followed by a reoxygenation period. Control hearts were perfused for a similar time but with oxygenated buffer. The control oxygenated mole rat heart had higher coronary flow (CF), systolic pressure and myocardial O2 consumption (VO2) and lower coronary resistance compared with the heart of the white rat. The hypoxic heart of the mole rat had higher CF, aortic flow, stroke volume, VO2, mechanical power and efficiency, and lower coronary resistance compared with the hypoxic heart of the white rat. The better performance of the hypoxic mole rat heart was not due to a more efficient O2 extraction but was associated with a lower coronary resistance. The findings correlate with the known cardiac physiology of the intact mole rat.

Animals

Talcosis presenting as pulmonary infiltrates in an HIV-positive heroin addict.

A case of an HIV-positive young drug addict presenting with fever, respiratory distress, and pulmonary infiltrates is reported. Pulmonary talcosis was diagnosed by transbronchial biopsy. The differential diagnosis of pulmonary infiltrates in HIV-positive patients is reviewed and the predisposition of drug addicts to develop both HIV infection, as well as pulmonary talcosis, is discussed. Pulmonary talcosis must be considered in the differential diagnosis of pulmonary infiltrates of HIV-positive drug addicts.

Adult

Beta-2 adrenergic responses to tulobuterol in airway smooth muscle, vascular smooth muscle and adrenergic nerves.

Experiments were designed to determine the mechanism of action of the bronchodilator drug tulobuterol. Tissues were suspended in organ chambers for isometric tension recording. Tulobuterol caused concentration-dependent relaxations of guinea pig tracheae, canine saphenous veins and canine bronchi; the compound relaxed canine coronary arteries only at high concentrations and did not affect spontaneously beating guinea pig atria. A metabolite of tulobuterol, 4-hydroxytulobuterol, was more potent in relaxing guinea pig tracheae than tulobuterol, salbutamol and isoproterenol. Other metabolites (3-hydroxy-, 5-hydroxy- and 4,5-dihydroxytulobuterol) were less efficacious than 4-hydroxytulobuterol. Both tulobuterol and 4-hydroxytulobuterol acted as partial agonists. The effects of tulobuterol in the saphenous vein (but not in the coronary artery) were antagonized by the selective beta-2 adrenergic blocker ICI 118,551 but were not affected by the selective beta-1 adrenergic inhibitor metoprolol. In bronchi, removal of the epithelium reduced the relaxations caused by tulobuterol. The drug did not inhibit responses of canine bronchi to electrical stimulation of the cholinergic nerves more than those to exogenous acetylcholine. Tulobuterol caused a moderate augmentation of the evoked release of [3H]norepinephrine in canine saphenous veins previously incubated with the labeled transmitter. Thus, tulobuterol is a selective beta-2 adrenergic agonist with minimal nonselective inhibitory effect on airway and vascular smooth muscle. It also facilitates adrenergic neurotransmission, which may help to explain its bronchodilator effect in the intact organism. Tulobuterol does not activate beta-1 adrenoceptors and has no direct positive chronotropic effect. A metabolite of tulobuterol, 4-hydroxytulobuterol, is more active than the parent compound.

Adrenergic Fibers

Inorganic phosphate inhibits sympathetic neurotransmission in canine saphenous veins.

Inorganic phosphate has been proposed as the initiator of metabolic vasodilatation in active skeletal muscle. The present study was primarily designed to determine if this substance has an inhibitory effect on adrenergic neurotransmission. Rings of canine saphenous veins were suspended for isometric tension recording in organ chambers. A comparison was made of the ability of inorganic phosphate (3 to 14 mM) to relax rings contracted to the same degree by electrical stimulation, exogenous norepinephrine, and prostaglandin F2 alpha. The relaxation during electrical stimulation was significantly greater at all concentrations of phosphate. In strips of saphenous veins previously incubated with [3H]norepinephrine, the depression of the contractile response caused by phosphate during electrical stimulation was accompanied by a significant reduction in the overflow of labeled neurotransmitter. Thus inorganic phosphate inhibits sympathetic neurotransmission and hence may have a key role in the sympatholysis in the active skeletal muscles during exercise. By contrast, in this preparation, it has a modest direct relaxing action on the vascular smooth muscle.

Animals

Peripartum congestive cardiomyopathy and endocardial fibroelastosis associated with ritodrine treatment. A case report.

Congestive cardiomyopathy from endocardial fibroelastosis occurred in a 24-year-old primigravida with a twin gestation and preeclampsia. The patient was taking ritodrine for premature labor. Cardiovascular evaluation should be performed during the course of ritodrine treatment, and no patient should be discharged if she does not have normal cardiovascular function.

Adult

Primary therapy for Cushing's disease with metyrapone.

A 13-year-old boy was diagnosed as suffering from pituitary-dependent Cushing's syndrome. He was treated with 2.0 g of metyrapone daily as the sole treatment for four years. All clinical and biochemical stigmata of Cushing's disease disappeared within a few months. The patient grew 23.0 cm in four years and regained normal health. No significant side effects of metyrapone were noticed. Administering the medication at 2 PM and 8 PM allowed higher cortisol levels in the morning and noon hours than in the evening and night, approximating the normal diurnal variation in cortisol production. We conclude that metyrapone may be considered the sole treatment in patients with Cushing's disease.

Adolescent

Serotonin reduces coronary flow in the isolated heart of the spontaneously hypertensive rat.

Serotonin may cause vasodilatation or vasoconstriction. In hypertension the vasoconstrictor effects of serotonin predominate. Experiments were designed to study the effects of serotonin on coronary flow in isolated hearts of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. The hearts were paced at constant rate and perfused by the Langendorff technique at constant pressure (75 cmH2O). In WKY rats serotonin (10-9 to 10-5 mol/l) caused concentration-dependent increases in coronary flow and a decrease in cardiac performance. In SHR, the monoamine caused concentration-dependent, partially reversible decreases in coronary flow, and a marked decrease in cardiac performance. The inhibitor of cyclo-oxygenase indomethacin prevented the decrease in coronary flow and cardiac performance caused by serotonin in SHR, but did not affect the increase in coronary flow in WKY rats. These experiments suggest that in the coronary circulation of SHR the response to serotonin is shifted from vasodilatation to vasoconstriction. The mediator of this vasoconstriction is probably a product of cyclo-oxygenase.

Animals

Autoregulation and vascular reserve in the coronary circulation of the spontaneously hypertensive rat.

Hypertension causes structural and functioning changes in blood vessels. Experiments were performed in isolated hearts of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats perfused by the Langendorff technique. Spontaneously hypertensive rats had significantly higher left heart to body weight ratios than WKY rats, indicating left ventricular hypertrophy. Coronary flow per unit cardiac mass was lower and vascular resistance was higher at 75 cm H2O perfusion pressure in SHR. This difference was maintained during maximal vasodilatation. In WKY rats, but not in SHR, autoregulation of flow was observed in the pressure range 75-150 cm H2O due to an increase in coronary vascular resistance. After maximal vasodilatation the pressure-flow relationship was linear in SHR and WKY rats, but less steep and shifted to the right in SHR. We conclude that structural adaptations of the coronary circulation in SHR lead to decreased coronary vascular reserve and a loss of autoregulation in the normal blood pressure range.

Animals

Contribution of echocardiography to cardiac diagnosis.

In order to quantify information provided by echocardiography for residents in internal medicine and for cardiologists, 150 selected patients were studied by echocardiography, and the ultrasonic diagnosis was compared with the clinical evaluation. Among 144 patients with adequate visualization of the heart, echocardiography provided findings that were totally unexpected to the residents in 13 (9%) and to the cardiologist in 9 (6%) patients. Echocardiography also provided information relevant to the management of the patient in another one-third of the cases. Both the residents and the cardiologist were able to correctly predict the cause of cardiomegaly and the mechanism of heart failure in most patients presenting with these findings. Despite the introduction of cross-sectional echocardiography, the amount of information contributed by echocardiography has not increased since 1978, when a similar study was performed at our institution. This may reflect increased clinical skill among residents, probably due to long-term exposure to echocardiography during their training.

Adolescent

Rare complications after transabdominal fine needle aspiration.

Fine needle aspiration is emerging as a useful diagnostic tool in the evaluation of tumor masses. This technique provides high diagnostic yield associated with only minimal side effects. Of 500 transabdominal aspirations conducted in our hospital over an 8-year period we have experienced four cases of unusual complications after this procedure. These included bile peritonitis, localized peritonitis and infection, perforation of small bowel, and pneumothorax. The last three cases have not yet been described in the literature as complications of transabdominal aspiration. Analysis of these complications illustrate the importance of careful patient selection and meticulous attention to the proper procedure.

Aged

Normothermic ischaemic cardiac arrest and reperfusion of the isolated working heart: effect of chlorpromazine on functional, metabolic and morphological recovery.

The effects of chlorpromazine, an inhibitor of both Ca2+ flux and phospholipase activity, on myocardial ultrastructure, function and metabolism were assessed during normothermic ischaemic cardiac arrest and reperfusion of the isolated working rat heart. Normothermic ischaemic cardiac arrest produced significant changes in myocardial ultrastructure, high energy phosphate contents and mitochondrial oxidative phosphorylation within 20 min. Reperfusion of untreated hearts subjected to 20 and 25 min ischaemia failed to restore mitochondrial function, mechanical activity and ATP content to control, pre-ischaemic levels. Morphological signs of ischaemic injury regressed, especially in the subendocardial layer. Pretreatment of hearts with chlorpromazine did not prevent the ischaemia-induced changes in myocardial ultrastructure and mitochondrial function. However, during reperfusion the chlorpromazine-treated, totally ischaemic heats (20 to 25 min) exhibited improved coronary flow rates, and ultrastructural and mechanical recovery. The mitochondrial oxidative phosphorylation process and tissue high energy phosphate contents were not affected by the drug.

Adenosine Triphosphate

Prognostic implication of detecting vegetations by M-mode echocardiography.

The prognostic significance of finding vegetations by M-mode echocardiography in patients with infective endocarditis remains controversial because many such patients are referred for early surgery. We detected vegetations in 7 of 25 consecutive subjects with active infective endocarditis (28.1%) studied by M-mode echocardiography. 11 patients died within 1 year and only 1 underwent surgery. Patients with vegetations had a higher likelihood of developing serious complications such as death, congestive heart failure or "severe congestive heart failure' when compared with patients without vegetation. This study validates previously reported series including a high percentage of patients "requiring surgery' and points to the serious prognostic implication of finding a vegetation by M-mode echocardiography.

Adolescent

Normothermic ischemic cardiac arrest of the isolated working rat heart. Effects of time and reperfusion on myocardial ultrastructure, mitochondrial oxidative function, and mechanical recovery.

The ischemic state of the myocardium of the isolated working rat heart after induction of normothermic ischemic cardiac arrest was assessed by the interrelationship among changes in myocardial ultrastructure, mitochondrial oxidative phosphorylation, and tissue high energy phosphate contents. At all time intervals (10-40 minutes) studied, the ultrastructural changes were more severe in the subendocardium than in the subepicardium. After 25-40 minutes of normothermic ischemic cardiac arrest, the mitochondrial oxygen uptake (state 3) became increasingly depressed, particularly in mitochondria isolated from the subendocardium. Mitochondrial oxidative function, as measured in vitro, did not correlate well with mitochondrial ultrastructural damage. In addition, the effects of coronary reperfusion on the ability of the ischemic heart to recover in terms of ultrastructure, mechanical, and metabolic function were evaluated. Hearts subjected to 10-40 minutes of normothermic ischemic cardiac arrest showed almost complete ultrastructural recovery of the subepicardium upon reperfusion; regression of ultrastructural changes occurred to a lesser extent in the subendocardium. Reperfusion for 30 minutes did not alleviate the depression in mitochondrial oxidative function, while tissue ATP levels did not return to control, preischemic levels. After 20 minutes of normothermic ischemic cardiac arrest, the mechanical performance of the working heart during reperfusion was significantly depressed, compared with pre-ischemic control values. Normal ultrastructure of the subendocardium always accompanied mechanical recovery, while improvement of mitochondrial oxidative function was not essential.

Adenosine Triphosphate

Normothermic ischaemic cardiac arrest of isolated working rat heart: effects of reserpine and propranolol on functional, metabolic and morphological recovery.

The ability to preserve myocardial structural and functional integrity during extended periods of total ischaemia has practical clinical significance. The role of endogenous catecholamines in the onset of irreversible damage in global ischaemia of the isolated rat heart was assessed by beta-blockade or catecholamine depletion. The effects of propranolol and reserpine pretreatment on myocardial ultrastructure, function and metabolism were studied during normothermic ischaemic arrest (NICA) and reperfusion of the isolated working rat heart. beta-Blockade as well as catecholamine depletion resulted in an increase in the percentage of totally ischaemic hearts which recovered mechanically upon reperfusion. In these studies mechanical recovery during reperfusion was associated with reversal of ultrastructural ischaemic alterations, but without an improvement in mitochondrial function. These findings support the concept that failure of mitochondria to recover functionally upon reperfusion is not the cause of either irreversible mechanical failure or ultrastructural damage of the ischaemic myocardium.

Animals