Biomedical subjects
A Simon
Publications and source records attributed to A Simon.
Untwinned single crystals of YBa2Cu3O7- delta : An optical investigation of the a-b anisotropy.
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[Imidazoles and cotrimoxazole].
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Unrelated responses of brachial artery hemodynamics and renin-angiotensin system to acute converting enzyme inhibition by enalaprilat in essential hypertension.
The simultaneous acute effects of converting enzyme inhibition by intravenous enalaprilat on the circulating renin-angiotensin system and on the brachial artery were studied in 12 hypertensive patients by a double-blind comparison with saline effects in 14 hypertensive patients. The brachial artery was investigated in terms of arterial section (measured by pulsed Doppler technique) and wall rigidity (assessed by pulse wave velocity). Arterial and biochemical parameters were measured in baseline before injection and at 20 to 40 minutes (t1) and 80 to 100 minutes (t2) after saline and drug injections. Compared with the saline vehicle, enalaprilat significantly decreased angiotensin enzyme converting activity (p less than 0.001), increased plasma renin activity (p less than 0.01) and decreased plasma aldosterone concentrations (p less than 0.01). The drug reduced blood pressure (p less than 0.01) and increased the brachial artery section (p less than 0.01), but did not change pulse wave velocity. In the enalaprilat group, significant postinjection relations were observed between: (1) enalaprilat concentration and plasma angiotensin converting enzyme activity (r = -0.72, p less than 0.001); (2) plasma renin activity and mean blood pressure (r = -0.46, p less than 0.02); (3) plasma enalaprilat concentration and pulse wave velocity (r = -0.50, p less than 0.01) and (4) pulse wave velocity and brachial artery section (r = 0.42, p less than 0.05). Thus, the brachial artery effects of enalaprilat were not directly related to the blockade of the renin-angiotensin system in plasma.(ABSTRACT TRUNCATED AT 250 WORDS)
Differential inactivation of plant lauric acid omega- and in-chain-hydroxylases by terminally unsaturated fatty acids.
The microsomal fraction from Vicia sativa L. cv. Septimane contains a cytochrome P-450-dependent lauric acid omega-hydroxylase that is inactivated in a time-dependent, pseudo-first-order manner when the microsomes are incubated with 11-dodecynoic acid. The rate constant for the inactivation is approximately 4.3-4.8 X 10(-3) s-1. In contrast, the olefinic analog 11-dodecenoic acid is primarily a time-independent inhibitor of the omega-hydroxylase. 1-Aminobenzotriazole, 3-phenoxy-1-propyne, and 3-(2,4-dichlorophenoxy)-1-propyne, mechanism-based inactivators of cinnamic acid 4-hydroxylase, and 9-decenoic acid, a mechanism-based inactivator of the lauric acid in-chain hydroxylase, are at best poor inactivators of the omega-hydroxylase. Conversely, cinnamic acid 4-hydroxylase is only slightly affected by concentrations of 11-dodecynoic acid that completely inactivate the omega-hydroxylase. 11-Dodecynoic acid is thus a potent, relatively specific, inactivator of the V. sativa lauric acid omega-hydroxylase.
Primary squamous cell carcinoma of the endometrium.
A case of squamous cell carcinoma of the endometrium which fulfills Fluhmann's criteria is presented. This case is reviewed together with additional 25 cases which had been already reported in various papers in the literature. The pathogenesis and the etiologic factors associated with primary squamous cell carcinoma of the endometrium are discussed. A review of the literature indicates that this rare malignancy is found in older patients, is highly malignant and carries a poor prognosis as myometrial invasion, and local extension or metastasis is found in 80% of the patients.
Opposite effects of hypertension and smoking on large artery wall shear conditions.
Wall shear phenomena were studied in the brachial artery in non-smoking and smoking normotensive and hypertensive subjects of similar age. Pulsed Doppler investigation revealed brachial artery diameter, and mean and systolic blood velocities (at the centerline of the vessel). A Poiseuillean blood velocity distribution was used to determine the wall shear rate and stress from velocity, diameter and viscosity. This was expressed in terms of mean and systolic values. Although hypertension and smoking both increased blood viscosity, hypertension reduced mean and systolic shear rates and stresses in non-smokers but not in smokers, and smoking increased mean and systolic shear rates and stresses in hypertensives but not in normotensives. Thus, the decreasing shear effect of hypertension was blunted by smoking, while the increasing shear effect of smoking was elicited by hypertension, suggesting an interaction of these factors on wall shear conditions.
Constricting and stiffening action of atropine on aortic response to angiotensin in dogs.
The elasticity of the thoracic aorta was studied in nine dogs instrumented with a pressure microtransducer and two ultrasonic crystals diametrically fixed in the adventitia. Systolic and diastolic changes in pressure and diameter were used to calculate Peterson and incremental elastic moduli. Acute hypertension was induced by infusions of angiotensin performed 1) during the control period, 2) after propranolol (1.5 mg/kg), 3) after atropine (0.2 mg/kg), and 4) after propranolol plus atropine. Absolute and percent variations of mean diameter were correlated to pressure in the control period and after autonomic blockade (p less than 0.01). The slopes of these correlations were not different between propranolol and control groups, but were lower with atropine (p less than 0.01) and with atropine plus propranolol (p less than 0.001) than in the control period. Correlations were also found between Peterson and incremental elastic moduli and mean pressure in the control period and after blockade (p less than 0.001). No differences of slopes existed between propranolol and control groups, but the slope of the correlation relative to the incremental elastic modulus was higher with atropine than in the control period (p less than 0.05), and the slopes of the correlations relative to the Peterson and the incremental elastic moduli were respectively higher with atropine plus propranolol than in the control period (p less than 0.05, p less than 0.05). Thus, atropine decreased the distention and increased the stiffness of the aorta in response to acute angiotensin-mediated hypertension.
Cefotaxime optimal dosage in adult patients. A reappraisal.
Cefotaxime, a third generation cephalosporin, is used throughout the world over a wide range of doses. The purpose of this paper is to discuss the rationale for determination of the optimal dosage and of adequate modes of administration. Among the factors determining in vivo activity, the most important are: (1) the time dependence of the antibacterial effect of cephalosporins, (2) the limited effect of increasing the drug concentration in contact with the bacteria and (3) the absence of a significant post-antibiotic effect. Combined with the rather short elimination half-life of cefotaxime, these factors argue for the use of a unitary dose of 1g in adult patients and for a 6- or 8-hour interval between doses. Information obtained from various animal models of infection are discussed. Clinical and bacteriological studies published in the international literature report a high rate of cure (between 80 and 100%) according to the type of infection and to the criteria of efficacy, with daily doses ranging from 2 to 4g bid or qid. The results obtained with the lowest doses are detailed, particularly for infections permitting the use of a low dosage. The necessity for increasing the dose is discussed in the following situations: (1) in specific infections requiring high local drug concentrations such as meningitis and endocarditis, (2) against micro-organisms exhibiting moderate susceptibility to cefotaxime (MIC greater than or equal to 1 mg/L) and (3) in immunocompromised patients. It is now well established that third generation cephalosporins have to be combined with other antimicrobial agents (e.g. aminoglycosides) for the treatment of patients with infections caused by bacteria able to become resistant. For susceptible strains, it has not been established that a synergistic effect of cefotaxime with another agent allows a reduction of the dosage of each member of the combination.
Heterogeneity of response of peripheral arteries to antihypertensive drugs in essential hypertension. Basic effects and functional consequences.
The vascular impact of different antihypertensive drugs was assessed in patients with mild to moderate essential hypertension by the use of the forearm circulation as a simple model to characterise the geometrical and distensible properties of the arterial system. The acute and chronic responses of the forearm arteries, expressed in terms of geometry (vasodilatation or vasoconstriction) and distensibility (arterial compliance, pulse-wave velocity), were not solely dependent on blood pressure levels. For similar blood pressure decreases, the dilatation of the forearm resistive vessels was associated either with an increase (calcium antagonists, angiotensin-converting enzyme inhibitors) or with a reduction (hydralazine-like drugs) or with no change (alpha- and beta-blocking drugs) in the calibre of the large forearm vessel. These non-homogeneous geometrical responses to antihypertensive drugs had important haemodynamic effects on the conduit, the buffering and the baroreflex functions of the arterial tree.
[Electron microscopy study of relations between prolongations of dopaminergic amacrine cells and blood vessels in the rat retina].
This immunohistochemical study by electron microscopy has shown the presence of tyrosine hydroxylase immunoreactive processes in more or less close contact with capillaries located in the two plexiform layers of the rat retina. These results, as compared to the literature on the innervation of small blood vessels in the brain, suggest that a dopaminergic innervation is modulating the retinal capillaries' vasomotricity.
Some comments on the compensation of bodily injury in the German Democratic Republic.
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[Ruptures and perforations of the thoracic and abdominal esophagus. Incidence and treatment].
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[Constrictive and stiffening effects of parasympathetic blockade on the pressure response of the aorta to angiotensin in the conscious dog ].
The elastic response of the thoracic aorta to increasing steps of angiotensin was studied in chronic instrumented conscious dogs with and without parasympathetic blockade by atropine. A pressure microtransducer and two ultrasonic crystals diametrically opposed and fixed in the adventitia enabled to determine the mean and systolic-diastolic changes of pressure (P) and diameter (D). By computing these measurements two representative indexes of dynamic elastic modulus in vivo were calculated; the elastic modulus of Peterson (Ep) Ep = delta P/D.D and the incremental elastic modulus (Ei) Ei = 0.75 EP/gamma, gamma being the ratio of the thickness to the external radius. A positive correlation (p less than 0.01) was obtained between pressure and diameter variations in the presence or absence of atropine but the slope of these relationship were lower with atropine than in controls. The slope of the positive correlations observed between Peterson and incremental elastic modulus and the increase in mean arterial pressure in response to angiotensin (p less than 0.01) was higher in the presence of atropine (p less than 0.05). These observations indicate that in response to angiotensin mediated high blood pressure, the cholinergic blockade of muscarinic receptors with atropine induce a contraction and increasing rigidity of the aorta.
[Shearing anomalies of the arterial endothelium in essential arterial hypertension].
Brachial artery wall shear rate and stress were studied in 20 untreated hypertensive patients and 11 normotensive controls of similar age. A pulsed Doppler velocimeter enabled to determine the internal diameter, the mean cross-sectional blood velocity and the systolic centerline blood velocity of the brachial artery. A coaxial cylinder viscosimeter provided blood viscosity at a shear rate of 96 s-1. A Poiseuille model of arterial flow was used for evaluating wall shear rate from the ratio between blood velocity and arterial diameter and wall shear stress from the product between shear rate and blood viscosity. Shear rate and stress were expressed in terms of systolic and mean values by using respectively systolic centerline and mean cross-sectional blood velocities. Comparatively to normal controls, hypertensive patients had higher blood viscosity (4.80 +/- 0.08 vs 4.28 +/- 0.09 cpoise, p less than 0.001) lower systolic wall shear rate (303 +/- 18 vs 413 +/- 20 s-1, p less than 0.001), lower mean wall shear rate (70 +/- 6 vs 109 +/- 16 s-1, p less than 0.01) and lower systolic wall shear stress (13.86 +/- 0.81 vs 17.02 +/- 1.26, p less than 0.001) but mean wall shear stress was not statistically different between patients and controls. Such wall shear abnormalities are described for the first time in large artery of hypertensive patients and merit attention because of the experimental critical role of low shear conditions on the atherogenic process.
[Significance of stomatological index cards for identification of unknown dead].
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[Combination of bupivacaine and fentanyl in long-term epidural analgesia during labor].
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The role of antihypertensive drugs in counteracting adverse influence on large arteries.
Studies in humans have shown that chronic elevation of blood pressure induces early alterations in the large arteries, consisting mainly of increased diameter, increased pulse wave velocity, and decreased arterial compliance. Acute reduction of blood pressure, per se, does not necessarily correct these alterations homogeneously. For instance, cadralazine reduced brachial artery diameter and urapidil decreased pulse wave velocity, without accompanying changes in forearm arterial compliance. In contrast, acebutolol, isosorbide dinitrate, nicardipine, and nitrendipine, for the same acute decrease in blood pressure, improved forearm arterial compliance by a concomitant decrease in pulse wave velocity and increase in arterial diameter. To determine whether or not these vascular effects persist with long-term acebutolol therapy, nine hypertensive patients were treated for a period of 3 months. Forearm hemodynamic and cytosolic free calcium concentrations in platelets were simultaneously assessed before and after treatment. Compared with placebo baseline values, chronic acebutolol therapy significantly decreased mean arterial pressure (p less than 0.01), pulse wave velocity (p less than 0.01), and platelet free calcium concentration (p less than 0.05); forearm arterial compliance was increased (p less than 0.01), but brachial artery diameter did not change. Platelet calcium concentration correlated closely with pulse wave velocity even at constant mean arterial pressure. These findings suggest a relaxant effect of acebutolol on the smooth musculature of large arteries, which is independent of changes in blood pressure and arterial diameter, and possibly mediated by changes in cytosolic calcium levels.