[Pericardial manifestations of toxoplasmosis]. / Manifestations péricardiques de la toxoplasmose.

A case of pericarditis due to toxoplasmosis in a 20 year old non-immune depressed man with a favourable outcome with specific antiparasitic treatment is reported. Pericarditis is rare in toxoplasmosis and does not require an associated immune deficiency. The clinical presentation is that of acute benign pericarditis, the diagnosis depending on positive toxoplasmosis serology (positive IgM or increasing IgG antibody titres) and the absence of another obvious cause. Isolation of the parasite by direct examination or animal inoculation is very rare. The spontaneous evolution is to pericardial constriction whilst specific antibiotic therapy (sulfadiazine-pyrimethamine) leads to a rapid cure in most cases. This underlines the necessity of searching for toxoplasmosis in patients with unexplained pericarditis.

[Arterial hypertension in black patients]. / L'hypertension artérielle du sujet noir.

Arterial hypertension in blacks seems to present a few peculiarities in comparison to that of caucasians, whether it is from the epidemiological point of view: greater frequency of the disease, more severe prognosis; from the physiopathological point of view with especially a definite prevalence of HBP with low renin and inflation of the plasma volume and increased tendency to sodium retention, or finally from the therapeutic point of view, since randomized studies have demonstrated that black patients respond better to diuretics than to beta-blockers. Currently, it is impossible to explain these differences in a simple fashion: is it a genetic factor or, on the contrary, environmental factors? Perhaps the response lies between those two extremes.

Effects of furosemide, piretanide, and water loading on urinary excretion of cefazolin in humans.

Antibiotics and diuretics are often prescribed concomitantly for humans. We compared the effects of two potent loop diuretics, furosemide and piretanide, with those of water loading on the urinary excretion of cefazolin. During a continuous infusion of inulin and cefazolin (10 mg/kg per h), six healthy male volunteers received a single intravenous injection of furosemide (0.3 mg/kg) or piretanide (0.1 mg/kg) or again an oral water load of 15 ml/kg over a 20-min period. In vitro, furosemide at all concentrations tested significantly reduced by about 10% the percentage of cefazolin bound to serum proteins. Piretanide exhibited such an effect only at a concentration of 2 micrograms/ml. Furosemide, piretanide, and water loading significantly and similarly increased the ratio of excreted to infused cefazolin up to 2 h after the injection of diuretic or after oral water intake. In each of the three parts of the experiment, the increase of the urinary flow rate was similar when compared with the control values. Furosemide significantly increased the cefazolin filtered load during the same time. Piretanide significantly enhanced the absolute rate of net cefazolin tubular secretion. Water loading increased the urinary excretion of cefazolin, probably through a reduction in tubular reabsorption. These results suggest that (i) furosemide and piretanide as well as water loading are capable of enhancing renal excretion of cefazolin by different complex mechanisms; (ii) cefazolin undergoes a bidirectional tubular transport; (iii) piretanide might act on the proximal tubule in addition to its main site of action on Henle's loop; and (iv) the effects of both diuretics and of water loading are unlikely to affect in vivo antibiotic activity in humans.

[Methodology of hemodynamic study of a vasodilator drug (author's transl)]. / Méthodologie d'étude hémodynamique d'un agent vasodilatateur.

The mechanism of action of a vasodilator drug is complex and depends on its predominant site of action: arterial or venous system. it leads to a) complex alteration of ventricular load that changes cardiac output, b) alteration of myocardial energetic metabolism. To classify a vasodilator drug, it is useful to study: a) its mechanism of action on the peripheral vascular system, b) the left ventricular function, and c) the coronary blood flow and the myocardial metabolism. The peripheral action of the drug is assessed by simultaneous measurement of peripheral blood flow, arterial pressure and venous pressure. From these data, arterial resistance (AR) and venous tone (VT) are calculated. A change of AR and for VT permits to classify a vasodilator drug as arterial, venous or both arterial and venous. Changes of factors of ventricular load are appreciated by measurement of aortic pressure, left ventricular pressure and ventricular volumes. If no change of heart rate occures, modification of stroke volume and cardiac output is due to a reduction of end diastolic volume (venous vasodilator drug) or of end systolic volume (arterial vasodilator drug).

[Hemodynamic changes during increasingly rapid atrial pacing]. / Modifications hémodynamiques lors de l'accroissement de fréquence cardiaque par stimulation auriculaire.

The cardiac output (Qc), indices of left ventricular function in the isovolumic period (dp/dt/Pt), max, and during the ejection period (EF, VCF), the end diastolic and end systolic ventricular volumes, the speed of ventricular filing, the module of elasticity of the ventricular chamber (kp) and the end systolic pressure-volume relationships were measured in 20 patients (11 normal in group I and 9 with and apparently primary cardiomyopathy in group II) at rest and during progressively rapid atrial pacing. The Qc was lower and the indices of left ventricular function in the isovolumic and ejectional phases, the end systolic pressure-volume relationship and speeds of ventricular filling were decreased in group II: kp was the same in both groups of patients. At progressively higher heart rates the cardiac output slightly in both groups, the systolic volume decreased, (dp/dt/Pt) max increased, the ejection fraction and VCF were unaltered. The speeds of filling and kp were unchanged. The end systolic pressure-volume relationship increased. In group I the reduction in systolic volume seemed to be related to a greater reduction in the end diastolic volume than in the end systolic volume. In group II, the reduction of the systolic volume was related only to a reduction of the end diastolic volume.

[Comparison of hemodynamic and coronary effects of 2 antianginal vasodilator drugs: nifedipine and trinitrine]. / Comparaison des effets hémodynamiques et coronariens de deux drogues vasodilatatrices anti-angineuses: la nifédipine et la trinitrine.

Twenty patients with coronary insufficiency had measurements taken while they were in normal rhythm (NR) and during atrial pacemaking (AP) before and after taking nifedipine (n: 12) or after intravenous perfusion of trinitrin (n: 8): measurements were taken of pulmonary capillary pressure (PCP), arterial femoral pressure (AFP), cardiac output (QC) and coronary sinus flow (QCS), coronary arterio-venous oxygen difference (DaVO2), myocardial oxygen consumption (MVO2) and the myocardial coefficient of extraction of lactates (K).--Under nifedipine in NR and AP, AFP was decreased and QC increased. QSC was increased in NR, but was not changed under AP. DaVO2 was shortened under both sets of conditions. MVO2 decreased only during AP. Nifedipine brought back to normal the lowering of K which occurred with pacemaking.--Under trinitrin, both in NR and under AP, AFP, PCP, QC, QSC and MVO2 were lowered. K and DaVO2 were unchanged.--A plethysmographic study in 13 patients showed that these haemodynamic effects could be explained by the arterial vasodilator action of nifedipine which occurred without changing the venous tone, and the mixed action of trinitrin.