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Heart rate (HR), cardiac output (CO), coronary sinus blood flow (CSF), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), mean arterial (MAP), and coronary arteriovenous difference for oxygen (AVDcO2) were measured in patients with stable angina pectoris without cardiac failure before and 40 to 60 minutes after administration of 2 or 3 mg of molsidomine. In 20 patients these measurements were made in basal state during spontaneous rhythm. In eight of these patients (including three receiving beta blockers) the measurements were made during atrial pacing. In eight other patients, all receiving long-term beta-blocker therapy, the measurements were made during cold pressor test. At the basal state in spontaneous rhythm, a gradual reduction in the LVSP to 70% or less of its initial value was observed in four patients receiving 3 mg of molsidomine (two of whom received beta-blocker treatment). The LVSP was immediately restored by vascular filling. In the 16 other patients molsidomine decreased LVSP, LVEDP, MAP, CO, and double product (DP = LVSP X HR). The AVDcO2 was unchanged. CSF and myocardial oxygen uptake index (MVO2 = CSF X AVDcO2) were decreased. During atrial pacing, hemodynamic and coronary effects were similar to those seen in the basal state. During the cold pressor test, the increases in LVSP, MAP, and LVEDP were significantly reduced by molsidomine. The variations in CSF and coronary resistance (MAP/CSF) were also significantly different after administration of molsidomine, with better metabolic regulation of the coronary circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

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The heart rate, cardiac output, coronary sinus blood flow, systolic and end diastolic left ventricular pressures, femoral arterial pressure and coronary oxygen arterio-venous difference were measured in 12 patients with stable coronary artery disease without cardiac failure on long-term betablocker therapy, before and 45 minutes after 2 or 3 mg sublingual molsidomine. The measurements were repeated in 8 patients during a cold pressor test. Under basal conditions, molsidomine decreased the systolic and end diastolic left ventricular pressures, mean femoral arterial pressure, cardiac output and double product. The coronary oxygen arterio-venous difference was unchanged. Coronary sinus flow and myocardial oxygen consumption decreased. In the 2 patients who were given 3 mg molsidomine, a progressive reduction in systolic left ventricular pressure to 70% or less than its initial value, necessitated immediate treatment with volume expanders. During the cold pressor test before molsidomine the systolic and end diastolic left ventricular pressures, mean femoral arterial pressure and the double product increased. Coronary sinus flow was unchanged overall: it decreased in 6 patients, increased in 2 patients and remained the same in 1 patient. Coronary resistance increased in 6 patients and decreased in only one patient. During the cold pressor test after molsidomine there was a significant reduction in the increase of systolic left ventricular pressure, mean femoral artery pressure and double product. Coronary sinus blood flow increased in 5 patients and decreased in only one case. Coronary resistance decreased in half the cases.(ABSTRACT TRUNCATED AT 250 WORDS)

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The heart rate (HR), the cardiac output (Qc) and the coronary sinus flow rate (Qcs), the left ventricular systolic and end-diastolic pressures (LVSP, LVEDP), the femoral artery pressure (FAP) and the difference between the coronary arterial and coronary venous oxygen tension (DAVcO2) were measured in patients with stable coronary insufficiency without cardiac failure, before and 40 to 60 minutes after 2 or 3 mg of molsidomine (M). In 20 patients, these measurements were made in the basal state, in spontaneous rhythm (SP). In 8 of these patient, (including 3 receiving beta-blockers) the measurements were made during an atrial stimulation test (ST) and in 8 other patients, all receiving long-term beta-blocker therapy, the measurements were made during a cold test (CT). At the basal state in SR, a gradual reduction in the LVSP to 70% or less of its initial value was observed in the patients receiving 3 mg of M (2 of whom received beta-blocker treatment). The LVSP was immediately restored by vascular filling. In 16 patients, M decreased the LVSP, the LVEDP, the FAP, the Qc and the double product (DP = LVSP X HR). The DAVcO2 was unchanged. Qcs and MVO2 (MVO2 = Qcs X DAVcO2) were decreased. In the course of ST, the haemodynamic and coronary changes are similar to those seen in the basal state. During the Ct, the increase in the LVSP, FAP and DP was significantly reduced by M. The variations in Qcs and coronary resistance (FAP/Qcs) were also significantly different after M., with better metabolic regulation of the coronary circulation.(ABSTRACT TRUNCATED AT 250 WORDS)

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Verapamil inhibits calcium influx through the slow calcium canals. The coronary an haemodynamic effects of intravenous Verapamil were studied in 8 patients with chronic coronary insufficiency documented by coronary arteriography. The following measurements were made in spontaneous rhythm and during atrial pacing under basal conditions and 10 minutes after intravenous Verapamil (0.10 to 0.17 mg/kg) relayed with a continuous infusion of 5 x 10(-3) mg/Kg/mn: heart rate, cardiac output, left ventricularr pressure (Millar 5 F micromanometer), femoral artery pressure, coronary sinus flow by continuous thermodilution, oxygen and lactate concentrations in arterial and arterio-venous oxygen difference, and index of myocardial oxygen consumption and the coefficient of lactate extraction were then calculated. The coronary and haemodynamic effects of atrial pacing were similar before and after Verapamil at a given rate. Left ventricula end diastolic pressure decreased, cardiac output and total systemic resistance were unchanged, dP/dt max increased but to a lesser degree after Verapamil (P less than 0.05). Coronary arterio-venous oxygen difference decreased after Verapamil. The coronary and haemodynamic effects of Verapamil were similar in spontaneous rhythm and during atrial pacing. In spontaneous rhythm, the heart rate and left ventricular end diastolic pressure increased. In spontaneous and paced rhythm, femoral artery pressure, total systemic resistance and dP/dt max decreased. Cardiac output remained the same. Myocardial oxygen consumption decreased mainly because of a reduced coronary arterio-venous oxygen difference and because of unchanged coronary flow in spontaneous rhythm oxygen consumption seems to have a favourable effect on the myocardial energy equilibrium as shown by the increased coefficient of lactate extraction during atrial pacing after Verapamil. This study shows the negative inotropic and arterial vasodilator effects of Verapamil to be responsible for the reduced myocardial oxygen consumption. It also caused coronary artery vasodilation.

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In 10 patients, 8 males and 2 females, suffering from idiopathic hemochromatosis (IH), the gonadotropic function has been studied using the GnRH test (iv administration of 100 micrograms) to make precise the pathogenesis of their hypogonadism. The FSH and LH mean basal levels were low and almost unaffected by GnRH (p < 0.001 at each time value when compared to controls). The hypogonadism often observed during the course of IH seems to be hypogonadotropic. Various factors could be responsible for this disturbance. The exact site of the lesion, whether hypothalamic or hypophyseal, remains unknown.

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Thirty-two patients (group I: 7 normal subjects; group II: 25 coronary subjects) underwent coronary arteriography, and measurements were made both in normal rhythm and under atrial stimulation of the pulmonary capillary pressure and the pressure in the femoral artery, of cardiac output, of coronary sinus flow (by continuous thermodilution), of the coronary arterio-venous oxygen difference, of oxygen consumption, and in 28 of the patients of the coefficient of extraction of K lactates. During stimulation, the only differences to appear between the subjects of group I and group II were an increase in capillary pressure (p less than 0.01) and a decrease in the coefficient of extraction of lactates (p less than 0.001) in the coronary patients. Similar differences were found between coronary patients with a stenosis greater than 70% in the anterior descending or circumflex artery (group IIa) and those without it (group 11b), and between the patients with pain during atrial stimulation (n = 9) and those without it. There was a good correlation between a double score (IVA + circumflex artery, Rowe's method) and the coefficient of extraction of lactates during atrial stimulation (n = 28, p less than 0.01).

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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.

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The desquamative intersitial pneumonia is a rare, sometimes curable from of diffuse interstitial fibrosis. A clinical, optical and ultrastructural, immunochemical and histo-enzymologic study of one case proved the macrophage nature of the intra-alveolar cells and suggested in the histo-genesis an immunological mechanism depending on lymphocytes.

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In the course of familial idiopathic haemochromatosis with diabetes, after stimulation with arginine, the alpha cell responds perfectly to stimulation, in contrast to the case of chronic pancreatic diseases. After an oral glucose load, there is no reduction in plasma glucagon concentrations, and a paradoxal increase is sometimes seen. These results are quite similar to those reported in common diabetes. Secretion of growth hormone after an infusion of arginine and insulin hypoglycaemia seem to be significantly reduced in comparison with normal subjects and those suffering from common diabetes, paired and explored using the same protocol. This may perhaps explain the low degree of severity and slow course of associated vascular disease.

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