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Biomedical subjects

F Blanchet

Publications and source records attributed to F Blanchet.

At least 55 records · Page 3Linked to original sources
PubMed1985

Alterations in contrast medium-induced coronary reactive hyperemia after bepridil in patients with coronary artery disease.

The acute effects of an intravenous infusion of bepridil (BEP) (4 mg . kg-1) on left ventricular (LV) hemodynamics, coronary sinus blood flow (CSBF), and myocardial metabolism were studied in eight patients with coronary artery disease. In contrast with data previously reported with calcium channel blockers, BEP induced an elevation in LV end-diastolic pressure from 12.0 +/- 7.1 to 20.1 +/- 7.2 mm Hg (mean +/- SD, p less than 0.001) and a fall in LV dp/dt max from 1339 +/- 302 to 1177 +/- 251 mm Hg . sec-1 (p less than 0.01). This significant alteration in LV function is likely to be explained by the lack of effect on heart rate and aortic pressure observed after an acute intravenous infusion of BEP. Myocardial oxygen consumption (MVO2) increased from 448 +/- 272 to 498 +/- 273 mumol . min-1/100 g LV (p less than 0.05) as did CSBF from 79.5 +/- 42.7 to 92.1 +/- 45.1 ml X min-1/100 g LV (p less than 0.01). Lactate extraction fell from 0.33 +/- 0.17 to 0.15 +/- 0.17 (p less than 0.05). A contrast medium-induced coronary reactive hyperemia (HPR) evidenced an increased hyperemic volume from 9.5 +/- 3.6 to 12.1 +/- 4.5 ml/100 g LV (p less than 0.01) and HPR duration from 23.3 +/- 6.9 to 32.3 +/- 15.4 sec (p less than 0.05) after BEP. However, the peak/resting CSBF ratio was blunted after BEP from 1.74 +/- 0.18 to 1.61 +/- 0.12 (p less than 0.05), evidencing a net effect of BEP on HPR.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Effects of hypocalcemia on diaphragmatic strength generation.

We studied the effects of hypocalcemia on diaphragmatic force and diaphragm blood flow (Qdi) in 12 anesthetized dogs. The diaphragm was electrically stimulated with intramuscular electrodes surgically implanted in the ventral surface of each hemidiaphragm. The transdiaphragmatic pressure (Pdi) during supramaximal (50 V) 2-s stimulations applied over a frequency range of 10-100 Hz was measured with balloon catheters during tracheal occlusion at functional residual capacity. A catheter was placed via the femoral vein into the left inferior phrenic vein, and Qdi was measured by timed volume collections of left inferior venous effluent. A catheter was introduced in a femoral artery to monitor blood pressure (BP). In five additional dogs, the force generated by the sartorius muscle during electrical stimulation was also studied concomitantly to diaphragmatic force. The animals were mechanically ventilated throughout the experiment, and the arterial blood gases and pH were maintained constant. Hypocalcemia was induced by a continuous infusion of EGTA (70 mg X kg-1 X h-1), which led to a progressive decrease (P less than 0.0001) of ionized calcium plasmatic level from 2.21 +/- 0.4 meq/1 during control to 1.69 +/- 0.06, 1.25 +/- 0.5, and 1.07 +/- 0.5 meq/1 after 30, 60, and 120 min, respectively. Hypocalcemia decreased progressively Pdi, which amounted to 84 +/- 3 (P less than 0.001) and 98 +/- 2% of control values for the low frequencies (10 and 20 Hz) and the high frequencies (50 and 100 Hz), respectively, after 30 min of EGTA infusion and to 74 +/- 5 and 79 +/- 6% for the low and high frequencies, respectively, after 120 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

[Screening for cancer of the upper aerodigestive tract in a high-risk population].

From the data collected in the Cancer Registry of Calvados, a screening program for neoplastic lesions of the whole upper digestive and respiratory tract was performed in a canton where esophageal cancer incidence is very high. 137 men underwent this examination for mouth, pharyngo-larynx and esophagus. None neoplastic lesion was revealed but histologic and cytologic swabs showed some abnormalities that are now being studied.

Adult↗
PubMed1984

Relative contribution of intrinsic lung dysfunction and hypoventilation to hypoxemia during hemodialysis.

Two mechanisms have been proposed to explain hemodialysis (HD)-induced hypoxemia: reversible lung damage due to intrapulmonary leukostasis as a consequence of the contact of blood with the dialyzer membrane, or alveolar hypoventilation due to the loss of carbon dioxide through the dialyzer. To assess the role of these factors, seven chronically uremic patients were studied before and during 4-hr HD sessions using a cuprophane membrane and either acetate (AHD) or bicarbonate (BHD) dialysate. In AHD only we observed, by comparison with predialysis values, a significant hypoxemia, and a decrease of alveolar ventilation (VA), lung carbon dioxide output, and respiratory exchange ratio. In both the AHD hypoxemic group and BHD nonhypoxemic group, there was a similar decrease in lung carbon dioxide diffusing capacity (DLCO) and of white blood cells (WBC), and a positive correlation between arterial oxygen pressure and VA without modification of alveolo arterial PO2 difference, an argument against the existence of ventilation-perfusion or ventilation-diffusion mismatching. We conclude that, although WBC sequestration induced a lung damage evidenced by DLCO impairment, the key factor of hypoxemia observed in AHD was the hypoventilation.

Acetates↗
PubMed1984

Analysis of increased myocardial contractility during sodium acetate infusion in humans.

To analyze the reported effects of acetate on left ventricular (LV) contractility during dialysis, LV function was studied before and after a 20-min sodium acetate (Na Ac) infusion (0.06 mmoles X kg-1 X min-1) in seven patients with heart rate (HR) controlled by atrial pacing. Angiographically determined LV volumes and LV pressures were used to calculate the LV function indices. A plasma acetate concentration of 3.13 +/- 1.05 (SD) mmoles X liter-1 induced an increase in cardiac index from 3.8 +/- 0.6 to 4.4 +/- 0.6 (SD) liter X min-1 X m-2 (P less than 0.01) and a rise in total body O2 consumption from 7.47 +/- 1.28 to 8.67 +/- 1.66 mmoles X min-1 X m-2 (P less than 0.05); there was no alteration of the volume elastic constant, of the end diastolic stress, and of the end systolic stress. There was an increase of the ejection fraction from 0.44 +/- 0.10 to 0.51 +/- 0.09 (P less than 0.01), the maximum velocity of shortening (Vmax, sec-1) from 1.37 +/- 0.25 to 1.55 +/- 0.28 (P less than 0.05), and of the end systolic stress-end systolic volume ratio (g X cm-2 X ml-1) from 2.99 +/- 0.76 to 3.40 +/- 0.98 (P less than 0.01). Hence, the enhancement of these indices was not the consequence of any alteration of HR, preload, or afterload.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗
PubMed1983

Effects of flunitrazepam on left ventricular performance, coronary haemodynamics and myocardial metabolism in patients with coronary artery disease.

The effects of flunitrazepam 15 micrograms kg-1, on left ventricular (LV) performance, coronary sinus blood flow (CSBF), myocardial oxygen uptake and myocardial lactate balance were studied in nine patients with coronary artery disease undergoing cardiac catheterization. Flunitrazepam produced a decrease in mean aortic pressure (MAP) and in systemic vascular resistance (SVR) with maximal changes from control value observed at 15 min for MAP and at 5 min for SVR. No change in cardiac index was observed. The following changes in variables related to LV performance were observed: (1) a transient increase in heart rate and left ventricular contractility (Vmax); (2) a sustained decrease of left ventricular end-diastolic pressure, maximum at 15 min. Myocardial oxygen consumption was decreased at 15 min but CSBF did not change, whereas total coronary vascular resistance was decreased. Since myocardial lactate extraction was increased and no change in ECG was observed, a coronary steal induced by coronary vasodilatation did not appear to take place.

Carbon Dioxide↗
PubMed1982

Effects of droperidol on left ventricular performance in humans.

The action of droperidol on left ventricular (LV) performance was examined before angiography in nine unpremedicated patients undergoing cardiac catheterization for stable uncomplicated coronary artery disease. Using local anesthesia, catheters were placed in the left ventricle, thoracic aorta, and pulmonary artery. Cardiac output (CO) and LV pressure derivatives were measured before and 2, 5, 10, 15, and 20 min after intravenous administration of 0.15 mg/kg droperidol. Droperidol administration induced a time-dependent decrease of mean arterial pressure (MAP) (significant at 2, 10, 15, and 20 min) and of cardiac index (CI) (significant at 15 and 20 min) with maximal changes observed at 20 min (-14 per cent for MAP and -15 per cent for CI). in addition, the following changes occurred in variables related to LV performance: 1) a transient increase in both heart rate (HR) (2, 5, and 10 min) and maximum rate of rise of left ventricular pressure/instantaneous left ventricular pressure (dP . dt-1 max . IP-1) (+ 15 per cent for HR and + 14 per cent for dP .dt-1 max . IP-1); 2) an early (2 min) and sustained (5, 10, 15, and 20 min) decrease of left ventricular end-diastolic pressure (LVEDP), maximum at 5 min (-30 per cent); 3) no change in systemic vascular resistance (SVR). This study shows that the fall in MAP which occurs after intravenous administration of clinical doses of droperidol is primarily due to decreased CO, secondary to decreased LVEDP and not to changes in cardiac contractility and in SVR.

Blood Pressure↗
PubMed1979

[Circulatory and respiratory effects of aspiration and reinfusion of ascites in cirrhosis. Apropos of 14 ascitic attacks treated by this method].

Aspiration and replacement of ascites in 14 patients with cirrhosis was carried out using a Rhodiascit (Rhône-Poulenc) apparatus. Hemodynamic studies were used to evaluate the effects of this therapy on circulatory and respiratory parameters. Results showed that the hemodynamic tolerance of the treatment, which produces a slow increase in blood volume, was excellent as there was an increase in the cardiac index without raising the pressure under which replacement was made. Futhermore, no adverse effects on blood respiratory functions were noted in these patients who had blood hypoxia before treatment, but the removal of ascitic fluid produced no improvement in arterial gasometric parameters which is contrary to what one would expect.

Adult↗
PubMed1978

Massive pulmonary embolism with circulatory failure: survival following sixty hours' support with a membrane lung.

A 62-year-old man had circulatory failure from massive pulmonary embolism following a road accident. Despite intensive therapy including urokinase infusion, inotropic drugs, and mechanical ventilation, the patient's circulatory status deteriorated. When it became impossible to maintain the mean systemic arterial pressure above 50 mm. Hg and the cardiac index above 1 L. per minute per square meter, circulatory support by partial cardiopulmonary bypass with a membrane lung was begun. Acute circulatory failure and acute pulmonary hypertension were promptly reduced by this procedure, and patient's status necessitated only intravenous heparin infusion and mechanical ventilation. After 60 hours of bypass the patient was weaned from the membrane lung, and 1 month later he was discharged from the hospital.

Extracorporeal Circulation↗
PubMed1977

[Hemodynamic profile in acute respiratory distress syndromes in the adult (author's transl)].

Hemodynamic, investigations carried out on 25 patients suffering from acute respiratory distress in the adult established a specific hemodynamic profile for that syndrome, including precapillary pulmonary artery hypertension and systemic arterial hypotension. The level of pulmonary vascular resistance (abnormally high) and systemic arterial resistance (abnormally low) were referred to the cardiac index (which may be increased in some patients due to infusions of Dopamine, or reduced in others due to an veno-arterial bypass). The observed hemodynamic disorders are not related to hypoxemia since this is corrected by permanent positive pressure breathing, or by extracorporeal oxygenation.

Acute Disease↗
PubMed1977

Massive pulmonary embolism without arterial hypoxaemia: pathophysiology in two cases.

Two cases of massive pulmonary embolism, confirmed by angiographic or necropsy findings, were remarkable by the absence of arterial hypoxaemia. The various mechanisms responsible for arterial hypoxaemia in pulmonary embolism are discussed. It is suggested that in patients with massive pulmonary embolism a markedly decreased cardiac output might account for the absence of arterial hypoxaemia. In the light of these two cases the finding of a normal PaO2 does not rule out the diagnosis of pulmonary embolism.

Aged↗