Search PubMed⌕ Search

Biomedical subjects

J P Merillon

Publications and source records attributed to J P Merillon.

At least 19 recordsLinked to original sources
PubMed1985

[Coronary and renal circulation in patients with cardiac failure after converting enzyme inhibitors].

The cardiac output and its peripheral distribution must fulfill the metabolic and/or functional requirements of the different organs. The various techniques used to measure blood flow rates in the coronary and renal arteries provide much information on this point, but they do not tell us all we would like to know about the distribution and "utilization" of these flows in tissues. In normal subjects the myocardial oxygen consumption is not markedly different from the renal oxygen consumption, but the mechanisms that regulate the coronary and renal circulations are not the same. The flow rate in the coronary vessels is about 10% of the cardiac output, the arteriovenous oxygen gradient is superior to 10 vol % and regulation is metabolic. In the renal vessels, which are primarily "functional", the flow rate is about 25% of the cardiac output and the arteriovenous oxygen gradient is inferior to 2 vol %. In heart failure patients, despite reduced cardiac output the blood pressure is kept normal for a long time by vasoconstriction of the arterioles, a process which involves, at least partly, the renin-angiotensin system. The vasoconstriction predominates in some circuits (the renal flow rate is less than 15% of the cardiac output) and spares the "privileged" circuits (the coronary flow rate is more than 15% of the cardiac output). Under the influence of angiotensin converting enzyme inhibitors, the cardiac output increases and its distribution is modified. The coronary flow rate remains stable or is reduced in proportion to the decrease in myocardial oxygen consumption, the metabolic regulation is preserved and there is no "coronary steal". The percent increase in renal flow rate is usually superior to that of the cardiac output. This peripheral redistribution of coronary and renal blood flow rates in heart failure patients after treatment with converting enzyme inhibitors seems to correspond to the physiological purposes of the two regional blood flows.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1985

Hemodynamic and coronary effects of molsidomine at basal state, during atrial pacing, and during cold pressor test in patients with stable angina pectoris.

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)

Adult↗
PubMed1985

Changes in left ventricular performance during chronic pressure or volume overload: importance of physical properties of the arterial system.

The present study was aimed at evaluation of changes in systolic and diastolic left ventricular function during chronic pressure of volume overload, in comparison with normal subjects. Sixty-two patients were included: group 1 was composed of 25 normal subjects, group 2 was composed of 20 subjects with essential hypertension, and group 3 was composed of 17 subjects with aortic regurgitation without congestive heart failure. Cardiac output, aortic and left ventricular pressures (micromanometers), ventricular volume and ascending aortic radius (cineangiography), ejection fraction (EF), mean velocity of fiber shortening (VCF), ventricular mass (m), and the ratio m/EDV (EDV, end diastolic volume) were determined. Also measured were maxima for end systolic pressure (ESP), end systolic stress (ESS), and end systolic volume (ESV) and radius (ESR), as well as the modulus of left ventricular chamber and muscle stiffness (method of Gaash et al.) (1) and characteristic impedance of the ascending aorta (Zc). In hypertensive patients, m and m/EDV were increased, as was the ESP/ESV ratio, whereas EF and VCF were not modified and the ESS/ESR was normal or sometimes decreased. The systolic "pump" function thus appeared to be increased, whereas the muscle function appeared normal or decreased. The moduli of left ventricular chamber stiffness and muscle stiffness were increased. Zc was increased because of a greater pulse wave velocity, although aortic radius was larger. A close relationship was found between Zc and the ratio m/EDV. In patients with aortic regurgitation, the increased left ventricular mass was closely related to the regurgitant fraction (RF). The m/EDV ratio was normal. EF was unmodified and VCF and the ESP/ESV ratio were decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Aortic input impedance in heart failure: comparison with normal subjects and its changes during vasodilator therapy.

This study was aimed at the evaluation of aortic impedance in patients with congestive heart failure. Aortic impedance (simultaneous measurements of aortic pressure and blood flow), mean (Wm) and pulsatile (Wp) powers were compared in 11 normal subjects and in 12 patients with heart failure. Pulse wave velocity (C: modified Moëns-Korteweg equation, simultaneous measurements of aortic pressure and radius) was determined under control conditions in all normal subjects and in 7 patients with heart failure. Impedance curves in patients with heart failure were characterized by increased values of the impedance modulus at 0 Hz (peripheral resistance) and at low frequencies. The characteristic impedance, C, and phase were not different from normal subjects. In six patients with heart failure, impedance curves were studied during nitroprusside infusion. During the infusion of the vasodilator, the impedance modulus at 0 Hz and at low frequencies decreased. The characteristic impedance was unchanged. The zero intercept of the phase was shifted towards lower frequencies. These results show that the changes in impedance curves in patients with heart failure are due to greater peripheral resistance and wave reflection. During nitroprusside infusion the stroke volume increased and the aortic blood flow became more pulsatile (greater values of low frequency components). This modification accounts for the increased values of Wm and Wp, and is related to decreased peripheral resistance and wave reflection.

Adult↗
PubMed1983

Forward and backward waves in the arterial system, their relationship to pressure waves form.

The purpose of this work was to analyze, in human subjects, the shape of the aortic pressure wave from its forward and backward components calculated by use of Westerhof's model. Twenty-nine patients were studied: 11 normal subjects, 11 hypertensive patients and 7 patients with congestive heart failure. The following measurements and calculations were performed both under control conditions and during either angiotensin infusion in 5 normal subjects or nitroprusside infusion in 6 hypertensive patients: cardiac output, aortic blood pressure (catheter tip micromanometer), blood flow velocity (electromagnetic catheter-tip velocity transducer) in the ascending aorta, aortic impedance and reflection coefficients allowing the calculation of the aortic forward and backward pressure waves. The results show that the shape of aortic pressure wave in hypertensive patients is related to increased arterial wall stiffness which determines greater values and overlap of the forward and backward waves. This result is corroborated by the changes observed during angiotensin infusion in normal subjects. The shape of pressure wave in heart failure patients is dicrotic. This shape is related to smaller values and overlap of forward and backward waves. This appears related to a reduced stroke volume. During peripheral vasodilation the shape of pressure wave in hypertensive patients becomes dicrotic. However, this was mainly related to later backward waves. These results confirm that the shape of pressure waves depends both on the arterial wall stiffness and on the left ventricular performance: mainly on the stroke volume. The calculation of forward and backward waves allows a quantitative analysis of pressure waves.

Adult↗
PubMed1982

Aortic input impedance in normal man and arterial hypertension: its modification during changes in aortic pressure.

The purpose of this work was to study the factors determining aortic input impedance in hypertensive patients. Aortic input impedance (simultaneous measurements of aortic pressure and blood flow), mean (Wm) and pulsatile (Wp) powers and the Wp/Wm ratio were compared in normal subjects (n = 13) and hypertensive patients (n = 12) under basal conditions and during blood pressure manipulation--angiotensin infusion in five normal patients and nitroprusside infusion in six hypertensive patients. Pulse wave velocity (Möens-Korteweg equation; simultaneous measurement of aortic pressure and radius) was determined under basal conditions in normal subjects and in 11 hypertensive patients. The results show that: 1) the changes in impedance curves in hypertensive patients are related to increased peripheral resistance, pulse wave velocity, wave reflection and aortic radius; 2) in most hypertensive patients impedance curves are normalised when blood pressure is reduced, whereas the Wp/Wm ratio remains higher. This latter result demonstrates that pulsatile energy losses are greater in hypertensive patients and suggests either that the aortic wall remains stiffer, despite the reduction in aortic pressure, or that the flow wave becomes more pulsatile since impedance curves of hypertensive patients seen after lowering blood pressure are similar to those of normal subjects.

Adult↗
PubMed1980

[Methodology of hemodynamic study of a vasodilator drug (author's transl)].

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).

Cardiac Output↗