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Biomedical subjects

A Nitenberg

Publications and source records attributed to A Nitenberg.

At least 109 records · Page 6Linked to original sources
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↗
PubMed1983

[Factors affecting the relaxation and diastolic properties of the left ventricle].

The myocardium is an integrated functional unit. The separation of the cardiac cycle into three phases on simultaneous ventricular and arterial pressure curves:contraction, relaxation, diastole, is an artificial distinction of interdependent functions which are superimposed in time in the real mechanical and biochemical phenomena. At the level of the sarcomeres and myofilaments, relaxation is the active process of liberation of the bridges formed between actin and myosin during contraction; diastole is the phase during which there is no cyclic renewal of these bridges, it is the passive phase. Myocardial relaxation in mammals is controlled by the rapid recapture of Ca2+ by the sarcoplasmic reticulum. It plays an important mechanical role during the closure of the aortic semilunar valves, the opening of the mitral valve, the rapid filling of the right ventricle and the diastolic perfusion of the coronary arteries. It is dependent on the load and is influenced by myocardial metabolism (hypoxia, acidosis, ischaemia), temperature and a number of pharmacological agents. Amongst the passive properties of the left ventricle, we need to distinguish between the distensibility of the left ventricle as a filling chamber (parietal rigidity) and the rigidity of each of the myocardial fibres which make up the ventricular wall (myocardial rigidity). The passive properties of the left ventricle can be modified by ventricular geometry, passive mechanical properties of the ventricular wall (thickening, myocardial changes, heart rate and filling rate, cellular oedema, hypoxia, ischaemia, coronary artery filling pressure), the interaction between the pericardium, the right ventricle and the left ventricle and intrathoracic pressure. The large number of factors which are capable of modifying left ventricular relaxation and diastole explains the problems associated with in vivo investigations, which depend on a large number of indices of limited value.

Calcium↗
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↗
PubMed1981

Myocardial oxygen extraction and oxygen-hemoglobin equilibrium curve during moderate exercise.

Conditions of oxygen extraction by the myocardium have been studied in 12 subjects (44 +/- 9 years old) with pure mitral stenosis without clinical, metabolic or electrical sign of coronary insufficiency. Oxygen-hemoglobin equilibrium curves (OHEC) have been determined on arterial, mixed venous and coronary sinus blood, at rest and during a moderate (60 W, 10 min) exercise performed on a bicycle ergometer in supine position. Physiological values, at rest and during exercise, of the following functional parameters of the OHEC were determined in the in-vivo conditions of pH and PCO2 : P50, nHill, DS max = maximal value of OHEC slope (DS = delta SO2/delta PO2), PDSmax, SDS max. The concentration of plasma electrolytes capable to modify one of these parameters was controlled in each blood sample. In coronary sinus blood, P50 rises from 27.5 +/- 1.7 to 28.9 +/- 1.6 Torr during exercise (p less than 0.01). At rest, Hill's n in myocardial venous blood (2.67 +/- 0.09) is significantly higher than in arterial blood (2.61 +/- 0.08, p less than 0.01). A decrease in DS max (2.67 +/- 0.20 to 2.53 +/- 0.12%. Torr -1; p less than 0.01) and an increase in PDSmax (20.9 +/- 1.9 to 22.6 +/- 2.1 Torr, p less than 0.01) are observed. At rest, the myocardial "venous point" (PCSO2, SCSO2) is not significantly distinct from the maximal slope point (PDSmax, SDS max). After 1 min of exercise, a small gap appears which becomes significant at the end of the exercise (PDS max-PCSO2 = 0.2 Torr at rest, 2.7 Torr after exercise; SDS max-ScsO2 = 4.1% at rest, 7.9% after exercise). DS value at the myocardial venous point is only 2% at rest and 6% after exercise, lower than its maximal value. The gap between venous point and DS max point could constitute an error signal in the regulation loop of the coronary circulation. The existence of a physiological receptor, sensitive to instant variations in myocardial tissue PO2 and able to maintain venous point near DS max point could be considered.

Acid-Base Equilibrium↗