M. Rapin
University of Paris
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Featured researches published by M. Rapin.
Intensive Care Medicine | 1977
Bernard Regnier; M. Rapin; G. Gory; François Lemaire; B. Teisseire; A. Harari
The Haemodynamic response to dopamine infusion has been assessed in 30 patients in septic shock with myocardial dysfunction. Dopamine infusion resulted in a haemodynamic improvement as indicated by significant increases in cardiac output of 38.4% (p>.001), stroke volume 18.7% (p<.001), and mean arterial pressure of 33% (p<.001). Despite the inotropic effect, left ventricular filling pressure did not change in 20 cases and increased in 10 cases. Mean peripheral resistance remained unchanged with a scatter of individual responses depending upon factors such as dopamine dose and initial vascular resistance.Dopamine increased intrapulmonary shunting by 48% (p<.001), insignificantly decreased PaO2, increased mixed venous oxygen saturation by 16% (p<.02) and decreased pulmonary vascular resistance by 15% (p<.02).Both isoprenaline and dopamine improve stroke volume by an inotropic action, with an increase in venous return in the case of the latter and a reduction in afterload in the former.It is cocluded that the usefulness of dopamine in septic shock may be limited in patients with previous myocardial disease because of the risk of increasing preload and in hypoxaemic patients because of the risk of increasing intrapulmonary shunting.
Critical Care Medicine | 1985
Christian Brun-Buisson; Francis Bonnet; Sabine Bergeret; François Lemaire; M. Rapin
Delayed-onset pulmonary edema complicating severe diabetic ketoacidosis was observed twice in one patient. Hemodynamic measurements during the second episode showed normal transmural pulmonary capillary wedge pressure, suggesting an alteration in alveolocapillary permeability. Hyperventilation and acidosis may underlie this alteration. Vigorous fluid therapy, while decreasing oncotic pressure, may also contribute to the pulmonary edema. The two episodes in one patient suggest that pulmonary microvascular diabetic angiopathy may predispose some diabetics with severe ketoacidosis to increased-permeability pulmonary edema.
Critical Care Medicine | 1985
Francis Bonnet; J. Bilaine; F. Lhoste; B. Mankikian; B. Kerdelhue; M. Rapin
A 0.01 and 0.1-mg/kg dose of iv naloxone was administered to seven patients in septic shock, in order to evaluate naloxones hemodynamic effect and possible relation to changes in plasma beta-endorphin and catecholamine levels. Naloxone failed to modify cardiac index, blood pressure, heart rate, and systemic vascular resistance. Plasma beta-endorphin, norepinephrine, and epinephrine were elevated but did not change after naloxone administration. These results suggest that beta-endorphin release is a consequence but not a cause of shock, and that the beneficial hemodynamic effects of naloxone in animal studies could be related to species differences or nociceptive stimulations.
Metabolism-clinical and Experimental | 1984
P. Trunet; François Lhoste; Jean-Claude Ansquer; Soline Kestenbaum; Catherine Sabatier; Jean-Paul Tillement; M. Rapin
Plasma levels of norepinephrine (NE), epinephrine (E), immunoreactive insulin (IRI), and glucose were measured in six healthy volunteers after glucose consumption and in six volunteers after a water solution. Ingestion of the glucose (100 g) solution significantly decreased E levels from 46.7 +/- 8.0 to 20.8 +/- 1.9 pg/mL (P less than 0.01). Three hours after the glucose ingestion, plasma E levels nearly returned to basal values. Plasma IRI and glucose levels peaked at 45 minutes after glucose consumption (P less than 0.01), then declined toward basal values. Plasma NE levels were unaffected by glucose consumption. There were no changes in glucose, IRI, NE, or E levels in the control group. These results suggest that E behaves as a counter-regulatory hormone to insulin under stimulation by glucose.
Intensive Care Medicine | 1986
P. Trunet; I. T. Borda; A.-V. Rouget; M. Rapin; F. Lhoste
All patients admitted during a 33-month period to a multidisciplinary intensive care unit were prospectively studied in order to determine the incidence and severity of drug-induced illness leading to the admission. The role of underlying diseases was assessed and the avoidability of drug-induced illness considered. Out of 1651 patients, 97 (5.88%) were admitted because of drug-induced illness; 74 of these had serious underlying diseases. 13 (13.4%) of the 97 patients died, but underlying diseases accounted for 4 of the 13 fatalities. In nearly half of the cases, the drug-induced illness appeared potentially avoidable.
Intensive Care Medicine | 1987
M. Rapin
An explanation is provided of the logical steps taken before assigning patients to critical care therapy in a major multidisciplinary intensive care unit of the University of Paris at the Hospital Henri Mondor. The factors considered by the staff in deciding to terminate intensive therapy are also enumerated. This system has not been influenced by the major legal pressures found in the United States but has been shaped by more chronic fiscal constraints.
Intensive Care Medicine | 1975
Alexandre Harari; Bernard Regnier; M. Rapin; François Lemaire; J. R. Le Gall
SummaryRight heart catheterisation was undertaken in six patients with accidental deep hypothermia. Studies were carried out before and after rapid blood volume expansion, with and without Isoproterenol infusion, and were repeated at normal body temperatures.The initial haemodynamic pattern indicated a marked hypovolemia with a simultaneous decrease of both cardiac output and ventricular filling pressures, and a decreased measured total blood volume. Rapid correction of the hypovolemia revealed cardiac insufficiency, in part due to the persisting bradycardia. Left ventricular function was depressed in patients with prolonged cold exposure and normal in patients with short exposure. These abnormalities disappeared after Isoproterenol infusion during hypothermia, and spontaneously after return to normothennia.No imbalance existed between the decreased cardiac output and oxygen uptake in hypothermia, arterio-venous oxygen difference being within normal limits.
Intensive Care Medicine | 1980
Claude George; Alain Sobel; Liliane Intrator; Michel Robin; Catherine Sabatier; Danièle Prevot; M. Rapin
SummaryIn order to explain complement components abnormalities observed during septic shock, circulating immune complexes (C.I.C.) were searched for in sera from 34 patients with gram negative sepsis by two different methods: polyethylene glycol precipitation test based on physical properties of C.I.C. and C1q deviation test based on the property of radiolabelled C1q to react with C.I.C. Serum immunoglobulins (IgG, IgA, IgM) and complement components (C1q, C3, C4) levels were simultaneously determined. Seventeen patients with minimal haemodynamic abnormalities had normal or increased levels (except C4 at 62% of normal) and in eleven cases both tests for C.I.C. were simultaneously positive. Seventeen patients with severe septic shock had a decrease in IgG, IgM, C1q, C3 and C4 and none had both tests for C.I.C. simultaneously positive (P<10−4). The disappearence of C.I.C. in patients with severe septic shock associated with evidence of complement activation suggests their involvement in the pathogenesis of septic shock in man.
Intensive Care Medicine | 1980
M. Francoual; F. Lhoste; Bernard Regnier; François Lemaire; M. Rapin
IntroductionA pathophysiological approach to pulmonary oedema (PO), discriminating in particular between cardiogenic pulmonary oedema (CPO) and non-cardiogenic pulmonary oedema (NCPO) has greatly enhanced our knowledge of this disease in the last few years [68]. In addition, the use of bedside haemodynamic measurements now enables treatment of CPO by new, potent, drugs such as vasodilators and catecholamines, and allows haemodynamic support during the management of NCPO by mechanical ventilation with positive end-expiratory pressure (PEEP).
Intensive Care Medicine | 1978
Kamran Samii; M. Rapin; Jean Roger Le Gall; Bernard Regnier
A study was perfomed in order to observe haemodynamic changes induced by haemodialysis in 14 patients with acute renal failure and severe sepsis. Left ventricular function, as assessed by changes in pulmonary wedge pressure and left ventricular stroke work index through plasma volume expansion, did not change during haemodialysis. Ultrafiltration-induced decreases in cardiac index provoked in 8 patients, with nearly normal initial systemic arteriolar resistance, had adequate and constant increase in their resistance (p<0.001), whereas 6 patients with low initial systemic arteriolar resistance did not increase their resistance and had a frequent (9/13 measurements) and significant (p<0.001) fall in mean aortic pressure. This abnormality of vascular tone is probably due to severe sepsis and explains why hypotension is a frequent occurrence during haemodialysis in such patients.