PubMed Health⌕ Search

Biomedical subjects

J L Vincent

Publications and source records attributed to J L Vincent.

At least 19 recordsLinked to original sources
PubMed1992

[Septic syndrome: cardiocirculatory assessment].

Severe sepsis is characterized by increased oxygen demand, alteration of oxygen extraction, and a diminution of myocardial contractility. The importance of each of these three factors is directly related to the severity of the sepsis. The combination of these factors may lead to tissue hypoxia, which is the shortest route to development of multiple organ failure (MOF). The presence of tissue hypoxia should be suspected in the presence of lactic acidosis. The phenomenon of dependence on oxygen consumption (VO2) in relation to oxygen transport (DO2) is detectable where there is a rise in DO2 induced by perfusion of liquids or administration of vasoactive agents. Study of the relationship between cardiac flow and oxygen extraction is a simple means of studying the relations between VO2 and DO2 at the patient's bedside.

Cardiac Volume↗
PubMed1992

Isolation by fluorescence-activated cell sorting of cells of a human lymphoblastoid cell strain containing mutations in the lambda immunoglobulin gene.

Fluorescence-activated cell sorting (FACS) was used to establish clonal populations of a human lymphoblastoid cell strain that contain spontaneously occurring and N-methyl-N'-nitro-N-nitrosoguanidine-induced mutations in the lambda immunoglobulin gene. Multiple rounds of FACS using a monoclonal antibody specific for the membrane-expressed human lambda immunoglobulin were used to enrich the population fraction of cells lacking a wild-type lambda immunoglobulin on the cell surface. Approximately 20% of the clonal populations established after five rounds of FACS-mediated enrichment did not express the lambda immunoglublin epitope recognized by the monoclonal antibody used for selection. However, evaluation of the FACS-selected mutant clonal populations with a polyclonal antilambda antibody, or a monoclonal antibody directed against a different epitope on the lambda immunoglobulin made by the T5-1 cells, indicated that the mutant clonal populations expressed lambda immunoglobulin on their cell surfaces. Additionally, the presence of lambda mRNA and of both secreted and cytoplasmic lambda protein confirmed the transcription and translation of the lambda immunoglobulin gene. These data suggest that FACS-mediated selection employing epitope-specific monoclonal antibodies provides a powerful technique for isolation of cell populations that express mutations within the coding region of the lambda immunoglobulin gene.

Blotting, Northern↗
PubMed1992

Atropine administration in experimental electromechanical dissociation.

Atropine can have a place during cardiopulmonary resuscitation (CPR) in the management of asystole, where parasympathetic influence might be excessive. However, the beneficial effects of atropine in electromechanical dissociation (EMD) have not been clearly demonstrated. The authors studied the effects of atropine in combination with epinephrine on an experimental model of EMD in the closed-chested dog. In 15 pentobarbital-anesthetized, mechanically ventilated dogs (mean weight 20 kg), EMD was induced by ventricular fibrillation followed by an external countershock, and was observed for 2 minutes before CPR was started. After 5 minutes of chest compression using a CPR thumper, either atropine 0.5 mg or D5W was administered, and the same injection was repeated every 5 minutes until recovery. Epinephrine 1 mg was administered in alternans. Each dog was submitted to two successive episodes of CPR, using either atropine or D5W, in a randomized order. Of a total of 28 CPRs, five were successful with chest compression alone. In the treatment groups, 10 of 11 were successful with atropine, but only eight of 12 with D5W (P < .01). The duration of CPR was also significantly shorter when atropine was used (9 minutes 56 seconds +/- 14 seconds versus 12 minutes 08 seconds +/- 43 seconds, P < .001). During the recovery period, atropine-treated animals had higher arterial pressure, heart rate, cardiac output and stroke volume. On this experimental model, the administration of high doses of atropine together with epinephrine enhances the recovery from EMD and results in a better cardiac function during recovery.

Animals↗
PubMed1992

Addition of enoximone to adrenergic agents in the management of severe heart failure.

OBJECTIVE: To assess the hemodynamic effects of the addition of small bolus doses of the phosphodiesterase inhibitor enoximone to adrenergic therapy in patients with severe heart failure. DESIGN: Open label, prospective study. SETTING: Multidisciplinary department of intensive care in a university academic hospital. PATIENTS: Twelve surgical patients after cardiac surgery and ten medical patients with ischemic or dilated cardiomyopathy who had signs of altered tissue perfusion associated with a low cardiac index (less than 2.25 L/min/m2), despite adrenergic therapy. INTERVENTIONS: Small iv bolus doses of 0.25 mg/kg of enoximone. MEASUREMENTS AND MAIN RESULTS: This treatment resulted in significant increases in cardiac index and left ventricular stroke work index without significant changes in heart rate or mean arterial pressure. Furthermore, the effects of half this dose (i.e., 0.125 mg/kg), studied in 11 patients, demonstrated a significant drug-induced increase in mean (+/- SD) cardiac index (from 1.58 +/- 0.29 to 1.84 +/- 0.27 L/min/m2, p less than .01) without change in mean arterial pressure (from 74.5 +/- 12.1 to 76.5 +/- 12.6 mm Hg, nonsignificant). CONCLUSIONS: Direct iv injections of enoximone can significantly increase the cardiac index in critically ill patients treated by adrenergic agents for severe heart failure. The administration of small doses of enoximone is effective and has minimal effect on arterial pressure.

Adult↗
PubMed1992

Addition of alinidine, a specific bradycardic agent, to dobutamine in a canine model of endotoxic shock.

BACKGROUND AND METHODS: Alinidine is a recently developed antiarrhythmic medication that acts directly on the cardiac pacemaker cells to reduce heart rate (HR). At effective doses, alinidine might have cardiodepressant actions that could be hazardous in the presence of hemodynamic instability. On the other hand, one limitation of the use of catecholamines is tachycardia, and alinidine could be beneficial in situations such as septic shock, where adrenergic agents are commonly required. The present study explored the hemodynamic and gasometric effects of alinidine during dobutamine administration in a canine model of septic shock induced by endotoxin administration. In ten pentobarbital-anesthetized, mechanically ventilated dogs (weight 28 +/- 4 kg), Escherichia coli endotoxin (3 mg/kg) injection was followed 30 mins later by saline infusion to restore and maintain pulmonary artery occlusion pressure at the baseline value. Sixty minutes after the endotoxin administration, a dobutamine infusion was started at a rate of 10 micrograms/kg/min. Thirty minutes later, alinidine was administered as a bolus dosage of 1 mg/kg in five dogs; the other five dogs served as a control group. RESULTS: Alinidine administration resulted in a decrease in HR from 157 +/- 20 to 138 +/- 27 beats/min (p less than .01) and a nonsignificant increase in cardiac output from 5.2 +/- 3.0 to 6.8 +/- 2.8 L/min, as a consequence of increases in stroke volume from 31.9 +/- 15.3 to 49.2 +/- 13.9 mL (p less than .01) and in left ventricular stroke work from 32.1 +/- 20.0 to 57.4 +/- 32.1 g.m (p less than .05). CONCLUSIONS: During experimental septic shock, alinidine administration can reverse dobutamine-induced tachycardia and simultaneously improve ventricular function.

Analysis of Variance↗
PubMed1992

Effect of positive end-expiratory pressure on right ventricular function in humans.

The effect of positive end-expiratory pressure (PEEP) on right ventricular (RV) function in humans is complex. Previous studies have been limited in their interpretation by not defining either pericardial pressure (Ppc) or RV volumes. Accordingly, we measured RV volumes and pressures and Ppc as PEEP was increased from zero to 15 cm H2O in 12 patients after thoracotomy, using a pulmonary arterial catheter equipped with a rapid responding thermistor that allowed measurement of RV ejection fraction (ef), while Ppc was measured via a pericardial balloon catheter. RV end-diastolic volume (EDV) was estimated as the ratio of stroke volume (SV) to RVef, whereas RV end-systolic volume (ESV) was estimated as RV EDV-SV. Right atrial pressure (Pra) was defined as end-diastolic pressure, and pulmonary arterial pressures (Ppa), both peak and mean, were used as end-systolic pressures. PEEP increased Ppc, Pra, and lung compliance (Cl). Cardiac output also decreased but not significantly. Neither mean nor peak systolic Ppa, nor RVef was significantly altered by PEEP. There was no relation between either RV filling pressure (Pra-Ppc) and EDV or the change in RV filling pressure and EDV, although EDV varied significantly as PEEP varied for individuals (p less than 0.05). Similarly, there was no relation between Ppa and ESV when either mean or peak Ppa values relative to Ppc were used. The relations between EDV and both SV and RVef were weak (r = 0.54 and 0.55, respectively). RVef varied inversely with ESV (r = -0.77), although it showed no relation to transmural peak Ppa (r = 0.28).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1992

Veno-arterial carbon dioxide gradient in human septic shock.

Recent reports have shown that venous hypercarbia, resulting in a widening of the veno-arterial difference in PCO2 (dPCO2), is related to systemic hypoperfusion in various forms of low-flow state. Although septic shock usually is a hyperdynamic state, other factors can influence the CO2 production and elimination, and thus dPCO2 in septic shock This study examined the dPCO2 and acid-base balance together with cardiac output measurements and oxygen-derived variables in 64 adult patients with documented septic shock. For a total of 191 observations, a significant exponential relation between dPCO2 and CO was found. At time of first measurement, 15 patients had an increased dPCO2 (above 6 mm Hg) and a higher mixed venous PCO2 (PvCO2) (47.2 +/- 10.0 vs 35.9 +/- 7.3 mm Hg, p less than 0.001). These patients had a lower cardiac index (2.9 +/- 1.3 vs 3.8 +/- 2.0 L/min.m2, p less than 0.01), a higher oxygen extraction ratio, but a similar VO2 than patients with normal dPCO2. The higher dPCO2 could also be related to an impaired CO2 elimination as indicated by a higher PaCO2 and a lower PaO2/FIO2 in these patients. Nonsurvivors had a significantly higher dPCO2 than survivors (5.9 +/- 3.4 vs 4.4 +/- 2.3 mm Hg, p less than 0.05) in the presence of similar cardiac output. The higher dPCO2 in these patients was probably related to the higher blood lactate levels (7.7 +/- 5.3 mmol/L vs 4.5 +/- 2.8 mmol/L, p less than 0.01) and the more severe pulmonary impairment (SaO2 90 +/- 8 percent vs 95 +/- 4 percent, p less than 0.001). Arteriovenous oxygen content difference (dAVO2) and VO2 were similar in survivors and nonsurvivors. In conclusion, dPCO2 patients with septic shock is related principally to cardiac output but apparently also to the degree of pulmonary impairment. Although dPCO2 is larger in nonsurvivors, its prognostic value is modest.

Adult↗
PubMed1992

Administration of anti-TNF antibody improves left ventricular function in septic shock patients. Results of a pilot study.

In this pilot study, murine monoclonal anti-TNF antibody (2 mg/kg) was administered to ten patients within 24 h of septic shock which persisted after initial resuscitation with intravenous fluids and adrenergic agents. This treatment resulted in a reduction in heart rate (from 122 +/- 10 to 113 +/- 10 beats per minute at 4 h, p less than 0.01) associated with an increase in LVSWI (from 26.5 +/- 5.6 to 31.5 +/- 10.5 g.m2 at 2 h, p less than 0.05), indicating in the absence of change in cardiac filling pressures, an improvement in ventricular function. Arterial oxygenation improved concurrently in six patients. These changes, however, appeared transient. The improvement in cardiac function following anti-TNF antibody administration in patients is in keeping with recent experimental studies indicating the role of TNF in the myocardial depression characterizing septic shock.

Aged↗
PubMed1992

A.R.D.S.

Explore the source record for details and available documents.

Anesthetics↗
PubMed1992

Myocardial depression characterizes the fatal course of septic shock.

The relationship between cardiac and vascular abnormalities was studied in 68 patients with established septic shock. At time of hemodynamic evaluation, after initial resuscitation, there was no significant difference in arterial pressure, pulmonary artery pressure, cardiac filling pressures, and cardiac index between the 38 survivors of shock and the 30 patients who died of shock, but the left ventricular stroke work index and the right ventricular (RV) stroke work index were higher in survivors than in those who died (mean +/- SD: 25.0 +/- 9.1 vs 20.1 +/- 9.4 gm/m2 [p less than 0.05] and 6.6 +/- 3.6 vs 4.8 +/- 2.8 gm/m2 [p less than 0.05], respectively). Survivors had also higher thermodilution RV ejection fraction and lower RV end-diastolic volumes than had those who died (43.9% +/- 16.3% vs 31.1% +/- 13.7% [p less than 0.01] and 82 +/- 30 vs 99 +/- 31 ml/m2 [p less than 0.05], respectively). Calculated systemic vascular resistance was similar in the two groups, but vasopressors had been required in 22 (58%) of 38 survivors and 25 (83%) of 30 patients who died (p less than 0.01). Moreover, when the patients were separated into two groups according to their cardiac output, higher or lower than 3 L/min/m2, in both subgroups patients who died had lower blood pressure than had survivors. Blood lactate levels were significantly lower in survivors than in nonsurvivors (5.1 +/- 2.1 vs 8.1 +/- 4.7 mEq/L, p less than 0.01). Final data obtained before recovery of shock or death indicated that the survivors had higher arterial pressure, lower pulmonary artery pressure and right atrial pressure, higher stroke volume, and higher RV ejection fraction than had the patients who died. No survivors but all patients who died had been treated with vasopressors. These data therefore indicate that death as a result of septic shock is characterized by both myocardial depression and altered vascular tone and both are probably interrelated.

Female↗
PubMed1992

Prostaglandin E1 infusion for right ventricular failure after cardiac transplantation.

The infusion of prostaglandin E1, a vasodilating substance with predominant effects on the pulmonary vasculature, has been found effective in the management of pulmonary hypertension associated with various diseases. The reported experience with prostaglandin E1 after cardiac transplantation is, however, limited. We used prostaglandin E1 in 18 patients in whom acute right ventricular failure developed after orthotopic cardiac transplantation. The infusion was started within 24 hours after operation in 16 patients and was continued for up to 7 days. Maximal doses of prostaglandin E1, administered via a central venous catheter, ranged from 30 to 120 ng/kg/min. Norepinephrine was simultaneously infused via a left atrial catheter in 10 patients to prevent a reduction in systemic arterial pressure. The prostaglandin E1 infusion resulted in significant reductions in mean arterial pressure and pulmonary vascular resistance and simultaneous increases in cardiac index and stroke index. Mean arterial pressure was stable and left ventricular stroke work increased. The alveolar oxygen tension/forced inspiratory oxygen index tended to decrease during the infusion. Three patients died, two of right heart failure and one of multiple organ failure associated with cardiac allograft rejection. In patients in whom right ventricular failure associated with pulmonary hypertension develops after cardiac transplantation, prostaglandin E1, combined with norepinephrine whenever the arterial pressure declines, can effectively reduce pulmonary artery pressures and improve global cardiac function without compromising systemic perfusion.

Adult↗
PubMed1991

Hemodynamic evaluation of bisoprolol after coronary artery surgery in patients with altered left ventricular function.

Bisoprolol is a new cardioselective beta1 adrenergic blocking agent without intrinsic sympathomimetic activity but with minimal effects on myocardial contractility. Bisoprolol was compared to propranolol in 24 patients after cardiac surgery for coronary artery bypass graft (CABG). Each patient had been treated preoperatively with beta-blocking agents and had a cineangiographic left ventricular ejection fraction between 35% and 55%. Patients were randomized to receive orally either 10 mg of propranolol three times a day or 5 mg of bisoprolol once a day. Both drugs resulted in a significant and similar decrease in heart rate. This was associated with significant decreases in cardiac index, stroke index, and thermodilution right ventricular ejection fraction 6 hours after administration of propranolol, but not after bisoprolol. Systolic function measured by Doppler techniques significantly increased in the 10 postoperative days in patients under bisoprolol but not significantly after propranolol. Each drug was well tolerated during the 10 postoperative days, and the recovery was uneventful in each patient. These results indicate that in patients with altered systolic function after CABG, bisoprolol is susceptible to reduce heart rate with less cardiovascular alteration than propranolol.

Adrenergic beta-Antagonists↗
PubMed1991

Interleukin-6 administration has no acute hemodynamic or hematologic effect in the dog.

To investigate the possible hemodynamic effects of interleukin-6 (IL-6), a single dose of 15 mcg/kg of recombinant IL-6 isolated from Escherichia coli was injected intravenously in six pentobarbital-anesthetized dogs. After 30 min, saline infusion was performed to maintain the pulmonary artery balloon-occluded pressure at baseline level. The animals were observed for up to 5 hours. No other hemodynamic alteration was observed than a gradual decline in cardiac output attributed to anesthesia. Hematologic variables, blood glucose, and total serum proteins were also constant. IL-6 levels were markedly elevated in the blood, but no tumor necrosis factor activity was detected. Thus a primary role for IL-6 in the early cardiovascular alterations associated with septic shock seems unlikely.

Animals↗