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Biomedical subjects

D Payen

Publications and source records attributed to D Payen.

At least 37 records · Page 2Linked to original sources
PubMed1999

A comparison of standard cardiopulmonary resuscitation and active compression-decompression resuscitation for out-of-hospital cardiac arrest. French Active Compression-Decompression Cardiopulmonary Resuscitation Study Group.

BACKGROUND: We previously observed that short-term survival after out-of-hospital cardiac arrest was greater with active compression-decompression cardiopulmonary resuscitation (CPR) than with standard CPR. In the current study, we assessed the effects of the active compression-decompression method on one-year survival. METHODS: Patients who had cardiac arrest in the Paris metropolitan area or in Thionville, France, more than 80 percent of whom had asystole, were assigned to receive either standard CPR (377 patients) or active compression-decompression CPR (373 patients) according to whether their arrest occurred on an even or odd day of the month, respectively. The primary end point was survival at one year. The rate of survival to hospital discharge without neurologic impairment and the neurologic outcome were secondary end points. RESULTS: Both the rate of hospital discharge without neurologic impairment (6 percent vs. 2 percent, P=0.01) and the one-year survival rate (5 percent vs. 2 percent, P=0.03) were significantly higher among patients who received active compression-decompression CPR than among those who received standard CPR. All patients who survived to one year had cardiac arrests that were witnessed. Nine of 17 one-year survivors in the active compression-decompression group and 2 of 7 in the standard group, respectively, initially had asystole or pulseless electrical activity. In 12 of the 17 survivors who had received active compression-decompression CPR, neurologic status returned to base line, as compared with 3 of 7 survivors who had received standard CPR (P=0.34). CONCLUSIONS: Active compression-decompression CPR performed during advanced life support significantly improved long-term survival rates among patients who had cardiac arrest outside the hospital.

Cardiopulmonary Resuscitation↗
PubMed1999

No evidence for cerebral hypoperfusion during cerebral malaria.

OBJECTIVE: Among the mechanisms suggested for altered consciousness during cerebral malaria is the hypothesis of cerebral ischemia, which remains controversial, with little supportive O2 conflicting hemodynamic data. The purpose of this study was to test the hypothesis that cerebral ischemia is a main mechanism for altered consciousness during cerebral malaria. SETTING: University hospital pediatric ward in a region with endemic cerebral malaria. DESIGN: Prospective evaluation of cerebral hemodynamics and cerebral oxygenation during cerebral malaria compared with severe malaria anemia without altered consciousness. PATIENTS: During a 2-wk period, we evaluated all patients who were admitted for cerebral malaria (n = 5). Age-matched patients admitted for severe malaria anemia without altered consciousness (n = 3) and outpatients (n = 3) were investigated for comparison. INTERVENTIONS: All patients received the usual treatment according to their needs, which was determined by the physician in charge. Repeated neurologic evaluations were performed during the early management period in patients with cerebral malaria. METHODS AND MAIN RESULTS: We repeatedly measured cerebral blood flow velocity (transcranial Doppler) and simultaneous systemic determinants of cerebral blood flow (arterial pressure, arterial oxygen saturation, PaCO2, rectal temperature, and hemoglobin concentration). The adequacy of cerebral blood flow to oxygen demands during cerebral malaria was assessed by continuous recording of jugular bulb venous oxygen saturation (using a fiberoptic device). Marked cerebral vasodilation was observed during cerebral malaria (systolic velocity, 1.45 +/- 0.09 m/s; diastolic velocity, 0.75 +/- 0.08 m/s; n = 4) and during severe malaria anemia (systolic velocity, 1.18 +/- 0.14 m/s; diastolic velocity, 0.55 +/- 0.05 m/s; n = 3) compared with control children (systolic velocity, 0.84 +/- 0.13 m/s; diastolic velocity, 0.35 +/- 0.06 m/s; n = 3; p < .05). During cerebral malaria, jugular bulb venous oxygen saturation remained stable, including during neurologic recovery, with initial values of 67.5 +/- 4.3%. CONCLUSIONS: Because jugular bulb venous oxygen saturation remained within the normal range, cerebral hyperemia seems to be an adaptive response to altered systemic determinants, which argues against a hemodynamic mechanism for altered consciousness during cerebral malaria.

Anemia↗
PubMed1999

Serum is more suitable than whole blood for diagnosis of systemic candidiasis by nested PCR.

PCR assays for the diagnosis of systemic candidiasis can be performed either on serum or on whole blood, but results obtained with the two kinds of samples have never been formally compared. Thus we designed a nested PCR assay in which five specific inner pairs of primers were used to amplify specific targets on the rRNA genes of Candida albicans, C. tropicalis, C. parapsilosis, C. krusei, and C. glabrata. In vitro, the lower limit of detection of each nested PCR assay was 1 fg of purified DNA from the corresponding Candida species. In rabbits with candidemia of 120 minutes' duration following intravenous (i.v.) injection of 10(8) CFU of C. albicans, the sensitivities of the PCR in serum and whole blood were not significantly different (93 versus 86%). In other rabbits, injected with only 10(5) CFU of C. albicans, detection of candidemia by culture was possible for only 1 min, whereas DNA could be detected by PCR in whole blood and in serum for 15 and 150 min, respectively. PCR was more often positive in serum than in whole blood in 40 culture-negative samples (27 versus 7%; P < 0.05%). Lastly, experiments with rabbits injected i.v. with 20 or 200 microgram of purified C. albicans DNA showed that PCRs were positive in serum from 30 to at least 120 min after injection, suggesting that the clearance of free DNA is slow. These results suggest that serum is the sample of choice, which should be used preferentially over whole blood for the diagnosis of systemic candidiasis by PCR.

Animals↗
PubMed1999

Sequential changes in autonomic regulation of cardiac myocytes after in vivo endotoxin injection in rat.

We report that in vivo injection of endotoxin (EDTX, 6 mg. kg(-)(1)) induces cardiovascular alterations in rats that closely mimic the clinical situation, as assessed by in vivo hemodynamic measurements in anesthetized and conscious, chronically instrumented animals. The patch-clamp technique was used to characterize the L-type calcium current (I(Ca)) and its autonomic regulation in isolated cardiac myocytes. The density of I(Ca) progressively decreased at 12 and 36 h after EDTX injection. However, the dihydropyridine (+/-)Bay K 8644 (100 nM) enhanced I(Ca) to levels similar to those in control and EDTX-treated myocytes. In addition, the net stimulatory effect of a beta-adrenergic agonist (isoproterenol) on I(Ca) was increased 12 h after EDTX injection. This change in the beta-adrenergic effect declined 24 h later. The potentiation in the beta-adrenergic stimulation of I(Ca) was mimicked by L858051 (10 microM), a direct activator of adenylyl cyclase, but not by IBMX (200 microM), a phosphodiesterase inhibitor. Besides, the antiadrenergic effect of acetylcholine on I(Ca) was unchanged 12 h after EDTX injection, but increased 36 h after EDTX injection. These results support the hypothesis that time-dependent changes in the adenylyl cyclase pathway in cardiac myocytes may contribute, via the autonomic regulation of I(Ca), to the severity of myocardial dysfunction during sepsis.

1-Methyl-3-isobutylxanthine↗
PubMed1999

[Management of severe post-partum hemorrhage using selective arterial embolization].

OBJECTIVES: To evaluate the efficacy and safety of uterine embolization in the management of intractable post-partum hemorrhage. MATERIALS AND METHODS: From July 1994 to December 1997, 51 patients with severe primary (n = 37) or secondary (n = 14) post-partum hemorrhage were treated by arterial uterine embolization. In all cases, hemostatic uterine embolization was performed because of persistent hemorrhage despite adapted obstetrical measures and early introduction of uterotonic drugs. RESULTS: In case of immediate post-partum hemorrhage, primary and secondary success rates were 89% et 97% respectively. In one patient with placenta accreta, delayed hysterectomy was necessary. One patient died of associated cerebral hemorrhage while vaginal bleeding had stopped. The success rate reached 100% in case of secondary post-partum hemorrhage. CONCLUSION: Emergency arterial embolization is a safe and effective means of controlling severe post-partum hemorrhage after failure with medical treatment.

Adult↗
PubMed1998

Reduced ex vivo interleukin-8 production by neutrophils in septic and nonseptic systemic inflammatory response syndrome.

Ex vivo cytokine production by circulating lymphocytes and monocytes is reduced in patients with infectious or noninfectious systemic inflammatory response syndrome. Very few studies have addressed the reactivity of polymorphonuclear cells (PMN). To analyze further the relative contribution of systemic inflammatory response syndrome alone or in combination with infection we studied the interleukin-8 (IL-8) production by PMN isolated from patients who had undergone cardiac surgery with cardiopulmonary bypass (CPB) and patients with sepsis. Cells were activated with either lipopolysaccharide (LPS) or heat-killed streptococci. Compared with healthy controls, the release of IL-8 by PMN in both groups of patients was significantly reduced whether activated by LPS, independently of its concentration and origin, or by heat-killed streptococci. These observations suggest that stressful conditions related to inflammation, independently of infection, rapidly dampened the reactivity of circulating PMN. We investigated whether the observed diminished reactivity of PMN might reflect an endotoxin tolerance phenomenon. Our in vitro experiments with PMN from healthy controls indicated that PMN could not be rendered tolerant stricto sensu. However, our data suggested that LPS-induced mediators such as IL-10 may be responsible for the observed anergy in patients.

Adult↗
PubMed1998

Chemical modifications of the vasoconstrictor peptide angiotensin II by nitrogen oxides (NO, HNO2, HOONO)--evaluation by mass spectrometry.

Nitric oxide (NO) and angiotensin II are natural regulators of blood pressure. Under aerobic conditions, NO is transformed into its higher oxides (N2O4, NO2, NO/NO2 or N2O3) and oxoperoxonitrate (currently named peroxynitrite) by coupling with superoxide. Previous studies have shown that these reactive nitrogen species should be involved in vivo in the transformation of cysteine and tyrosine into the corresponding nitrosothiol and 3-nitrotyrosine. In the present study, attention has been focused on the relative reactivities of HNO2, peroxynitrite, and NO in the presence of dioxygen, towards the arginine and tyrosine residues of the peptide angiotensin II. Nitration of the tyrosine residue is clearly the main reaction with peroxynitrite. By contrast, besides 20% of nitration of the tyrosine residue, NO in the presence of dioxygen leads to nitrosation reactions with the arginine residue similar to those observed with HNO2 at pH 5, possibly through the intermediate N2O3 reactive species. Angiotensin II is converted for the most part to peptides having lost either a terminal amine function or the whole guanido group, leading respectively to citrulline-containing angiotensin II or to a diene derivative. Identification established mainly by tandem mass spectrometry of peptidic by-products allows us to propose a cascade of nitrosations of all the amine functions of the arginine residue. Further in vivo studies show that transformations of the arginine residue in angiotensin II do not alter its vasoconstrictive properties, whereas nitration of the tyrosine residue totally inhibits them.

Angiotensin II↗
PubMed1998

Systemic pressure-flow reactivity to norepinephrine in rabbits: impact of endotoxin and fluid loading.

OBJECTIVE: This study aimed to evaluate the impact of fluid loading on hemodynamics and vascular hypocontractility to norepinephrine (NE) in an endotoxic shock model. DESIGN: Mean arterial pressure (MAP), aortic blood flow velocity (AoV, 20 MHz Doppler) and aortic conductance (AoC = AoV/MAP) were studied during 180 min (T0-T180) in 41 anesthetized and ventilated rabbits. INTERVENTIONS: Shock was induced by a 600 micrograms/kg bolus injection of endotoxin. Fluid loading (20 ml/kg colloids) was infused from T90 to T120. Dose-response curves to NE were performed at T0, T60 and T120 in endotoxic and non-endotoxic animals with or without fluid loading. MEASUREMENTS AND RESULTS: Endotoxin decreased pressure (-23%, p < 0.05) and flow (-42%, p < 0.05) corresponding to a decrease in conductance (-19%, p < 0.05). Fluid loading did not improve hypotension but markedly increased systemic flow (+51%, p < 0.01), corresponding to a hyperkinetic syndrome. Vascular reactivity to NE was impaired after endotoxin at T60 since the pressure response to NE was depressed (p < 0.01) and flow did not decrease. In non-fluid-loaded groups, the pressure response to NE recovered at T120, with no reduction in flow. In fluid-loaded endotoxic animals, however, the pressure response to NE was still impaired at T120 (p < 0.05), but with a decrease in flow. CONCLUSIONS: Fluid loading transformed the hypodynamic profile of endotoxic shock into a hyperdynamic state without improving blood pressure. Depressed vascular reactivity to NE was observed in both hyperdynamic and hypodynamic states, suggesting that a reduced vascular reactivity does not necessarily imply systemic vasodilation.

Animals↗
PubMed1998

Prolonged severe hypercapnia complicating near fatal asthma in a 35-year-old woman.

OBJECTIVE: We describe a patient with a prolonged and severe hypercapnia occurring during an episode of status asthmaticus induced by ophthalmic instillation of carteolol. SETTING: Prehospital Emergency Medical Service and Pulmonary Intensive Care Unit in a university hospital. PATIENT: A 35-year-old female developed an acute asthma attack while at home, which required advanced life support. INTERVENTION: On hospital admission, arterial blood gases revealed a PaCO2 of 208 mmHg. Hypercapnia persisted with a PaCO2 of more than 190 mmHg for 10 h, with pH always less than 7.00. The patient was finally discharged after 26 days without sequelae. CONCLUSION: This case illustrates the cerebral and cardiovascular tolerance of severe and prolonged hypercapnia associated with major acidosis.

Acidosis, Respiratory↗
PubMed1998

[Monitoring and maintenance of blood volume in intracranial surgery].

Intraoperative monitoring usually does not assess intravascular blood volume of the patient. The variations of the systolic blood pressure and the right auricular pressure allow to appreciate the intravascular blood volume changes and their consequences on the cerebral perfusion pressure. However, when the autoregulation of the cerebral blood flow is strongly depressed, the evaluation of the cerebral perfusion pressure alone is inadequate. In this case, the optimal monitoring should be metabolic (jugular bulb venous oxygen saturation) to finally assess the cerebral flow-metabolic coupling.

Anesthesia, General↗
PubMed1998

Paracrine regulation of cardiac myocytes in normal and septic heart.

A paracrine pathway for the regulation of cardiac contractile function by nonmuscle cells is documented in the heart. Coronary and endocardial endothelium release several diffusible agents, such as prostaglandins, endothelin-1, and nitric oxide, with an action on cardiac myocyte function. Cardiac diseases involving an immune or inflammatory mechanism, such as endotoxic shock, are now seen as conditions in which cross-talk between different cell types in the heart is clearly implicated. The potential biological relevance of inducible nitric oxide synthase in the myocardium, and the subsequent production of nitric oxide has been proposed as a mechanism of the cardiac depression observed in septic shock. In addition to cardiac myocytes, activated microvascular endothelial cells and cardiac endothelial cells may contribute to nitric oxide generation and, ultimately, to the depression of myocardial contractile activity during sepsis. This article reviews the local intercellular communication between cardiac myocytes and endothelial cells in the normal heart and discusses some of the mechanisms potentially claimed to depress heart function in sepsis.

Endothelium↗
PubMed1998

Intravenous almitrine bismesylate reversibly induces lactic acidosis and hepatic dysfunction in patients with acute lung injury.

BACKGROUND: Intravenous almitrine, which augments hypoxic pulmonary vasoconstriction, is used for short-term improvement of arterial oxygenation. However, recent research has suggested a potentially harmful effect on lactate metabolism and hepatic function. METHODS: Arterial oxygenation, hemodynamic parameters, plasma lactate, and hepatic function were monitored prospectively in 25 patients with acute lung injury (defined as a ratio of arterial oxygen pressure to inspiratory oxygen fraction < or = 150 mmHg) who where treated with intravenous almitrine. In 21 of 25 patients, acute lung injury was related to primary lung lesions, including pneumonia, postcardiosurgical atelectasis, and lung contusions. RESULTS: Intravenous almitrine increased the ratio of arterial oxygen pressure to inspiratory oxygen fraction from 93 +/- 33 mmHg to 207 +/- 107 mmHg (mean +/- SD). In eight patients (three men), the plasma lactate concentration increased by an average of +3.5 +/- 1.8 mM, and the pH and bicarbonate concentration both decreased during the first 24 h of treatment. In this group of patients, the total bilirubin concentration was elevated before almitrine administration, and the results of other hepatic function tests, such as aspartate aminotransferase, alanine aminotransferase, and prothrombin time, were altered by almitrine administration. Therefore, intravenous almitrine was discontinued. Lactic acidosis and hepatic dysfunction improved. In the other 17 patients (14 men), the plasma lactate concentration and the hepatic function tests remained unaltered during intravenous almitrine therapy for > 60 h. Univariate and multivariate analyses revealed that an abnormal plasma concentration of total bilirubin before almitrine administration and female gender were the two factors significantly linked with lactic acidosis during almitrine infusion. CONCLUSIONS: This study confirms that intravenous almitrine greatly improves arterial oxygenation in patients with acute lung injury but may also induce lactic acidosis and hepatic dysfunction. The coexistence of lactic acidosis and hepatic dysfunction in the same patients strongly suggests that the liver is the primary source of intravenous almitrine-induced lactic acidosis.

Acidosis, Lactic↗
PubMed1998

Life-threatening primary postpartum hemorrhage: treatment with emergency selective arterial embolization.

PURPOSE: To prospectively evaluate the efficacy and safety of emergency selective arterial embolization in the management of intractable primary postpartum hemorrhage. MATERIALS AND METHODS: Twenty-seven consecutively seen women with life-threatening primary postpartum hemorrhage underwent uterine embolization. In all cases, hemostatic embolization was performed because of intractable hemorrhage that could not be controlled with vaginal packing and administration of uterotonic drugs. The mean hemoglobin level before embolization was 7.48 g/dL +/- 2.39 (74.8 g/L +/- 23.9) (1 standard deviation). Hysterectomy performed in two patients before embolization failed to stop the bleeding. RESULTS: Angiography revealed extravasation in nine patients and spasm of the branches of the internal iliac artery in five. The procedure consisted of embolization of uterine (n = 46), vaginal (n = 5), or ovarian (n = 2) arteries or anterior division of internal iliac arteries (n = 8). Immediate disappearance or dramatic diminution of external bleeding was observed in all cases. Two patients needed repeated embolization the next day. No major complication related to embolization was found. In one patient with placenta accreta, delayed hysterectomy was necessary. Normal menstruation resumed in all women except the two who underwent hysterectomy. One woman became pregnant after embolization. CONCLUSION: Emergency arterial embolization is a safe and effective means of control of primary postpartum hemorrhage. The procedure obviates high-risk surgery and allows maintenance of reproductive ability.

Adult↗
PubMed1998

Impact of inhaled nitric oxide on platelet aggregation and fibrinolysis in rats with endotoxic lung injury. Role of cyclic guanosine 5'-monophosphate.

As inhaled nitric oxide (iNO) may differently increase bleeding time (BT) and inhibit platelet aggregation in normal and lung-injured patients or experimental models, we studied the effects of iNO on hemostasis in presence and absence of an endotoxic lung injury in the rat. Eight hours after intratracheal administration of endotoxin (lipopolysaccharide [LPS]) or its solvent (phosphate-buffered solution [PBS]), four groups of rats were randomized according to the presence or absence of 15 ppm iNO added for an additional 10 h. We measured BT, ex vivo platelet aggregation, plasma fibrinogen, euglobulin clot lysis time (ECLT), and platelet and aortic cyclic guanosine 5'-monophosphate (cGMP) contents. Acute lung inflammation did not influence BT, but increased platelet aggregability, fibrinogen levels, and platelet and aortic cGMP. In control and endotoxic rats, iNO increased BT, reduced platelet aggregability, and increased platelet cGMP. iNO increased aortic cGMP only in healthy rats. ECLT was increased by LPS and unchanged with iNO. These results suggest that the extrapulmonary "systemic" effects induced by iNO on hemostasis were not strictly similar in healthy and LPS rats, inflammation inducing proper changes in coagulation parameters. However, iNO attenuated the procoagulant activity induced by acute lung inflammation, suggesting a potentially beneficial effect of this therapy.

Administration, Inhalation↗
PubMed1997

Benefit of active compression-decompression cardiopulmonary resuscitation as a prehospital advanced cardiac life support. A randomized multicenter study.

BACKGROUND: We compared short-term prognosis of active compression-decompression (ACD) and standard (STD) cardiopulmonary resuscitation (CPR) in out-of-hospital cardiac arrests. METHODS AND RESULTS: We randomized advanced cardiac life support (ACLS) with ACD ACLS CPR on odd days and STD ACLS CPR on even days. We measured the rates of return of spontaneous circulation (ROSC), survival at 1 hour (H1), at 24 hours (H24), and at 1 month (D30): hospital discharge (HD); neurological outcome; and complications. Mean times from collapse to basic cardiac life support CPR was 9 minutes and from collapse to ACLS CPR was 21 minutes. Compared with the STD ACLS patients (n = 258), ACD ACLS patients (n = 254) had higher survival rates (ROSC, 44.9% versus 29.8%, P = .0004; H1, 36.6% versus 24.8%, P = .003; H24, 26% versus 13.6%, P = .002; HD without neurological impairment, 5.5% versus 1.9%, P = .03) and a trend for improvement in neurological outcome at D30 (Glasgow-Pittsburgh Outcome Categories = 1.6 +/- 0.8 versus 2.3 +/- 1.1. P = .09). Sternal dislodgements (2.9% versus 0.4%, P = .03) and hemoptysis (5.4% versus 1.3%, P = .01) were more frequent in the ACD ACLS group. CONCLUSIONS: Despite long time intervals, ACD significantly improved short-term survival rates in out-of-hospital cardiac arrests compared with STD CPR.

Adult↗