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Biomedical subjects

F Hinder

Publications and source records attributed to F Hinder.

At least 19 recordsLinked to original sources

[Evidence-based infection control methods using spa genotyping for MRSA spread in hospitals].

BACKGROUND AND OBJECTIVE: Isolation of methicillin resistant Staphylococcus aureus (MRSA) often implies rigorous infection control measures. The use of rapid and accurate typing is required to monitor their spread. Prompt identification of epidemic MRSA is crucial to control an outbreak, in order to avoid unnecessary interventions in patients and staff. In this study we evaluated protein A ( spa) gene repeat sequence analysis for MRSA typing in a hospital. METHODS: In 2003, all non-replicate MRSA-strains from staff and patients admitted to the University Hospital Münster (1480 beds), Germany, were spa typed. The spa types were assigned using the Ridom StaphType software. Typing results were correlated with the epidemiological findings of each MRSA isolate. RESULTS: Assignment of spa types was possible for all 175 MRSA isolates and provided rapid (mean, 2 days) typing results. spa typing method yielded 34 spa types. Synchronizing the sequencing results with a central database (http://www.spaServer.ridom.de) created a reproducible and uniform nomenclature for easy intra- and inter-hospital comparisons. CONCLUSION: spa typing makes continuous and fast MRSA typing possible for hospital isolates. The differentiation between outbreaks and accidental accumulations due to imported MRSA was easily possible and allowed implementation of focused and evidence-based infection control measures.

Bacterial Typing Techniques↗

Fat elimination from autologous blood.

Bowl-based autotransfusion devices reduce the amount of fat found in shed blood, but cannot completely eliminate fat particles. When fat is seen on the surface of the processed blood, this blood should be filtered with a leukocyte removal filter before retransfusion.

Blood Transfusion, Autologous↗

The inhibitory effect of bupivacaine on prostaglandin E(2) (EP(1)) receptor functioning: mechanism of action.

Prostaglandin E(2) receptors, subtype EP(1) (PGE(2)EP(1)) have been linked to several physiologic responses, such as fever, inflammation, and mechanical hyperalgesia. Local anesthetics modulate these responses, which may be due to direct interaction of local anesthetics with PGE(2)EP(1) receptor signaling. We sought to characterize the local anesthetic effects on PGE(2)EP(1) signaling and elucidate mechanisms of anesthetic action. In Xenopus laevis oocytes, recombinant expressed PGE(2)EP(1) receptors were functional (half maximal effect concentration, 2.09 +/- 0.98 x 10(-6) M). Bupivacaine, after incubation for 10 min, inhibited concentration-dependent PGE(2)EP(1) receptor functioning (half-maximal inhibitory effect concentration, 3.06 +/- 1.26 x 10(-6) M). Prolonged incubation in bupivacaine (24 h) inhibited PGE(2)-induced calcium-dependent chloride currents (I(Cl(Ca))) even more. Intracellular pathways were not significantly inhibited after 10 min of incubation in bupivacaine. But I(Cl(Ca)) activated by intracellular injection of GTPgammaS (a nonhydrolyzable guanosine triphosphate [GTP] analog that activates G proteins, irreversible because it cannot be dephosphorylated by the intrinsic GTPase activity of the alpha subunit of the G protein) was reduced after 24 h of incubation in bupivacaine, indicating a G protein-dependent effect. However, inositol 1,4,5-trisphosphate- and CaCl(2)- induced I(Cl(Ca)) were unaffected by bupivacaine at any time points tested. Therefore, bupivacaine's effect is at phospholipase C or at the G protein or the PGE(2)EP(1) receptor. All inhibitory effects were reversible. We conclude that bupivacaine inhibited PGE(2)EP(1) receptor signaling at clinically relevant concentrations. These effects could, at least in part, explain how local anesthetics affect physiologic responses such as fever, inflammation, and hyperalgesia during the perioperative period.

Anesthetics, Local↗

Thoracic, but not lumbar, epidural anesthesia improves cardiopulmonary function in ovine pulmonary embolism.

UNLABELLED: We hypothesized that sympathetic stimulation is the main mechanism contributing to hemodynamic failure in pulmonary embolism. We investigated the effects of epidural anesthesia-induced sympathetic blockade, restricted to thoracic and lumbar levels, during pulmonary embolism. Two experiments were performed in chronically instrumented ewes. In the first experiment, six sheep received 6 mL bupivacaine 0.175% (Thoracic Epidural Anesthesia [TEA] group), and six sheep received 6 mL saline 0.9% (TEA-Control group), respectively, via an epidural catheter (T3 level). In the second experiment, six sheep received 2.8 mL bupivacaine 0.375% (Lumbar Epidural Anesthesia [LEA] group), and six sheep received 2.8 mL saline 0.9% (LEA-Control group) epidurally (L4 level). Embolization was performed by IV injection of autologous blood clots (Experiment 1, 0.75 mL/kg; Experiment 2, 0.625 mL/kg). TEA was associated with significantly slower heart rates, decreased mean pulmonary artery pressures and central venous pressures, and significantly higher stroke volume index and oxygenation in comparison with the TEA-Control group. By contrast, LEA was associated with significantly faster heart rates and increased central venous pressures and with a significantly lower stroke volume index in comparison with the LEA-Control group. TEA significantly reduced, and LEA significantly increased, hemodynamic deterioration, suggesting beneficial effects of TEA on cardiopulmonary function during pulmonary thromboembolism. IMPLICATIONS: Thoracic (but not lumbar) epidural anesthesia was associated with beneficial cardiopulmonary effects during experimental pulmonary thromboembolism in sheep.

Anesthesia, Epidural↗

Noradrenaline and nomega-monomethyl-L-arginine (L-NMMA): effects on haemodynamics and regional blood flow in healthy and septic sheep.

This prospective, non-randomized, controlled experimental study looks at the effects of N(omega)-monomethyl-L-arginine (L-NMMA) on haemodynamics, oxygen transport and regional blood flow in healthy and septic sheep, and compares these effects with those of noradrenaline (NA; norepinephrine). All sheep were chronically instrumented. Six sheep received L-NMMA (7 mg.kg(-1).h(-1)), six sheep received NA, and seven sheep received the carrier alone (0.9% NaCl). The NA dosage was continuously and individually adjusted to achieve the same increase in blood pressure as observed in matched sheep of the L-NMMA group (non-septic phase). Treatment was discontinued after 3 h. Sepsis was initiated and maintained by a continuous infusion of live Pseudomonas aeruginosa. After 24 h of sepsis, the sheep were again challenged over a treatment period of 3 h with their previously assigned drug (septic phase). During the non-septic phase of the experiment, NA and L-NMMA both caused an increase in mean arterial pressure (MAP) through vasoconstriction. Ater 24 h of sepsis, all sheep developed a hyperdynamic circulatory state. While L-NMMA caused an increase in MAP through intense vasoconstriction, NA caused MAP to increase through a further elevation of the cardiac index. The NA dosage needed was significantly higher in the septic phase compared with the non-septic phase, reflecting a reduced vascular responsiveness to catecholamines during sepsis. Renal blood flow remained unchanged during either treatment in both the non-septic and the septic phases. Nevertheless, urine output increased during NA treatment in both the non-septic and the septic phases, while L-NMMA caused urine output to increase only under septic conditions.

Animals↗

[Venous paradoxical air embolism].

Paradoxical air embolism may occur with any venous air embolism. Air may either enter the systemic circulation through a patent foramen ovale or through transpulmonary passage of air. While small venous air emboli are mostly well tolerated, even the smallest paradoxical air emboli can have fatal consequences in the systemic circulation. Therapy and prophylaxis of paradoxical air embolism equal those of venous air embolism. This is especially true, since paradoxical air embolism may not become obvious under general anesthesia. More specific therapeutic regiments, such as hyperbaric oxygenation and the infusion of perfluorocarbons, are still in an experimental stage.

Embolism, Air↗

A comparison of transoesophageal echocardiographic Doppler across the aortic valve and the thermodilution technique for estimating cardiac output.

This study was undertaken in order to elucidate the differences between various planes of measurement and Doppler techniques (pulsed- vs. continuous-wave Doppler) across the aortic valve to estimate cardiac output. In 45 coronary artery bypass patients, cardiac output was measured each time using four different Doppler techniques (transverse and longitudinal plane, pulsed- and continuous-wave Doppler) and compared with the thermodilution technique. Measurements were performed after induction of anaesthesia and shortly after arrival in the intensive care unit. Optimal imaging was obtained in 91% of the patients, in whom a total of 82 measurements of cardiac output were performed. The respective mean (SD) areas of the aortic valve were 3.77 (0.71) cm2 in the transverse plane and 3.86 (0.89) cm2 in the longitudinal plane. A correlation of 0.87 was found between pulsed-wave Doppler cardiac output and the thermodilution technique in either transverse or longitudinal plane. Correlation coefficients of 0.82 and 0.84 were found between thermodilution cardiac output and transverse and longitudinal continuous-wave Doppler cardiac output, respectively. Although thermodilution cardiac output is a widely accepted clinical standard, transoesophageal Doppler echocardiography across the aortic valve offers adequate estimations of cardiac output. In particular, pulsed-wave Doppler cardiac output in both the transverse and longitudinal plane provides useful data.

Aged↗

Selective inhibition of inducible nitric oxide synthase: effects on hemodynamics and regional blood flow in healthy and septic sheep.

OBJECTIVES: To investigate the effects of S-ethylisothiourea (S-EITU) on hemodynamics, oxygen transport, and regional blood flow in healthy and septic sheep. DESIGN: Prospective, randomized, controlled experimental study with repeated measures. SETTING: Investigational intensive care unit at a university medical center. SUBJECTS: Eleven healthy, female adult sheep of the Merino breed, divided into a control group (n = 5) and into a group treated with S-EITU (n = 6). INTERVENTIONS: All sheep were chronically instrumented. After a 5-day recovery period, they were randomly assigned to either control or S-EITU groups. While control sheep received only saline, S-EITU was administered in increasing doses of 1, 3, and 9 mg/kg/hr over 1 hr each (nonseptic phase). After 2 days of recovery, a continuous infusion of live Pseudomonas aeruginosa (2.5 x 106 colony-forming units/min) was started in all sheep and maintained for the remainder of the experiment. After 24 hrs of sepsis, the sheep again received their assigned treatment (septic phase). In both the nonseptic and septic phases, the sheep received colored microspheres through a left atrial catheter to allow analysis of regional blood flows. All animals were autopsied at the end of the experiments, and organ probes were removed for blood flow analyses. MEASUREMENTS AND MAIN RESULTS: The administration of S-EITU caused a dose-dependent vasoconstriction in the nonseptic phase. After 24 hrs of Pseudomonas infusion, all sheep developed a hyperdynamic circulatory state, with increased cardiac indices and reduced arterial pressures and systemic vascular resistances. Oxygen extraction decreased significantly, preventing an increase in oxygen consumption, despite an increased oxygen delivery. The hyperdynamic circulation was dose dependently reversed by S-EITU, causing an increase in arterial pressure by peripheral vasoconstriction. Sheep in the control group showed a continuation of the hyperdynamic circulation. The effects of S-EITU on hemodynamics and regional blood flows were comparable under septic and nonseptic conditions. CONCLUSIONS: With the inducible form of nitric oxide synthase expressed under septic, but not under nonseptic conditions, S-EITU was expected to have vasoconstrictive properties only in the septic phase. It produced a comparable vasoconstriction during the nonseptic phase of the experiment. Thus, either S-EITU does not selectively block the inducible nitric oxide synthase in sheep, or other vasodilators besides nitric oxide play an important role in septic vasodilation.

Animals↗

Role of nitric oxide in sepsis-associated pulmonary edema.

Transient pulmonary hypertension after inhibition of nitric oxide synthase (NOS) does not alter pulmonary reflection coefficients or lymph flows in endotoxemic sheep. To test the effects of persistent pulmonary hypertension induced by N omega-nitro-L-arginine methylester (L-NAME) and of inhaled NO on pulmonary edema, 18 sheep (three groups) were chronically instrumented with pulmonary artery catheters, femoral arterial fiberoptic thermistor catheters, and tracheostomy. The awake, spontaneously breathing animals received Salmonella typhi endotoxin (lipopolysaccharide; LPS) (10 ng/kg/ min) for 28 h. After 24 h, an airflow of 6 L/min was delivered through the tracheostomy. One group of animals (L-NAME/air) received L-NAME intravenously (25 mg/kg + 5 mg/kg/h) and breathed air. The second group (L-NAME/NO) was given L-NAME and NO (40 ppm) was added to the airflow. The third group was given NaCl 0.9% and breathed air (NaCl/air). Extravascular lung water was measured through the double-indicator dilution technique. Endotoxemia caused pulmonary edema, which was aggravated by L-NAME. Breathing of NO normalized pulmonary artery pressure (Ppa) and ameliorated pulmonary edema. Inhalation of NO may therefore be a therapeutic option for pulmonary edema associated with pulmonary hypertension.

Administration, Inhalation↗

Inhaled prostaglandin E1 for treatment of acute lung injury in severe multiple organ failure.

UNLABELLED: Acute lung injury is characterized by hypoxemia due to pulmonary ventilation/perfusion-mismatching. I.v. administered prostaglandin E1 (PGE1), a vasodilator with a high pulmonary clearance, has been studied in acute lung injury. Inhalation of the vasodilators nitric oxide and prostacyclin improved oxygenation by selective dilation of the pulmonary vasculature in ventilated lung areas. In the present study, PGE1 inhalation was used for treatment of acute lung injury. Fifteen patients with acute lung injury defined as PaO2/fraction of inspired oxygen (FIO2) <160 mm Hg were treated with PGE1 inhalation in addition to standard intensive care. The drug was continuously delivered via a pneumatic nebulizer. Acute physiology and chronic health evaluation system II and multiple organ failure scores were (mean +/- SEM) 33 +/- 2 and 10 +/- 0.3, respectively. Inhaled PGE1 was administered for 103 +/- 17 h at a dose of 41 +/- 2 microg/h. The PaO2/FIO2 ratio increased from 105 +/- 9 to 160 +/- 17 mm Hg (P < 0.05) and to 189 +/- 25 mm Hg (P < 0.05) after 4 h and 24 h, respectively. PGE1 inhalation decreases in mean pulmonary artery pressure and central venous pressure were not statistically significant. Mean arterial pressure, pulmonary capillary wedge pressure, cardiac output, and heart rate remained unchanged. Intensive care unit mortality was 40%. The present data suggest that inhaled PGE1 is an effective therapeutic option for improving oxygenation in patients with acute lung injury. Whether inhaled PGE1 will increase survival in acute lung injury should be investigated in a controlled prospective trial. IMPLICATIONS: In patients with severe acute lung injury and multiple organ failure, inhaled prostaglandin E1 improved oxygenation and decreased venous admixture without affecting systemic hemodynamic variables. Controlled clinical trials are warranted.

APACHE↗

Assessment of cardiovascular volume status by transoesophageal echocardiography and dye dilution during cardiac surgery.

Conventional evaluation of cardiovascular volume status by filling pressures is unreliable in critically ill patients. Measurements of left ventricular end diastolic area index by transoesophageal echocardiography and of intrathoracic blood volume index by dye indicator dilution are new approaches to this problem. In this study, different indices of cardiovascular volume status were analysed to define their relation during the pronounced haemodynamic changes associated with systemic inflammation after cardiopulmonary bypass. Correlations were performed with left ventricular end diastolic area index, intrathoracic blood volume index, central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP). Data from 15 patients receiving coronary artery bypass grafts were compared after induction of anaesthesia and in the intensive care unit. Spearman's correlation coefficient for perioperative absolute changes in left ventricular end diastolic area index and intrathoracic blood volume index was 0.87 (P < 0.05). However, an increase in intrathoracic blood volume index by 125 mL m-2 was necessary to maintain a baseline left ventricular end diastolic area index. Absolute values of all variables varied widely, with the only significant correlation found between CVP and PCWP. Changes in CVP and PCWP did not correlate with changes in left ventricular end diastolic area index or intrathoracic blood volume index. Provided simultaneous baseline measurements are available and a supranormal intrathoracic blood volume index compensates for the haemodynamic changes in systemic inflammation, left ventricular end diastolic area index and intrathoracic blood volume index may substitute for each other during the evaluation of cardiovascular volume status in patients with stable cardiac function.

Anesthesia↗

Endogenous nitric oxide and the pulmonary microvasculature in healthy sheep and during systemic inflammation.

Nitric oxide (NO) influences microvascular integrity. NO synthase inhibitors are regarded as therapeutic options, but their impact on the pulmonary microvasculature is not well defined. We studied the microvascular effects of the nonselective NO synthase inhibitor N(omega)-nitro L-arginine methylester (L-NAME) in healthy sheep and during systemic inflammation. Permeability analysis was performed in 30 adult ewes with chronic lung lymph fistulas and pulmonary venous occluders. Experiment 1: 20 sheep received Escherichia coli endotoxin (lipopolysaccharide, 10 ng/kg/min) for 32 h. After 24 h of endotoxemia, 10 sheep were given L-NAME (25 mg/kg), and 10 sheep received NaCl 0.9%. Experiment 2: six sheep were treated with L-NAME (25 mg/kg), and four animals received NaCl 0.9%. Endotoxin induced a phasic pulmonary microvascular response with early transiently increased endothelial permeability at 4 h and late normalization of microvascular integrity to large molecules after 24 h. At that time systemic vasodilation had occurred. L-NAME raised pulmonary artery pressure and pulmonary vascular resistance index without signs of increased permeability in either experiment. NO is involved in vascular tone in healthy sheep and during systemic inflammation, but it does not seem to play a role in the integrity of the pulmonary microvascular barrier function to large molecules.

Animals↗

[Prolonged muscle weakness in intensive care patients with special attention to the so-called intensive care polyneuromyopathy].

Generalized muscle weakness in critically ill patients can result in prolonged periods of artificial ventilation and longer stays in the intensive care unit. Both neuropathic (critical illness polyneuropathy) and myopathic (critical illness myopathy) abnormalities seem to play an important role for this prolonged weakness. This article reviews its complex differential diagnosis with special emphasis on the current understanding of the neuromuscular syndromes. An efficient diagnostic plan is necessary for the exclusion of other curable causes of prolonged muscle weakness even in the presence of polyneuromyopathic changes. Psychological support of the patient and prophylaxis of secondary complications of prolonged immobilization are crucial when specific therapy is not possible.

Critical Care↗

The atrial natriuretic peptide receptor antagonist HS 142-1 improves cardiovascular filling and mean arterial pressure in a hyperdynamic ovine model of sepsis.

OBJECTIVE: To test whether systemic vascular resistance and mean arterial pressure increase during the administration of the atrial natriuretic peptide antagonist, HS 142-1, in ovine experimental hyperdynamic sepsis. DESIGN: Prospective trial. SETTING: Research laboratory at a large university medical center. SUBJECTS: Chronically instrumented Merino breed ewes (n = 14). INTERVENTIONS: Continuous infusion of Pseudomonas aeruginosa (2.5 x 10(6) colony-forming units/min) for the experimental period of 48 hrs. One group (HS 142-1) received a continuous infusion of HS 142-1 (3 mg/kg/hr) from 40 to 48 hrs; the remaining sheep ("control") were given the vehicle sodium chloride 0.9%. MEASUREMENTS AND MAIN RESULTS: All sheep developed a hyperdynamic cardiovascular response by 40 hrs that was characterized by low values of systemic vascular resistance index (p < .05) and mean arterial pressure (p < .05), and an increased cardiac index (p < .05). HS 142-1 increased cardiac filling pressures (p < .05) without apparent effects on fluid balance, and was associated with a significantly (p < .05) higher mean arterial pressure than was found in the control group at 44 and 48 hrs. HS 142-1 did not change systemic vascular resistance index. At 44 and 48 hrs, cardiac index values were found to have significantly (p < .05) increased in the animals receiving HS 142-1, when these data were compared with cardiac output values at 40 hrs. CONCLUSION: HS 142-1 increases cardiac filling pressures and maintains mean arterial pressure in hyperdynamic sepsis without reversal of sepsis-induced vasodilation.

Animals↗