[Reticulocyte hemoglobin equivalent as a diagnostic marker for the current iron deficiency : Old wine in new bottles]. / Retikulozyten-Hämoglobin-Äquivalent als diagnostischer Marker der aktuellen Eisendefizienz : Alter Wein in neuen Schläuchen.

The reticulocyte hemoglobin equivalent (RET-He) is presented as a biomarker for the diagnostics and monitoring of iron deficiency. The marker is independent of the acute phase and can be determined within a few minutes by a blood count. Due to the approximately 120-day lifetime of erythrocytes, iron deficiency and changes in the iron status of erythropoiesis can first be recognized at a relatively late stage using classical hematological parameters, such as hemoglobin, mean corpuscular volume, mean cellular hemoglobin content and also with determination of hypochromic erythrocytes (% hypo). The RET-He is a cost-effective parameter for the diagnosis and monitoring of the iron supply for erythropoiesis. Reticulocytes, the precursors of mature erythrocytes, are washed out of the bone marrow into the peripheral blood and normally mature within 2 days to mature erythrocytes. The determination of the reticulocyte number therefore enables a timely statement about erythropoiesis. A measurement of the hemoglobin content of reticulocytes therefore reflects the actual iron metabolism of erythropoiesis and enables assessment of the quality of the cells. Changes in the iron status of erythropoiesis can thus be detected much earlier than by determining only the hemoglobin content of mature erythrocytes, i.e. the mean cellular hemoglobin content. It is recommended that the evaluation of RET-He should be carried out as an inexpensive routine preoperative marker of latent anemia in order to identify patients at risk. In the sense of a perioperative prehabilitation and the enhanced recovery after surgery (ERAS) concept, patients with iron deficiency can be treated proactively at an early stage in order to prevent complications and extended hospital stays.

[Costs of delivering allogenic blood in hospitals]. / Kosten der Verabreichung von Blutkonserven im Krankenhaus.

INTRODUCTION: In clinical practice there are medical and economic reasons against the thoughtless use of packed red blood cells (rbc). Therefore, in searching for alternatives (therapy of anemia) the total costs of allogeneic blood transfusions must be considered. Using a practical example this article depicts the actual costs and possible alternatives from the point of view of a hospital in Germany. METHOD: To determine the total costs of allogeneic blood transfusions the actual resource consumption associated with blood transfusions was collated and analyzed at the St. Marien-Hospital in Vechta. RESULTS: The authors were able to show that the actual procurement costs (average. 97 EUR) represent only 55 % of the total costs of 176 EUR. The additional expenses are allocated to personnel (78 %) and materials (22 %). Alternatives, such as i.v. iron substitution or stimulation of erythropoesis might be the more economical solution especially if only purchase prices are compared and the total costs of allogeneic blood transfusions are not considered. DISCUSSION: Analyzing a single hospital limits generalization of the results; however, in the international context the results can be recognized as plausible. So far there have been no comprehensive studies on the true costs of blood preparations, therefore, this article represents a first starting point for closing this gap by conducting additional studies.

Local anesthetic actions on thromboxane-induced platelet aggregation.

UNLABELLED: Some local anesthetics (LA), in concentrations present in blood during IV or epidural infusion, inhibit thrombus formation in the postoperative period. Studies on thromboxane A2 (TXA2) signaling in a recombinant model suggest that interference with TXA2-induced platelet aggregation may explain, in part, the antithrombotic actions of epidural analgesia and IV LA infusion. In this study we investigated the effects of clinically used LAs (lidocaine, ropivacaine, and bupivacaine) on TXA2-induced early platelet aggregation (1-5 s) by using quenched-flow and optical aggregometry. Our findings demonstrate that the LAs tested seem to have only a limited ability to inhibit TXA2-induced platelet aggregation assessed at early times (1-5 s). Therefore, the clinical effects of LAs on thrombi formation are unlikely to be explained by this manner alone. At large LA concentrations, moderate effects were obtained. Prolonged incubation with LA did not significantly increase effectiveness, and the lack of an effect could not be explained by generation of secondary mediators. The results were independent of the anesthetic studied. Local anesthetic effects on TXA2-induced early platelet aggregation (1-5 s) are unlikely to play a major role in the clinically observed antithrombotic effects of local anesthetics. IMPLICATIONS: Local anesthetic effects on thromboxane A2-induced early platelet aggregation (1-5 s) are unlikely to play a major role in the clinically observed antithrombotic effects of local anesthetics. Thus, other potential targets need to be explored.

Effect of different anaesthetic regimes on the oculocardiac reflex during paediatric strabismus surgery.

The oculocardiac reflex (OCR) is induced by mechanical stimulation and therefore is frequently encountered during strabismus surgery. This study was designed to determine how various anaesthetic regimes modulate the haemodynamic effects of the OCR during paediatric strabismus surgery. Thirty-nine patients (4-14 years, ASA I) were randomized to one of four anaesthetic regimes: group P: propofol (12 mg.kg(-1).h(-1)) and alfentanil (0.04 mg.kg(-1).h(-1)); group S: sevoflurane 1-1.2 MAC in 30% O(2)/70% N(2)O; group K: ketamine racemate (10-12 mg. kg(-1).h(-1)) and midazolam (0.3-0.6 mg.kg(-1).h(-1); group H: halothane 1-1. 2 MAC in 30% O(2)/70% N(2)O. Electrocardiogram (ECG), beat-to-beat heart rate (HR) and blood pressure (BP) changes were measured during and after a standardized traction was applied to an external eye muscle (4-6 Newton, 90 s). OCR was defined as a 10% change in HR induced by traction. OCR occurred in 77% of patients. Whereas virtually all patients in the P, H and S groups developed OCR, only 22% developed it in group K. Median HR change in group P (-37 bpm) was significantly greater (P < 0.05) than in group H (-17 bpm) or group K (-7 bpm). Median BP change in group K (+10 mmHg) was significantly different (P < 0.05) from group H (-5 mmHg), group S (-3 mmHg) and group P (-8 mmHg). Atrioventricular rhythm disorders were significantly more frequent in group P compared with group K (P < 0.02). Respiration-induced sinus dysrhythmia was significantly less frequent (P < 0.001) in group K (0%), compared with group P (100%), group H (56%) and group S (55%). Of the anaesthetic techniques studied, ketamine anaesthesia is associated with the least haemodynamic changes induced by OCR during strabismus surgery in paediatric patients.

Ropivacaine attenuates pulmonary vasoconstriction induced by thromboxane A2 analogue in the isolated perfused rat lung.

BACKGROUND AND OBJECTIVES: Thromboxane A2 (TXA2) activation is involved in several pathophysiological states in producing pulmonary hypertension. Local anesthetics (LA) inhibit signaling of TXA2 receptors expressed in cell models. Therefore, we hypothesized that LA may inhibit pulmonary vasoconstriction induced by the TXA2 analogue U 46619 in an isolated lung model. METHODS: Isolated rat lungs were perfused with physiological saline solution and autologous blood with or without the LA lidocaine, bupivacaine, ropivacaine, or the permanently charged lidocaine analogue QX 314 (all 1 microg/mL) as a pretreatment. Subsequently, pulmonary vasoconstriction was induced by 3 concentrations of U 46619 (25, 50, and 100 ng/mL) and the change in pulmonary artery pressure (Pa) was compared with each LA. In a second experiment, Pa responses to angiotensin II (0.1 microg), hypoxic pulmonary vasoconstriction (HPV, 3% O2 for 10 minutes), or phenylephrine (0.1 microg) were assessed to determine the specificity of ropivacaine effects on TXA2 receptors. Finally, reversibility of pulmonary vasoconstriction was determined by adding ropivacaine to the perfusate after pulmonary vasoconstriction was established with U 46619. RESULTS: Ropivacaine, but not bupivacaine, lidocaine, or QX 314 significantly attenuated pulmonary vasoconstriction induced by 50 ng/mL U 46619 (35.9%, P<.003) or 100 ng/mL U 46619 (45.2%, P<.001). This effect of ropivacaine was likely to be specific for the thromboxane receptor because pulmonary vasoconstriction induced by angiotensin II, HPV, or phenylephrine was not altered. Ropivacaine did not reverse vasoconstriction when it was administered after U 46619. CONCLUSIONS: Ropivacaine, but not lidocaine, bupivacaine, or QX 314 at 1 microg/mL, attenuates U 46619-induced pulmonary vasoconstriction in an isolated perfused rat lung model. These results support evidence that the clinically used enantiomer S(-)-ropivacaine may inhibit TXA2 signaling.

Characterization of a receptor subtype-selective lysophosphatidic acid mimetic.

Despite an intriguing cell biology and the suggestion of a role in pathophysiological responses, the mechanism of action of such lipid phosphoric acid mediators as lysophosphatidic acid (LPA) remains obscure, in part because of an underdeveloped medicinal chemistry. We report now the agonist activity of a synthetic phospholipid in which the glycerol backbone of LPA is replaced by L-serine. Like LPA, the L-serine-based lipid mobilizes calcium and inhibits activation of adenylyl cyclase in the human breast cancer cell line MDA MB231. Treatment with LPA desensitizes MDA MB231 cells to subsequent application of the L-serine compound; when the order of application is reversed, however, the L-serine compound does not prevent calcium mobilization by LPA, which might indicate the existence of two LPA receptors in these cells. The analogous D-serine-based phospholipid was distinctly less potent than the L-isomer in those assays; this finding demonstrates stereoselectivity by an LPA receptor. Unlike LPA, the L-serine-based lipid does not evoke a chloride conductance in Xenopus laevis oocytes, but injection of poly(A)+ RNA from HEK 293 cells confers this phenotype on the oocyte. The latter result has practical importance in that it allows use of the frog oocyte for expression cloning of an LPA receptor DNA, an assay system made problematic by the oocyte's strong endogenous response to LPA.