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ABSTRACT: We report on a 20-year-old patient with McCune-Albright syndrome suffering from global respiratory insufficiency who required continuous mask ventilation and where intubation had to be avoided. Perivascular axillary anesthesia according to Weber was performed for a double corrective osteotomy of the humerus. During plexus anesthesia the patient was positioned on the non-anesthesized side in a 15 degrees Trendelenburg position. An extension of analgesia was observed up to the complete upper arm region. Using the modified positioning an extension of brachial plexus anesthesia is possible.
Der Anaesthesist 10/2005; 54(9):889-94. · 0.99 Impact Factor
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ABSTRACT: Thoracic epidural analgesia (TEA) provides optimal perioperative anaesthesia and analgesia after thoracic and major abdominal surgery and decreases postoperative morbidity and mortality, mainly by blocking sympathetic nerve fibres. Surgery leads to a stress response characterized by sympathetic arousal, altered balance of catabolic and anabolic hormones, hypermetabolism, negative protein economy, and altered carbohydrate metabolism and immune function. A threefold increase of the plasma level of norepinephrine (noradrenaline) was detected up to 24 hours after surgery. These elevated catecholamine plasma levels are a risk, especially to patients with coronary artery disease, because unlike healthy coronary arteries, the stress response causes a vasoconstriction in arteriosclerotic coronary arteries. TEA results in a vasodilation in stenotic coronary arteries. In patients with instable angina pectoris, TEA reduced the number as well as the duration of episodes of cardiac ischaemia. Furthermore, TEA improves myocardial structure and function after coronary artery bypass grafting. Plasma levels of troponin T and I, as well as of atrial natriuretic peptides, were reduced and echocardiographic parameters of the ventricular wall motion were improved by TEA. Patients showed fewer arrhythmic episodes and postoperative myocardial infarction, and could be extubated earlier. The positive effects of TEA after coronary artery bypass grafting are not limited to a short postoperative period, the 2-year mortality rate also seems to be reduced. Optimized pain control and early mobilization decrease the riskof pulmonary complications, resulting in a shortened stay in intensive care units. In combination with early enteral nutrition, TEA leads to an earlier return of gastrointestinal function. Patients treated with thoracic epidural anaesthesia and analgesia have a better health-related quality of life.
Baillière' s Best Practice and Research in Clinical Anaesthesiology 07/2005; 19(2):201-13.
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ABSTRACT: Bei einem 20-jhrigen Patienten mit McCune-Albright-Syndrom und respiratorischer Globalinsuffizienz mit Dauermaskenbeatmung musste eine Intubationsnarkose vermieden werden. Zur operativen Korrektur einer schwergradigen Oberarmfehlstellung erfolgte eine perivaskulre axillre Plexusansthesie nach Weber. Mit der Lagerung des Patienten auf die nichtbetroffene Seite und Kopftieflagerung von 15 (modifizierte Lagerungstechnik) konnte eine Ausbreitung der Analgesie bis auf die Oberarmregion erreicht werden.We report on a 20-year-old patient with McCune-Albright syndrome suffering from global respiratory insufficiency who required continuous mask ventilation and where intubation had to be avoided. Perivascular axillary anesthesia according to Weber was performed for a double corrective osteotomy of the humerus. During plexus anesthesia the patient was positioned on the non-anesthesized side in a 15 Trendelenburg position. An extension of analgesia was observed up to the complete upper arm region. Using the modified positioning an extension of brachial plexus anesthesia is possible.
Der Anaesthesist 01/2005; 54(9):889-894. · 0.99 Impact Factor
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ABSTRACT: 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 & Analgesia 01/2002; 93(6):1460-5, table of contents. · 3.29 Impact Factor
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ABSTRACT: Although hemoglobin-based oxygen carriers (HBOC) are now being investigated, the effects of HBOC solutions during regional anesthesia have never been analyzed. Therefore, we investigated the hemodynamic changes after HBOC infusion during general anesthesia and thoracic epidural anesthesia. Sheep were assigned to three different groups: a) a control group with six unanesthetized sheep; b) six sheep with a halothane anesthesia (2.0 vol.% in oxygen); and c) six awake sheep with a thoracic epidural anesthesia with bupivacaine. After a period of stabilization, all 18 animals received 100 mg/kg of the HBOC pyridoxalated hemoglobin polyoxyethylene conjugate. The infusion of the HBOC caused a significant increase in mean arterial pressure and pulmonary artery pressure in both the control and epidural anesthesia groups. Anesthesia with halothane reduced the effects of the HBOC-solution on mean arterial pressure but did not abolish the increase in pulmonary artery pressure. Our results demonstrate that vasoconstriction caused by HBOC solutions is not abolished by epidural anesthesia, but halothane anesthesia may alter the hemodynamic effects of HBOC solutions. IMPLICATIONS: We evaluated the effects of epidural anesthesia and halothane anesthesia on the vasoconstrictive properties of a cell-free hemoglobin solution. The vasoconstriction caused by a cell-free hemoglobin solution was similar in unanesthetized sheep and sheep with thoracic epidural anesthesia and was reduced in sheep with halothane anesthesia.
Anesthesia & Analgesia 12/1999; 89(5):1131-6. · 3.29 Impact Factor
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ABSTRACT: The aim of the study was to investigate the effects of the putative protein phosphatase (PP) activator 2,3-butanedione monoxime (BDM) in vascular smooth muscle. BDM concentration-dependently increased PP activity in homogenates of bovine coronary arteries and led to dephosphorylation of various smooth muscle proteins in 32P-labelled bovine aortic smooth muscle cells. In isolated bovine coronary artery rings (CARs) the effects of 10 mmol/l BDM on force of contraction (FOC) under conditions of depolarization by 75 mmol/l KCl and PP inhibition by 100 micromol/l cantharidin were investigated. At the end of contraction experiments CARs were freeze-clamped and myosin light chain (MLC20) phosphorylation was determined by two-dimensional gel electrophoresis. Pretreatment of CARs with BDM reduced KCl-induced FOC to 42+/-4% vs. 118+/-1% (no BDM) and cantharidin-induced FOC to 102+/-2% vs. 120+/-7% (no BDM) compared to a former KCl contraction (= 100%). Moreover, BDM increased the amount of unphosphorylated MLC20 up to 56+/-2% vs. 36+/-5% (no BDM) and 28+/-2% vs. 21+/-1% (no BDM), respectively, demonstrating the central role of MLC20 phosphorylation in initiating smooth muscle contraction. In KCl precontracted CARs BDM decreased FOC to 47+/-4% vs. 100+/-1% (no BDM) but did not affect MLC20 phosphorylation, suggesting an uncoupling of force maintenance and MLC20 phosphorylation. In contrast, BDM neither affected FOC nor MLC20 phosphorylation in CARs precontracted with cantharidin. These results strengthen the hypothesis that PP activation by BDM only occurs on the holoenzyme level, e.g. by affecting regulatory subunits.
Archiv für Experimentelle Pathologie und Pharmakologie 07/1999; 359(6):484-92. · 2.65 Impact Factor
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Critical Care 04/1999; 3:1-2. · 4.93 Impact Factor
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ABSTRACT: 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.
American Journal of Respiratory and Critical Care Medicine 02/1999; 159(1):252-7. · 11.08 Impact Factor
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ABSTRACT: 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.
Anesthesia & Analgesia 05/1998; 86(4):753-8. · 3.29 Impact Factor
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ABSTRACT: Carbon monoxide is hypothesized to be produced by the enzyme heme oxygenase predominantly in liver and spleen, bound to hemoglobin, and excreted by the lungs. Thus, venous carboxyhemoglobin is expected to be higher or equal to arterial carboxyhemoglobin. Unspecific inflammatory stimuli have been shown to induce heme oxygenase in lung tissue possibly leading to pulmonary carbon monoxide production. Arterial and central venous carboxyhemoglobin levels were measured in critically ill patients on the third day of ICU stay (n = 59) as well as in otherwise healthy humans prior to orthopedic surgery (n = 29). Arterial and central venous carboxyhemoglobin were higher in ICU patients than in healthy humans, respectively. In both groups, arterial carboxyhemoglobin was significantly higher than central venous carboxyhemoglobin. The arteriovenous carboxyhemoglobin differences were similar in both groups. The data suggest (a) increased CO-generation in critical illness and (b) pulmonary CO-production in healthy and critically ill humans.
Biochemical and Biophysical Research Communications 03/1998; 244(1):230-2. · 2.48 Impact Factor
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ABSTRACT: The present study compared the effects of nitric oxide (NO) synthase inhibition and NO scavenging with haemoglobin in endotoxaemic sheep.
12 sheep were instrumented for chronic study. Six sheep received LG-nitro-arginine-methylester (L-NAME, 2.5 mg/kg bolus followed by a continuous infusion of 0.5 mg/kg per h), the other 6 sheep received pyridoxalated haemoglobin polyoxyethylene conjugate (PHP, 100 mg/kg bolus followed by a continuous infusion of 20 mg/kg per h).
Haemodynamic and oxygenation parameters were measured in healthy sheep, after infusion of Salmonella typhosa endotoxin (10 ng/kg per min) for 24 h and after infusion of L-NAME or PHP. The infusion of endotoxin resulted in a hypotensive, hyperdynamic circulation. Infusion of L-NAME increased mean arterial pressure (MAP) from 76.1 +/- 4.2 mmHg to normal values of 95.8 +/- 5.7 mmHg (p < 0.05). PHP increased MAP from 73.0 +/- 3.0 to 88.6 +/- 4.7 mmHg (p < 0.05). This increase in MAP was associated in the L-NAME group with a more prominent drop in cardiac index (from 10.2 +/- 0.4 to 7.0 +/- 0.51.min-1.m-2; p < 0.05) than in the PHP group (from 10.7 +/- 0.2 to 9.3 +/- 0.61.min-1.m-2). During the first 90 min of infusion, cardiac index remained lower in the L-NAME group than in the PHP group. The increase in pulmonary vascular resistance was also higher in the L-NAME group.
These results suggest, that at the doses used in the experiment, NO scavenging with PHP has smaller effects on cardiac index and pulmonary vascular resistance than NO synthase inhibition with L-NAME. Therefore, the concept of NO scavenging in hyperdynamic sepsis should be further evaluated.
Intensive Care Medicine 01/1998; 24(1):48-54. · 5.40 Impact Factor
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ABSTRACT: Inhibition of nitric oxide synthase causes intense vasoconstriction. This effect is thought to be dependent on sympathetic nerve activity. Thus, we investigated the vasoconstrictive effects of the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) in sheep, in which a reversible sympathetic block was established by thoracic epidural anesthesia.
Sheep (n = 11) were surgically prepared for chronic study. After at least 5 days of recovery, L-NAME was continuously administered and hemodynamics were monitored. This was done in sheep with and without sympathetic blockade in randomized order.
The vasoconstrictive effects of L-NAME were similar in sheep with and without sympathetic blockade.
The obtained results suggest that the vasoconstrictive properties of nitric oxide synthase inhibitors are independent of sympathetic tone.
Cardiovascular Research 11/1997; 36(1):111-7. · 6.06 Impact Factor
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ABSTRACT: Chronically instrumented awake healthy sheep (n = 6) received the synthetic catecholamine, dopexamine, during or without a background infusion of the nitric oxide synthase inhibitor. L-nitro-arginine-methylester (L-NAME). Three days later, hypotensive-hyperdynamic circulation was induced and maintained by continuous infusion of Salmonella typhosa endotoxin (10 ng/kg per min). After 24 h of continuous endotoxin infusion, the dopexamine L-NAME protocol was repeated. In healthy and endotoxaemic animals with and without nitric oxide synthase inhibition dopexamine caused the same haemodynamic changes: heart rate and cardiac output increased, mean arterial pressure and systemic vascular resistance decreased. L-NAME infusion induced normalisation of the hypotonic-hyperdynamic circulation in endotoxaemic animals. Dopexamine reduced some adverse effects of L-NAME treatment, like increased pulmonary vascular resistance and decreased oxygen delivery. In conclusion the haemodynamic effects of dopexamine are independent of the amount of nitric oxide production. Dopexamine may attenuate some of the adverse effects of nitric oxide synthase inhibition.
European Journal of Pharmacology 09/1997; 333(2-3):181-6. · 2.52 Impact Factor
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ABSTRACT: To investigate the hypothesis that nitric oxide synthase (NOS) inhibition restores the vasopressor response to norepinephrine (NE) in ovine hyperdynamic sepsis, eight sheep were chronically instrumented. In the non-septic portion of the study, NE was titrated to achieve an increase in mean arterial pressure (MAP) by 15 mm Hg ("small dose"). Small-dose NE was repeated 1 h after administration of the NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME; bolus 5 mg/kg, followed by 1 mg.kg-1.h-1). After 3 days of recovery, sepsis was induced by a continuous endotoxin infusion (Salmonella typhosa, 10 ng.kg-1.h-1). Three animals died during this period (data excluded). After 24 h, small-dose NE was given. If MAP increased less than 15 mm Hg, the NE dose was increased to achieve the targeted MAP change ("large dose"). Finally, both doses of NE were given after L-NAME administration. To increase MAP by 15 mm Hg in nonseptic animals, the rate of NE infusion was 0.18 +/- 0.03 microgram.kg-1.min-1 (small dose). During L-NAME infusion, this NE dose increased MAP by 32 +/- 8 mm Hg. In septic animals, small-dose NE increased MAP by only 9 +/- 2 mm Hg (P < 0.05 versus nonseptic state). To increase MAP by 15 mm Hg, the NE dose had to be increased to 0.34 +/- 0.06 microgram.kg-1.min-1 (large dose). During L-NAME infusion, NE administration increased MAP by 16 +/- 2 mm Hg and 28 +/- 4 mm Hg (small and large dose, respectively). Thus, L-NAME restored the vasopressor response to NE in sepsis, and increased the vasopressor response to NE in a similar fashion in healthy and septic sheep.
Anesthesia & Analgesia 12/1996; 83(5):1009-13. · 3.29 Impact Factor
