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1.
Anaesthesist ; 69(5): 316-322, 2020 05.
Article in German | MEDLINE | ID: mdl-32333024

ABSTRACT

The current coronavirus disease 2019 (Covid-19) pandemia is a highly dynamic situation characterized by therapeutic and logistic uncertainties. Depending on the effectiveness of social distancing, a shortage of intensive care respirators must be expected. Concomitantly, many physicians and nursing staff are unaware of the capabilities of alternative types of ventilators, hence being unsure if they can be used in intensive care patients. Intensive care respirators were specifically developed for the use in patients with pathological lung mechanics. Nevertheless, modern anesthesia machines offer similar technical capabilities including a number of different modes. However, conceptual differences must be accounted for, requiring close monitoring and the presence of trained personnel. Modern transport ventilators are mainly for bridging purposes as they can only be used with 100% oxygen in contaminated surroundings. Unconventional methods, such as "ventilator-splitting", which have recently received increasing attention on social media, cannot be recommended. This review intends to provide an overview of the conceptual and technical differences of different types of mechanical ventilators.


Subject(s)
Anesthesia, General , Coronavirus Infections , Critical Care , Pandemics , Pneumonia, Viral , Respiration, Artificial/instrumentation , Ventilators, Mechanical , Betacoronavirus , COVID-19 , Coronavirus Infections/epidemiology , Coronavirus Infections/therapy , Humans , Pneumonia, Viral/epidemiology , Pneumonia, Viral/therapy , SARS-CoV-2
2.
Acta Anaesthesiol Scand ; 60(1): 103-16, 2016 Jan.
Article in English | MEDLINE | ID: mdl-26190257

ABSTRACT

BACKGROUND: Late ischemic preconditioning is mediated via nuclear transcription factor signal transducer and activator of transcription 3 (STAT3). Pim-1 kinase reduces infarct size in cardiomyocytes and is regulated by STAT3. We tested the hypothesis that late desflurane-induced preconditioning (DES-SWOP) is mediated via STAT3 and Pim-1. METHODS: After institutional approval, pentobarbital-anesthetized male C57BL/6 mice were subjected to 45 min coronary artery occlusion (CAO) and 3 h reperfusion. Control animals received no additional intervention. Desflurane was administered 48 h before CAO either alone or in combination with the janus kinase/STAT3 inhibitor AG-490 (40 µg/g i.p., 20 min before desflurane administration) or the Pim-1 kinase inhibitor II (PIM-Inh.II, 10 µg/g i.p., 15 min before CAO). Infarct size (IS) and area at risk were determined with triphenyltetrazolium chloride and Evans blue, respectively. Additionally, cytosolic and nuclear fractions were separated at two different time points and expression of STAT3, phospho-STAT3(Ser727) , phospho-STAT3(Tyr705) , Pim-1, Bad and phospho-Bad(Ser112) were determined by Western Blot analysis. Data were analyzed with one-way or two-way ANOVA and post hoc Duncan test and are presented as mean ± SEM. RESULTS: IS was 47 ± 2% (n = 7-8 per group) in control animals (CON). DES-SWOP reduced myocardial infarct size to 23 ± 4%* (*P < 0.05 vs. CON). AG-490 alone did not affect myocardial infarct size (44 ± 7%), but abolished DES-SWOP (44 ± 4%). Blockade of Pim-1 did not affect the protection by DES-SWOP (34 ± 4%*). Desflurane reduced cytosolic content and enhanced nuclear content of phospho-STAT(S) (er727) . After 48 h, desflurane enhanced Pim-1 activity, whereas Pim-1 expression remained unchanged. CONCLUSION: These data suggest that DES-SWOP is mediated by activation and nuclear translocation of STAT3. The impact of Pim-1 in DES-SWOP signaling remains unclear.


Subject(s)
Anesthetics, Inhalation/pharmacology , Ischemic Preconditioning, Myocardial , Isoflurane/analogs & derivatives , Proto-Oncogene Proteins c-pim-1/metabolism , STAT3 Transcription Factor/metabolism , Animals , Blood Pressure , Desflurane , Heart Rate , Isoflurane/pharmacology , Male , Mice , Mice, Inbred C57BL , Myocardial Infarction/pathology , Myocardial Infarction/prevention & control , Myocardial Reperfusion , Proto-Oncogene Proteins c-pim-1/drug effects , STAT3 Transcription Factor/antagonists & inhibitors , STAT3 Transcription Factor/drug effects , Tyrphostins/pharmacology , bcl-Associated Death Protein/metabolism
3.
Acta Anaesthesiol Scand ; 56(7): 904-13, 2012 Aug.
Article in English | MEDLINE | ID: mdl-22385356

ABSTRACT

BACKGROUND: Anaesthetic-induced (APOST) and ischaemic postconditioning (IPOST) against myocardial infarction are mediated via phosphatidylinositol-3-kinase/Akt. Pim-1 kinase is acting downstream of Akt and has recently been demonstrated to enhance cardiomyocyte survival. We tested the hypothesis that both APOST and IPOST are mediated by Pim-1 kinase. METHODS: Pentobarbital-anaesthetized male C57BL/6 mice were subjected to 45-min coronary artery occlusion (CAO) and 3-h reperfusion. Animals received either no intervention, the Pim-1 kinase inhibitor II (10 µg/g intraperitoneally) or its vehicle dimethy sulfoxide (10 µl/g intraperitoneally). Three minutes prior to the end of CAO, 1.0 minimum alveolar concentration desflurane was administered for 18 min alone or in combination with Pim-1 kinase inhibitor II. IPOST was induced by three cycles of each 10-s ischaemia/reperfusion, and animals received either IPOST alone or in combination with Pim-1 kinase inhibitor II. Infarct size was determined with triphenyltetrazolium chloride and area at risk with Evans blue. Protein expression of Pim-1 kinase, Bad, phospho-Bad(Ser112) and B-cell lymphoma 2 was determined using Western immunoblotting analysis. RESULTS: Infarct size in control animals (CON) was 46 ± 3%. Dimethylsulfoxide (47 ± 3%) and Pim-1 kinase inhibitor II (44 ± 5%) did not significantly reduce infarct size. Desflurane (16 ± 2%*; *P < 0.05 vs. CON) and IPOST (21 ± 2%*) significantly reduced infarct size compared with CON. Inhibition of Pim-1 kinase abolished desflurane-induced postconditioning (46 ± 4%) and IPOST (44 ± 5%). Western blot analysis revealed that only desflurane enhances phosphorylation of Bad at serine 112 that was abrogated by Pim-1 kinase inhibitor II. CONCLUSION: These data suggest that Pim-1 kinase mediates both desflurane-induced postconditioning and IPOST in mice.


Subject(s)
Anesthetics, Inhalation/therapeutic use , Ischemic Postconditioning/methods , Isoflurane/analogs & derivatives , Proto-Oncogene Proteins c-pim-1/physiology , Anesthetics, Inhalation/administration & dosage , Anesthetics, Inhalation/pharmacology , Animals , Desflurane , Gene Expression Regulation/drug effects , Genes, bcl-2 , Injections, Intraperitoneal , Isoflurane/administration & dosage , Isoflurane/pharmacology , Isoflurane/therapeutic use , Male , Mice , Mice, Inbred C57BL , Myocardial Infarction/pathology , Phosphorylation/drug effects , Protein Kinase Inhibitors/pharmacology , Protein Processing, Post-Translational/drug effects , Proto-Oncogene Proteins c-bcl-2/biosynthesis , Proto-Oncogene Proteins c-pim-1/antagonists & inhibitors , Pyridines/pharmacology , Random Allocation , Signal Transduction/drug effects , bcl-Associated Death Protein/biosynthesis , bcl-Associated Death Protein/genetics
4.
Br J Anaesth ; 108(4): 594-601, 2012 Apr.
Article in English | MEDLINE | ID: mdl-22315330

ABSTRACT

BACKGROUND: Desflurane (DES)-induced preconditioning is mediated by large-conductance calcium-activated potassium channels (BK(Ca)). Whether BK(Ca) are involved in anaesthetic-induced post-conditioning is unknown. We tested the hypothesis that DES-induced post-conditioning is mediated by BK(Ca) upstream of the mitochondrial permeability transition pore (mPTP). METHODS: Pentobarbital-anaesthetized male C57Black/6 mice were subjected to 45 min coronary artery occlusion (CAO) and 3 h reperfusion. Animals received either no intervention or dimethylsulphoxide (DMSO, 10 µl g(-1)). DES (1.0 MAC, 7.5 vol%) was administered for 18 min, starting 3 min before the end of CAO. The following agents were given either alone or in combination with DES: the BK(Ca) activator NS1619 (1 µg g(-1)), the BK(Ca) inhibitor iberiotoxin (IbTx, 0.05 µg g(-1)), the mPTP opener atractyloside (ATRA, 25 µg g(-1)), and the mPTP inhibitor cyclosporine A (CYC A, 10 µg g(-1)). Infarct size (IS) was determined with triphenyltetrazolium chloride and the area at risk with Evans Blue, respectively. RESULTS: IS in control animals was 48(6)%. Neither DMSO, IbTx nor ATRA affected myocardial IS. DES alone or NS1619 alone or the combination reduced IS (P<0.05), CYC A alone or in combination with IbTx or DES also reduced IS (P<0.05). DES-induced reduction of myocardial IS was completely abolished by IbTx and was partially blocked by ATRA and ATRA partially blocked IS reduction by NS1619. CONCLUSIONS: These data suggest that DES-induced post-conditioning against myocardial infarction is mediated by BK(Ca) and mPTP. Cardioprotection by BK(Ca) activator NS1619 might occur, at least in part, independently of mPTP.


Subject(s)
Anesthetics, Inhalation/pharmacology , Isoflurane/analogs & derivatives , Mitochondrial Membrane Transport Proteins/metabolism , Myocardial Infarction/metabolism , Myocardial Infarction/prevention & control , Potassium Channels, Calcium-Activated/metabolism , Analysis of Variance , Animals , Desflurane , Disease Models, Animal , Ischemic Preconditioning, Myocardial/methods , Isoflurane/pharmacology , Male , Mice , Mice, Inbred C57BL , Mitochondrial Permeability Transition Pore
5.
Pathol Res Pract ; 188(8): 1083-7; discussion 1087-90, 1992 Dec.
Article in English | MEDLINE | ID: mdl-1300603

ABSTRACT

In a 50-year-old man without bronchopulmonary symptoms a round mass lesion close to the hilum of the right lung was detected in a routine chest x-ray and confirmed by computed tomography. Histological examination of two biopsy specimens did not result in a definitive diagnosis. Therefore thoracotomy with enucleation of the focus was performed. The histological picture of the lesion is characterized by connective tissue proliferation, multinucleated giant cells, ossification, localised hemorrhage, deposits of hemosiderin and foci of foam cells. The findings are interpreted as a giant cell granuloma of the lung.


Subject(s)
Granuloma, Giant Cell/pathology , Lung Diseases/pathology , Granuloma, Giant Cell/diagnostic imaging , Humans , Lung Diseases/diagnostic imaging , Male , Middle Aged , Radiography
6.
Pneumologie ; 43(1): 32-5, 1989 Jan.
Article in German | MEDLINE | ID: mdl-2710766

ABSTRACT

We describe the case of a 53-year-old woman patient with recurrent attacks of fever, in whom, both roentgenologically and computer-tomographically, a shadow was found in the anterior upper lobe segment of the right lung, and a presumptive diagnosis of a tumour in underlying retention pneumonia was established. For this reason, this segment was resected. The histologic work-up of the surgical specimen revealed bronchocentric granulomatosis. The clinical and morphological findings, together with differential diagnostic considerations of this relatively rare disease, are discussed.


Subject(s)
Granuloma, Giant Cell/pathology , Lung Diseases/pathology , Biopsy , Diagnosis, Differential , Female , Humans , Middle Aged , Pulmonary Alveoli/pathology
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