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  • 1
    German Medical Science GMS Publishing House; Düsseldorf
    In:  130. Kongress der Deutschen Gesellschaft für Chirurgie; 20130430-20130503; München; DOC13dgch113 /20130426/
    Publication Date: 2013-04-27
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 2
    ISSN: 0020-711X
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1435-1420
    Keywords: Key words Emergency surgery – pulmonary embolectomy – vena cava filter
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary  Pulmonary embolism is a common event in hospitalized patients. In most cases, pulmonary embolism is asymptomatic and undergoes spontaneous resolution. Pulmonary embolectomy is required when refractory hypotension persists, despite all resuscitative efforts, and a thrombus has clearly been documented by angiography, computed tomography or magnetic resonance angiography. Embolectomy for massive embolism is performed through median sternotomy with the use of cardiopulmonary bypass. Usually the common pulmonary artery is incised and the emboli are extracted using forceps, suction or Fogarty catheters. For chronic embolisation or if no cardiopulmonary bypass is available, a lateral thoracotomy may be performed. The embolus may be removed after proximal occlusion of the pulmonary artery while normal circulation continues in the opposite lung. In patients with high risk of recurrence, the vena cava inferior may be interrupted or a vena cava filter may be implanted. Postoperatively, systemic anticoagulation should be administered for 3 months or longer depending on the patient’s risk profile. Interventional approaches for the treatment of pulmonary embolism are currently under investigation. Their benefit over surgical embolectomy remains to be established.
    Type of Medium: Electronic Resource
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  • 4
    Publication Date: 2020-11-01
    Description:   Low exercise capacity is a strong predictor of all-cause cardiovascular mortality and morbidity. In contrast, high exercise capacity is protective and “physical fitness” is considered beneficial. These effects seem to be mediated through mitochondrial function. Importantly, exercise capacity consists of an intrinsic (genetic) and an extrinsic (exercise, environmental) part. In humans, these two parts cannot be truly separated. The rat model of high (HCR) and low (LCR) capacity runners allows to distinguish between the two parts. We assessed mitochondrial function in this model, specifically investigating the impact of exercise training on mitochondrial respiratory capacity. HCR and LCR were divided into control and exercised groups. Exercise capacity was determined individually using a ramped test. Animals were trained five times a week for four weeks on a treadmill. Mitochondria were isolated from heart, M. gastrocnemius and liver. Citrate synthase activity and protein content were determined photometrically and respiratory capacity was measured using a Clark-type electrode. At the same age and tibia length, LCR-C were heavier and had a lower heart to body weight ratio than HCR-C. Citrate synthase activity was lower in skeletal muscle of LCR but cardiac citrate synthase was not different between sedentary HCR and LCR. Respiratory capacity in heart and liver was not different between sedentary HCR and LCR but was lower in skeletal muscle in LCR compared to HCR with all selected substrates (glutamate: 86,0±17,6 vs. 63,7±8,0; succinate: 203±19 vs. 136±17 nAO/min/mg Protein). Exercise training led to an increase in body weight in HCR but did not change body weight in LCR. Similarly, gastrocnemius and soleus weights only increased with exercise in HCR. Exercise led to an increase in citrate synthase activity in hearts of HCR (0,78±0,07 vs. 1,58±0,45 U/mg Protein) but not of LCR. Consistently, mitochondrial respiratory capacity was found increased in HCR with exercise in heart with all substrates (glutamate: 261±43 vs. 305±35; succinate 417±32 vs. 539±65 nAO/min/mg Protein). Liver was not affected by exercise. Conclusion Our data suggest that genetic predisposition for aerobic capacity additionally affects the response of mitochondria to exercise. Thus, it may be possible that the “born runner” benefits more from aerobic exercise training than the “less genetically equipped counterpart”. Funding Acknowledgement Type of funding source: None
    Print ISSN: 0195-668X
    Electronic ISSN: 1522-9645
    Topics: Medicine
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