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  • 1
    Electronic Resource
    Electronic Resource
    Effects of ischaemia and preservation on the ultrastructure of the bronchiolar epithelium (1996)
    Springer
    Virchows Archiv 429 (1996), S. 109-118 
    Details
    ISSN: 1432-2307
    Keywords: Lung-transplantation pathology ; Bronchi-epithelium ; Ischaemia ; Mitochondrial swelling ; Scanning electron microscopy ; Transmission electron microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In ten cases of clinical human single-lung transplantation, the nontransplanted Euro-Collins-preserved contralateral lungs were examined using electron microscopy to determine the effects of ischaemia on the bronchiolar epithelium. Existing structural damage at the time of transplantation was characterized using this approach, and nine nonpreserved canine single lungs were also investigated to identify the impact of ischaemia. The study revealed a significant correlation between the duration of ischaemia and the mitochondrial surface-to-volume ratio, which can serve as a morphometric criterion for mitochondrial damage, in canine lungs. However, this correlation was not found in the human donor lungs. Further examination of human donor lungs showed slight to moderate damage to the endoplasmic reticulum and nuclear chromatin. In addition, various degrees of damage to mitochondrial structure, ranging from inconspicuous to severe, were found. The mitochondrial surface-to-volume ratio can be considered to be a suitable criterion for the quantification of ischaemic damage of the bronchiolar epithelium under experimental conditions. Ultrastructural analysis of human donor lungs revealed intact bronchiolar epithelial cell structures at the time of transplantation, reflecting adequate organ preservation with Euro-Collins solution.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00192433
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  • 2
    Electronic Resource
    Electronic Resource
    The surface to volume ratio of mitochondria, a suitable parameter for evaluating mitochondrial swelling (1990)
    Springer
    Virchows Archiv 416 (1990), S. 305-315 
    Details
    ISSN: 1432-2307
    Keywords: Myocardial ultrastructure ; Mitochondrial swelling ; Stereology ; Correlations of structural parameters ; Cardiac arrest and global ischaemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Cellular changes occuring in the left ventricular myocardium during ischaemia after different methods of cardiac arrest have been evaluated by morphological and morphometric parameters: volume densities of mitochondria (VVMi), sarcoplasm (VVSp), myofibrils (VVMf), surface densities of mitochondria (SVMi). The surface to volume ratio of mitochondria (SVratioMi) has been used as an independent parameter of mitochondrial swelling. Since ischaemic swelling of myocardial cells increases the volume of the reference space and ischaemic swelling of mitochondria decreases the free sarcoplasm, VVMi and VVSp cannot be considered as reliable indicators of the degree of oedema. SVMi/VVMf remains nearly constant after different forms of cardiac arrest, demonstrating the integrity of mitochondrial outer membranes. The inverse linear ratio between SVratioMi and the mean mitochondrial volume indicates that the increase in mitochondrial volume is achieved by surface smoothing. Loss of matrix structure and fragmentation of cristae occur at an SVratioMi of about 5.8, cristolysis at 5.5 to 5.6 and amorphous matrix densities at an SVratioMi of less than 5.5 μm2/μm3. The SVratioMi is a suitable parameter for evaluating mitochondrial swelling both at the onset and during global myocardial ischaemia, independent of the method of cardiac arrest used. It serves as an indicator of the state of structural preservation of mitochondria during ischaemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01605291
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  • 3
    Electronic Resource
    Electronic Resource
    Morphometric evaluation of volume shifts between intra- and extra-cellular space before and during global ischemia (1995)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 241 (1995), S. 319-327 
    Details
    ISSN: 0003-276X
    Keywords: Heart ; Dog ; Cardioplegia ; Cardiac arrest ; Ischemia ; Morphometry ; Interstitial space ; Contraction state ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Background: It is well known that all forms of cardiac arrest lead to global ischemia combined with alterations in cellular and interstitial volume. The aim of this study was to investigate the nature of these alterations with respect to different methods of cardiac arrest and establish the extent of their mutual influence at the onset as well as during the course of global ischemia.Methods: Three tested clinical methods were employed to induce cardiac arrest by a) aortic cross clamping, b) coronary perfusion with the cardioplegic solution St. Thomas, and c) coronary perfusion with the cardioplegic solution histidine-tryptophane-ketoglutarate (HTK). The arrested hearts were subjected to global ischemia at 25°C. The size of the myocytes, as well as the interstitial space of myocytes, was determined morphometrically. The contraction state of myocytes was evaluated according to a score.Results: We found that the degree of contraction, as well as nature of alterations in the cellular and interstitial volumes, depended both on the form of cardiac arrest and on the duration of ischemia. The following relationships were established. High contraction at the onset of ischemia leads to expulsion of fluid from the interstitium between bundles of myocytes into the tissue clefts increasing their size. The decrease in contraction during ischemia leads to narrower tissue clefts. Cellular swelling at the onset of and during ischemia is caused by volume shifts between intracellular and interstitial space. An increase in cellular volume during global ischemia and/or additional contraction reduce the interstitium within bundles of myocytes. Sufficient relaxation and/or interstitial edema enlarge the interstitium.Conclusions: Cellular and intersticial alterations seen at the onset and during the course of ischemia are dependent upon the method of cardiac arrest. Furthermore, a considerable mutual influence is exerted by the alterations in cellular and interstitial spaces. © 1995 Wiley-Liss, Inc.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1092410305
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  • 4
    Electronic Resource
    Electronic Resource
    Cellular distribution patterns of lanthanum and morphometry of rat hearts exposed to different degrees of ischemic stress (1995)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 243 (1995), S. 496-508 
    Details
    ISSN: 0003-276X
    Keywords: Heart ; Ischemia ; Lanthanum ; Tracer ; ESI ; EELS ; Morphometry ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Background: The element lanthanum (La) can be used as a tracer for verification of membrane permeability. The aim of this study was to establish whether (1) distribution of La in the myocardium of rat hearts depends on the degree of ischemic stress and (2) morphometrically determined cell and mitochondrial swelling correlates with the La distribution.Materials and Methods: Isolated beating rat hearts were arrested by coronary perfusion with the cardioplegic solution Custodiol® (controls) or by aortic cross clamping followed by exposur to different degrees of ischemic stress. The solutions for perfusion-and postfixation as well as for rinsing contained 1.1% La(NO3)3. Cellular and mitochondrial swelling were determined morphometrically and myocytes exhibiting intracellular La were quantified and stated as percentage of test fields.Results: Immediately after cardiac arrest La was present as precipitates only in a few myocytes adjacent to the outer mitochondrial membrane as seen by cTEM and ESI. In such cells La was also detected by EELS in mitochondrial matrix and myofibrils. Advanced ischemic stress led to an increase of the percentage of myocytes containing detectable intracellular La. After 45 min ischemia at 30°C, myocytes and mitochondria showed a remarkable edema and different intracellular distribution patterns of La. After 90 min of ischemia at 20°C interruptions of sarcolemma could only be detected in a few of the swollen myocytes. Roundish La granules were seen in the myofibrils. The percentage of myocytes containing intracellular La and the extent of cellular and mitochondrial swelling showed a significant correlation.Conclusions: Patterns of intracellular La distribution depend on the degree of ischemic stress and correspond to the degree of cellular as well as mitochondrial edema. These results point at a direct relation between alterations of membrane permeability and development of edema. © 1995 Wiley-Liss, Inc.
    Additional Material: 9 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1092430412
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