Experimental Studies on the Endothelium Ultrastructure of Heart Capillaries under Moderate (28–30°) and Deep (22–24°) Hypothermia without Perfusion
Ultrastructural changes in endothelial cells (EC) of myocardial capillaries were studied in 24 dogs which underwent hypothermia without perfusion. Biopsy specimens for electron microscopy were taken from the left ventricle of each dog in the control group, during anesthesia (prior to active cooling)...
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Published in: | Microvascular research Vol. 58; no. 3; pp. 250 - 267 |
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Main Authors: | , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Amsterdam
Elsevier Inc
01-11-1999
Elsevier |
Subjects: | |
Online Access: | Get full text |
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Summary: | Ultrastructural changes in endothelial cells (EC) of myocardial capillaries were studied in 24 dogs which underwent hypothermia without perfusion. Biopsy specimens for electron microscopy were taken from the left ventricle of each dog in the control group, during anesthesia (prior to active cooling), and at the end of moderate (28–30°) and deep (22–24°) artificial body cooling. The following morphological types of the EC were identified both in the control group and in all test groups: those with moderately dense cytoplasm, light, dark, and irreversibly damaged cells. Dark cells showed increased numbers of plasmalemmal vesicles and appeared to be more transport-specialized as opposed to other types. In all stages of the experiment the amount of dark cells continuously increased (to 23.80, 34.62, and 47.17%, respectively). On cooling to 28–30°, subcellular manifestation of reduced synthetic activity of organelles (nucleus, Golgi complex, and rough endoplasmic reticulum) was observed in all types of the EC. These changes persisted, or even increased, at the end of deep hypothermia. The transport activity of the EC changed differently in three experimental groups in all cell types. Micropinocytotic activity increased under spontaneous mild hypothermia (34–35°) during anesthesia and tended to decrease with subsequent artificial lowering of the temperature to 22–24°. These ultrastructural changes seem to make up an integral part of the process of capillary endothelium adaptation to body surface cooling, and they might contribute to the development of tolerance to subsequent ischemic exposure during cardiac arrest. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0026-2862 1095-9319 |
DOI: | 10.1006/mvre.1999.2181 |