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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ultrastructure of the rat fasciculata cells in stress situations, such as catabolism and hypothermia was compared descriptively and quantitatively by stereological methods with that of the nonstimulated rat fasciculata cell. The volume and surface densities are expressed per cm3 of cytoplasm, mitochondria and smooth endoplasmic reticulum. Furthermore, absolute values are given. In both stress situations the volume density of the mitochondria compared to the controls is enlarged significantly (H: 37% CA: 50%). The significant increase of the average single mitochondrium of the fasciculata cell (H: 58% CA: 58%) shows a real growth of the mitochondria in these stress situations. Also the surface density of the mitochondrial inner membranes--the mitochondrial enzymes for steroid genesis are partly located in these membranes--shows a significant increase (H: 31%, CA: 84%). Whereas the volume density of the smooth endoplasmic reticulum remains unchanged, the surface density is significantly raised (H: 44%, CA: 60%). An attempt was made to draw up a relationship between stereological and known biochemical data of steroid genesis within the fasciculata cell. An activation in both stress situations could be observed. The stereological data reflect a subcellular reaction pattern, which is similar to exogenous ACTH administration, thus indicating an endogenous ACTH liberation due to these stress conditions.
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PMID:Stereological study of the zona fasciculata of the adrenal cortex in stress situations (hypothermia, catabolism). 73 37

In rats, restraint for 48 h elicits hepatic glycogen depletin, autophagy and other ultrastructural changes (e.g. mitochondrial enlargement and rough endoplasmic reticulum disorganization) associated with marked hypothermia. By restoring the body temperature of these animals, all the hepatocytic alterations are abolished.
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PMID:Temperature-dependence of stress-induced hepatic autophagy. 86 91

The left adrenal medullas of 20 (5 litters of 4) day-old dogs were studied with the electron microscope. The right adrenal medullas of the same animals had been examined by fluorescence microscopy and the results reported previously. In each litter one animal served as a coenothermic (37 degrees C) and one a hypothermic control (15 degrees C). The third animal (at 37 degrees C) was asphyxiated until twice its time of last gasp (about 32 min) and the fourth was cooled to 15 degrees C and asphyxiated for the same length of time as the third animal. The induction of hypothermia (to 15 degrees C) in unanesthetized puppies results in a decrease (32%) in dense-cored granules, an enlargement of mitochondria, and slight dilation of the endoplasmic reticulum. In coenothermic puppies asphyxiation to twice the time of last gasp is accompanied by the following changes: loss of dense-cored granules (52%); swelling of nuclei; clumping and marginal aggregation of nuclear chromatin material; dilation of the endoplasmic reticulum; swelling, loss of cristae and rarefaction of the matrices of mitochondria. The changes in some cells were greater than others. Many of these changes are considered to demonstrate anoxic damage. Under the conditions of the present experiments, hypothermia protected most of the adrenal medullary cells from anoxic damage.
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PMID:Electron microscopy of the adrenal medulla of the newborn dog under hypothermia and asphyxia. 117 93

As basic studies of hyperthermia and hypothermia on malignant tumor, the kinetics of proliferative activity, the morphologic changes in the two cell lines, SGF-3 and SGF-5, established in our department after the change of culture temperature were examined. The results obtained were: a) A significant difference was found in the sensitivity to temperatures between the two cell lines originated from human esophageal squamous cell carcinoma. The temperature range allowing cultured cell to proliferate were from 31 degrees to 39 degrees C in SGF-3 and from 29 degrees to 41 degrees C in SGF-5. b) Minor difference occurred in the results between the two cell lines examined during the recovery of proliferative activity, but no proliferative activity was discovered after the cells were exposed to 42 degrees C for 72 h. Two cell lines resumed their proliferation after having been exposed to 27 degrees or 28 degrees C for 72 h. c) Morphologic changes of the cell lines cultured at high temperature were cytoplasmic vacuolation and cell aggregation by phase contrast microscope and the increase of heterochromatin, the decrease of granular formation in nucleoli, and nucleolar vacuolation by transmission electron microscopy (TEM). At low temperatures the changes observed included cytoplasmic ballooning and circumnuclear halo formation by phase contrast microscope, and the increase of heterochromatin, nucleolar segregation, swelling of mitochondria, and dilatation of rough endoplasmic reticulum (rER) by TEM.
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PMID:Temperature sensitivity on proliferation and morphologic alteration of human esophageal carcinoma cells in culture. 231 1

Circulatory arrest to the lumbar spinal cord of adult cat was produced by occlusion of the descending aorta and concurrent arterial hypotension. Local hypothermia of the cord was induced by paraffin oil at 5 C, which was circulated over the exposed surface of the cord, using the laminectomy wound as a trough. Intramedullary temperature was 15 C at a depth of 5 mm. In 10 control animals oil at 37 or 5 C was circulated over the exposed cords (normal-normothermic and normal-hypothermic controls with 1 and 2 hours hypothermia). Three animals had circulatory arrest and recirculation in normothermia (ischemic-normothermic) and 3 in hypothermia (ischemic-simultaneous hypothermia). Three had circulatory arrest and 15 minutes of recirculation in normothermia followed by 1 hour of hypothermia (ischemic-delayed hypothermia). The medial and lateral portions of the anterior gray horns of the last lumbar spinal segment were studied in the light and electron microscopes. Ischemic-normothermic tissue showed 20% shrinkage in mean areas of neuronal perikarya and massive "watery" swelling of astrocytic cell bodies and processes. Within neuronal perikarya and dendrites, cytoplasm increased in electron density, ribosomes dispersed, Golgi apparatus swelled and mitochondria swelled with loss of matrix density and disruption of cristae. Axons and axon terminals did not increase in size, but mitochondria within these structures doubled in size without loss of matrix density or change in pattern of cristae. Synaptic vesicles were no longer uniform in size, and they were clumped away from the synaptic cleft and diminished in number. Lysosomes were unchanged in appearance and size. Mitochondria of astrocytes underwent approximately fourfold enlargement without loss of matrix density or pattern of cristae. Bundles of astrocytic microfilaments were fragmented, spread apart and diminished in quantity. Oligodendroglia and endothelial cells were unchanged. Normal-hypothermic animals were similar to normal-normothermic except for clefts in rough endoplasmic reticulum of neurons and dendrites. These clefts were formed by a separation of the cisternal membrane from the adjacent row of ribosomal rosettes. Ischemic-simultaneous hypothermia animals had findings identical to normal-hypothermic animals. Ischemic-delayed hypothermia animals were similar to ischemic-normothermic animals except for less swelling of astrocytic processes, greater swelling of astrocytic mitochondria and less alteration of microfilaments. The findings show that ischemia in normothermia brings about alterations in virtually every organelle of the neurronal perikaryon except the lysosome. Simultaneous hypothermia in ischemia prevents the protean alterations of ischemia, whereas hypothermia delayed until after the ischemic episode only slightly modifies the cellular lesions found in ischemic-normothermic animals.
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PMID:Electron microscopy of cat spinal cord subject to circulatory arrest and deep local hypothermia (15 C). 472 89

An ultrastructural, morphologic and histochemical study was made on the livers of rats exposed to eight different acute stressors: fasting, cortisol injecions, reserpine injections, restraint, spinal cord transection, immersion in hot water, exposure to cold and forced muscular exercise in a revolving drum. After 48 hours of exposure to stress, electron microscopy of the liver revealed rough endoplasmic reticulum fragmentation and dilatation, glycogen depletion, and mitochondrial enlargment. The most striking change, however, was an increase in the number and size of autophagic vacuoles which were limited by single or multiple membranes. A cytochemical study revealed that in the former case, the vacuolar membranes did not show a glucose-6-phosphatase positive reaction, whereas they did in the latter case. The vacuoles contained acid phosphatase positive material as well as organelles in various stages of degradation. Following exposure to most of the stressors, a marked increase of plasma corticosterone was noted, with a lowered rectal temperature and the appearance of the typical stress triad (adrenal hypertrophy, thymicolymphatic involution and gastrointestinal ulcers). The severity of the morphologic changes appeared to parallel the degree of hypothermia caused by the stressor. The results suggest that autophagy in the liver may be an adaptive response to stressors at the subcellular level.
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PMID:Liver ultrastructure during acute stress. 743 33

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 degrees ) and deep (22-24 degrees ) 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 degrees, 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 degrees ) during anesthesia and tended to decrease with subsequent artificial lowering of the temperature to 22-24 degrees. 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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PMID:Experimental studies on the endothelium ultrastructure of heart capillaries under moderate (28-30 degrees) and deep (22-24 degrees) hypothermia without perfusion. 1052 68

Intracellular Ca(2+) homeostasis is a prerequisite for a healthy cell life. While cells from some mammals may suffer dysregulation of intracellular Ca(2+) levels under certain deleterious and stressful conditions, including hypothermia and ischemia, cells from mammalian hibernators exhibit a remarkable ability to maintain a homeostatic intracellular Ca(2+) environment. Compared with cells from non-hibernators, hibernator cells are characterized by downregulation of the activity of Ca(2+) channels in the cell membrane, which helps to prevent excessive Ca(2+) entry. Concomitantly, sequestration of Ca(2+) by intracellular Ca(2+) stores, especially the sarcoplasmic/endoplasmic reticulum, is enhanced to keep the resting levels of intracellular Ca(2+) stable. An increase in stored Ca(2+) in heart cells during hibernation ensures that the levels of Ca(2+) messenger are sufficient for forceful cell contraction under conditions of hypothermia. Maintenance of Na(+) gradients, via Na(+)-Ca(2+) exchangers, is also important in the Ca(2+) homeostasis of hibernator cells. Understanding the adaptive mechanisms of Ca(2+) regulation in hibernating mammals may suggest new strategies to protect nonhibernator cells, including those of humans, from Ca(2+)-induced dysfunction.
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PMID:Adaptive mechanisms of intracellular calcium homeostasis in mammalian hibernators. 1220 Mar 99

Cold ischemia--warm reperfusion (CI/WR) injury of liver transplantation involves hepatocyte cell death, the nature and underlying mechanisms of which remain unclear. Isolated hepatocytes and isolated perfused livers were used to determine the prevalence of necrosis and apoptosis as well as mitochondrial dysfunction. In isolated cells, propidium iodide and Hoechst 33342 staining showed a cold-storage, time-dependent increase in necrosis, whereas apoptosis was minimal even after 48 h of hypothermia. Nonetheless, a progressive loss of mitochondrial membrane potential was observed. Translocation of mitochondrial cytochrome c toward microsomes occurred within 24 h of CI/WR, with cytochrome c reaching the cytosol later. Mitochondria isolated from whole livers subjected to CI/WR also display reduced metabolic parameters and increased susceptibility to swelling. These events are associated with increased activity of major initiator (caspase 9) and effector (caspase 3) caspases. The results demonstrate that CI/WR induces mitochondrial dysfunction in isolated cells and in the whole organ; only in the latter is that sufficient to trigger the classical mitochondrial pathway of apoptosis. Our study also provides evidence for the involvement of endoplasmic reticulum stress in CI/WR hepatocyte injury. Combined protection of mitochondria and endoplasmic reticulum may thus represent an innovative therapeutic avenue to enhance liver graft viability and functional integrity.
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PMID:Implication of mitochondrial dysfunction and cell death in cold preservation--warm reperfusion-induced hepatocyte injury. 1690

The conditions of the protein-synthesizing system in neurons of the hippocampus (areas CA1 and C A3) and of the cortex (sensomotor region) in rats subjected to y-irradiation at a dose of 8 Gy under hypothermia (16 - 18 degrees C) and hypoxia-hypercapnia were investigated by fluorescent and electron microscopy. Under hypothermia, the protein-synthesizing system was shown to be damaged to a lesser degree and to be restored faster in comparison with similar neurons in rats irradiated at room temperature. In rats irradiated under hypothermia, the rRNA biogenesis and the protein-synthesizing activity of polyribosomes were restored in two days. The protective influence of hypothermia did not spread to changes in membrane structures (endoplasmic reticulum and Golgy apparatus); i.e., a partial loss of integrity and possible transformation of their structure caused by the irradiation and the restoration of these structures occurred at a lower rate.
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PMID:[Protective effect of hypothermia on brain neurons of rats exposed to ionizing radiation]. 1763 50


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