The use of fluorescent-protein conjugates for staining brain capillaries in hypo- and hyperthermia (26–42°)

Metzger, Hermann; Brüggemann, Helmut; Plewnia, Anke

doi:10.1016/0026-2862(87)90064-1

Cited by 5 publications

(2 citation statements)

References 12 publications

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“…13 Given that the 1 H ADC for H 2 O in rat brain is roughly 1ϫ10 Ϫ3 mm 2 /s, and assuming that the proportionality is maintained, we estimate the ADC for Na ϩ in vivo to be 0.55ϫ10 Ϫ3 mm 2 /s. In reperfused cortex, the average distance between active capillaries is 50 m, 14 and it would take Ϸ1 second for Na ϩ to diffuse into the intervening space. In unperfused cortex, the distance to the nearest collateral vessel is Ϸ0.5 mm, and it would take 8 minutes for Na ϩ to permeate the ischemic tissue.…”

Section: Na Imagesmentioning

confidence: 99%

Direct, Longitudinal Comparison of ¹ H and ²³ Na MRI After Transient Focal Cerebral Ischemia

Lin

Song

Miller

et al. 2001

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Background and Purpose — 23 Na MRI may offer new insight into the evaluation of tissue injury. We performed a direct, longitudinal, morphological comparison of 1 H T2 relaxation, 1 H apparent diffusion coefficient (ADC), 23 Na content, and histopathology after cerebral ischemia to address the hypotheses that (a) 23 Na MRI is unique in comparison to 1 H MRI, and (b) accumulation of 23 Na is an unambiguous marker for dead tissue. Methods —Rats underwent 30 minutes of focal ischemia. MRIs of 1 H T2, 1 H ADC, and 23 Na content were acquired from 12 hours up to 1, 2, or 14 days after reperfusion. On excision, brains were stained with triphenyltetrazolium chloride (TTC). Results —In all cases, the region of abnormality increased in size for 2 days. On day 5, both 1 H T2 and ADC temporarily appeared normal despite the presence of TTC-defined infarction. By comparison, the volume of tissue exhibiting abnormally intense 23 Na signal mirrored the TTC-defined infarct at all time points. Conclusions —Regions of high 23 Na content correlate well with the TTC-defined infarct and may be a quantitative in vivo marker for dead tissue. In contrast, the dynamics of the 1 H T2 and ADC make it difficult to interpret these images without additional information because they may appear normal despite infarction. Neither type of 1 H image delineates dead tissue, and none of these methods predicts the potential infarct size at early time points.

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Section: Na Imagesmentioning

confidence: 99%

Direct, Longitudinal Comparison of ¹ H and ²³ Na MRI After Transient Focal Cerebral Ischemia

Lin

Song

Miller

et al. 2001

Stroke

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“…While the experimental evidence of a significant microhemodynamic impact seems poor at present for the first of these two factors, the enhanced capability of white blood cells and platelets to adhere to the vascular endothelium may lead to an elevation of local flow resistance and thereby enhance perfusion heterogeneity [15]. The latter phenomenon could be of particular significance during a chronic exposure to low temperatures, because the microvasculature would be plugged by blood cells, resulting in tissue hypoxia [12,23]. The mechanism of such microvascular occlusion, however, remains obscure, because an analysis of capillary ultrastructure during chronic, repeated cold exposure is not available.…”

Section: Introductionmentioning

confidence: 99%

Microvascular ultrastructure in non-freezing cold injuries

1990

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The effects of repeated local exposure to cold on the integrity of the subcutaneous microcirculation were studied in a model using a transparent tissue chamber implanted into a dorsal skin fold of Syrian hamsters. A detailed study of the vascular ultrastructure within the chamber revealed the following features: Endothelial damage was prominent in true capillaries and venous vessels, while arterioles remained unaffected. The endothelial lining appeared extremely attenuated around the entire vascular perimeter causing the development of "gaps", some of which contained leukocytes or platelets. Smaller vessels were often completely filled with blood cells with leukocytes integrated into the endothelial wall. Fibrin was never observed within these occluded vessels. Finally, only veil-like remnants of the endothelium persisted, and compressed erythrocytes were still mimicking the original vascular outline. It is concluded that the ultrastructural changes observed after a repeated non-freezing cold injury closely resemble those observed during ischemia/reperfusion injury.

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Measurement of cerebral capillary perfusion with a fluorescent label

Weiss¹

1988

Microvascular Research

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The use of fluorescent-protein conjugates for staining brain capillaries in hypo- and hyperthermia (26–42°)

Cited by 5 publications

References 12 publications

Direct, Longitudinal Comparison of ¹ H and ²³ Na MRI After Transient Focal Cerebral Ischemia

Direct, Longitudinal Comparison of ¹ H and ²³ Na MRI After Transient Focal Cerebral Ischemia

Microvascular ultrastructure in non-freezing cold injuries

Measurement of cerebral capillary perfusion with a fluorescent label

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The use of fluorescent-protein conjugates for staining brain capillaries in hypo- and hyperthermia (26–42°)

Cited by 5 publications

References 12 publications

Direct, Longitudinal Comparison of 1 H and 23 Na MRI After Transient Focal Cerebral Ischemia

Direct, Longitudinal Comparison of 1 H and 23 Na MRI After Transient Focal Cerebral Ischemia

Microvascular ultrastructure in non-freezing cold injuries

Measurement of cerebral capillary perfusion with a fluorescent label

Contact Info

Product

Resources

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Direct, Longitudinal Comparison of ¹ H and ²³ Na MRI After Transient Focal Cerebral Ischemia

Direct, Longitudinal Comparison of ¹ H and ²³ Na MRI After Transient Focal Cerebral Ischemia