A comparison of measurements of cerebral blood flow in the rabbit using laser Doppler spectroscopy and radionuclide labelled microspheres

Eyre, J A; Essex, T.; Flecknell, P. A.; Bartholomew, P.; Sinclair, J I

doi:10.1088/0143-0815/9/1/006

Cited by 101 publications

(35 citation statements)

References 10 publications

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“…Recently, the validity of this technique was confirmed for measurement of the cerebral microcirculation under physiological and pathological conditions by demonstrating a close correlation with blood flow values obtained by the hydrogen clearance 11 or microsphere 12 techniques. The sensitive volume of laser Doppler flowmetry is less than 1 mm 3 , 11 and the main signal received from tissue originates from a depth of less than 1 mm.…”

Section: Discussionmentioning

confidence: 68%

Laser doppler flowmetry in CA1 sector of hippocampus and cortex after transient forebrain ischemia in gerbils.

Kuroiwa

Bonnekoh

Hossmann

1992

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Background and Purpose: Local differences in the hemodynamic response to transient ischemia could be involved in the development of selective vulnerability. These differences were studied in vulnerable and nonvulnerable regions of the brain.Methods: Five gerbils were subjected to 10 minutes of bilateral forebrain ischemia, and cerebral blood flow was measured continuously in the frontal cortex and CA1 sector of the hippocampus using laser Doppler flowmetry. Carotid artery pressure was recorded simultaneously with a pressure transducer.Results: After induction of ischemia, blood flow in the cortex and CA1 sector decreased to 11.8% and 18.0% of the baseline value, respectively. After release of the vascular occlusion, blood flow in the cortex returned to the preischemic level at 7.5 minutes (recovery time), reached the hyperemic peak (123.8%) at 12.4 minutes (peak latency), and again decreased to the preischemic level at 27.2 minutes. In the CA1 sector, blood flow returned to the preischemic level at 2.1 minutes, reached the hyperemic peak (122.2%) at 5.7 minutes, and decreased again to the preischemic level at 21.3 minutes. In both the cortex and CA1 sector, recovery time and peak latency correlated inversely with the amount of residual blood flow during ischemia. Histologically, cortical neurons were not injured but only 14.6% of CA1 neurons survived 1 week after ischemia.Conclusions: CA1 neurons were selectively injured despite the milder percentage decrease of blood flow during ischemia and the more prompt recovery of flow after ischemia. These findings stress the importance of intrinsic rather than hemodynamic factors in the pathogenesis of selective vulnerability of CA1 neurons after transient bilateral forebrain ischemia. (Stroke 1992;23:1349-1354

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Section: Discussionmentioning

confidence: 68%

Laser doppler flowmetry in CA1 sector of hippocampus and cortex after transient forebrain ischemia in gerbils.

Kuroiwa

Bonnekoh

Hossmann

1992

Stroke

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“…The absolute flow values differ from those yielded by other methods and probably should be considered as unitless, but there is little doubt that LDF is an accurate method for quantitating changes in CBF relative to some reference point. [22][23][24][25] Some caution must be exercised with respect to our results. For example, we have reported absolute CBFLDF values in Figure 1 and in Table 1.…”

Section: Resultsmentioning

confidence: 79%

Cerebral autoregulation during moderate hypothermia in rats.

Verhaegen

Todd

Hindman

et al. 1993

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“…The linear channels of the analog digital converter were reconverted to log values for this purpose Measurement of cortical microvascular blood perfusion. LDF has been established as a reliable method for the measurement of regional microvascular blood perfusion (14). The two-channel laser Doppler flowmeter (Periflux 4001 Master, Perimed AB, Stockholm, Sweden) emits a low-power 2-mW helium-neon laser light with a wavelength of 632.8 nm, which is directed to the tissue by the optical fibers (PF 319:0, 210 mm long and 0.5 mm in diameter).…”

Section: Animal Preparationmentioning

confidence: 99%

Hydrogen Peroxide Production in Leukocytes during Cerebral Hypoxia and Reoxygenation with 100% or 21% Oxygen in Newborn Piglets

et al. 2001

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The aim of this study was to investigate whether reoxygenation with 21% O 2 rather than 100% O 2 results in reduced hydrogen peroxide (H 2 O 2 ) concentrations in neutrophils (PMN). Piglets (2-4 d old) exposed to severe hypoxia (inspired fraction of oxygen, 0.08) were randomized to resuscitation with 21 (n ϭ 13) or 100% O 2 (n ϭ 12). Five animals served as controls. H 2 O 2 concentrations in PMN in terms of rhodamine 123 (Rho 123) fluorescence intensity from arterial and superior sagittal sinus blood were quantified by flow cytometry. Laser Doppler flowmetry (LDF) was used to assess cortical blood perfusion. During hypoxia, Rho 123 increased in arterial PMN in both study groups by 15 and 32%, respectively (p Ͻ 0.05). In cerebral venous PMN, the increase was less dominant (p ϭ 0.06). Reoxygenation with 100 or 21% O 2 had no different effect on Rho 123 in arterial PMN. In cerebral venous PMN, Rho 123 was approximately 40% higher after 60 min and 30% higher after 120 min compared with corresponding data in the 21% O 2 group (p Ͻ 0.05), which were close to baseline levels. Further, O 2 treatment in both groups induced PMN accumulation in arterial blood (p Ͻ 0.05). Laser Doppler flowmetry signals increased during transient hypoxia (p Ͻ 0.0001 compared with baseline) and were normalized after reoxygenation in both study groups. The primary release of products of the sequential reduction of oxygen, superoxide radical (O 2 -) and H 2 O 2 , and the secondary production of hydroxyl radical (HO -) constitute the molecular mechanism of oxygen toxicity. Any system producing O 2 -will, as a result of the dismutase reaction, also produce H 2 O 2 . Although stable, the damaging redox properties of H 2 O 2 and its ability to form highly reactive free radicals in the presence of transition metal ions have caused the body to form defenses against it. The role of oxygen toxicity in the development of perinatal hypoxic-ischemic encephalopathy is still a matter of debate. The principal hypothesis put forward to explain this process is the oxygen free radical theory (1, 2).Stimulation of PMN during hypoxia-reoxygenation may increase the concentration of reactive oxygen species (3) in these cells. To date, the production of H 2 O 2 in PMN during hypoxia and resuscitation with pure or air-mixed O 2 has not been studied in detail. Reoxygenation is necessary to prevent further injury to neuronal tissue, but the renewed availability of O 2 to previously hypoxic brain tissue may also have detrimental effects both with respect to the microcirculation and to the parenchyma of the brain. The production of reactive oxygen metabolites may be proportional to PaO 2 , and the oxygen tension achieved during reactive hyperemia and reoxygenation with O 2 concentrations higher than 21% may generate a correspondingly higher burst of these metabolites. However, we

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A comparison of measurements of cerebral blood flow in the rabbit using laser Doppler spectroscopy and radionuclide labelled microspheres

Cited by 101 publications

References 10 publications

Laser doppler flowmetry in CA1 sector of hippocampus and cortex after transient forebrain ischemia in gerbils.

Laser doppler flowmetry in CA1 sector of hippocampus and cortex after transient forebrain ischemia in gerbils.

Cerebral autoregulation during moderate hypothermia in rats.

Hydrogen Peroxide Production in Leukocytes during Cerebral Hypoxia and Reoxygenation with 100% or 21% Oxygen in Newborn Piglets

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