Arteriovenous differences of oxygen and transcranial Doppler sonography in the management of aneurysmatic subarachnoid hemorrhage

Oertel, Matthias F.; Scharbrodt, Wolfram; Wachter, Dorothee; Stein, Marco; Schmidinger, A.; Böker, Dieter-Karsten

doi:10.1016/j.jocn.2007.04.003

Cited by 1 publication

(1 citation statement)

References 38 publications

(37 reference statements)

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“…92 Parallel recordings of arteriovenous oxygen differences and TCD flow velocities in the first days after SAH, however, show decreased OEF during the gradual increase in flow velocity, consistent with such relative hyperemia. 93 Similarly, direct measurements of CBF show occasional hyperemia and early reductions in OEF in patients after SAH. 94 The molecular underpinnings of the early vasodilation after SAH have been explored in animal models: within the first few days of SAH, the production of NO indeed appears to be upregulated in the walls of pial arterioles (in contrast to the subsequent downregulation reviewed above), as evidenced by increased expression of endothelial endothelial NOS and increased levels of NO breakdown products.…”

Section: The Dynamics Of Cerebral Blood Flow Cerebral Blood Flow Resmentioning

confidence: 96%

The Role of the Microcirculation in Delayed Cerebral Ischemia and Chronic Degenerative Changes after Subarachnoid Hemorrhage

Østergaard

Aamand

Karabegovic

et al. 2013

J Cereb Blood Flow Metab

140

147

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The mortality after aneurysmal subarachnoid hemorrhage (SAH) is 50%, and most survivors suffer severe functional and cognitive deficits. Half of SAH patients deteriorate 5 to 14 days after the initial bleeding, so-called delayed cerebral ischemia (DCI). Although often attributed to vasospasms, DCI may develop in the absence of angiographic vasospasms, and therapeutic reversal of angiographic vasospasms fails to improve patient outcome. The etiology of chronic neurodegenerative changes after SAH remains poorly understood. Brain oxygenation depends on both cerebral blood flow (CBF) and its microscopic distribution, the so-called capillary transit time heterogeneity (CTH). In theory, increased CTH can therefore lead to tissue hypoxia in the absence of severe CBF reductions, whereas reductions in CBF, paradoxically, improve brain oxygenation if CTH is critically elevated. We review potential sources of elevated CTH after SAH. Pericyte constrictions in relation to the initial ischemic episode and subsequent oxidative stress, nitric oxide depletion during the pericapillary clearance of oxyhemoglobin, vasogenic edema, leukocytosis, and astrocytic endfeet swelling are identified as potential sources of elevated CTH, and hence of metabolic derangement, after SAH. Irreversible changes in capillary morphology and function are predicted to contribute to long-term relative tissue hypoxia, inflammation, and neurodegeneration. We discuss diagnostic and therapeutic implications of these predictions.

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Section: The Dynamics Of Cerebral Blood Flow Cerebral Blood Flow Resmentioning

confidence: 96%

The Role of the Microcirculation in Delayed Cerebral Ischemia and Chronic Degenerative Changes after Subarachnoid Hemorrhage

Østergaard

Aamand

Karabegovic

et al. 2013

J Cereb Blood Flow Metab

140

147

View full text Add to dashboard Cite

show abstract

Arteriovenous differences of oxygen and transcranial Doppler sonography in the management of aneurysmatic subarachnoid hemorrhage

Cited by 1 publication

References 38 publications

The Role of the Microcirculation in Delayed Cerebral Ischemia and Chronic Degenerative Changes after Subarachnoid Hemorrhage

The Role of the Microcirculation in Delayed Cerebral Ischemia and Chronic Degenerative Changes after Subarachnoid Hemorrhage

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