2002
DOI: 10.1097/00006123-200211000-00023
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Cerebral Venous Steal: Blood Flow Diversion with Increased Tissue Pressure

Abstract: Cerebral venous steal is a potential cause of secondary brain injury in areas of increased tissue pressure. It can be eliminated with increased venous pressure. Increased venous pressure may recruit the collapsed vascular network and correct perifocal perfusion maldistribution. This resembles how positive end expiratory pressure recruits collapsed airways and decreases the ventilation/perfusion mismatch.

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Cited by 33 publications
(27 citation statements)
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“…Hypoxia may indeed induce matrix fragmentation by activation of tissue metalloproteases [1]. Therefore, initial interstitial oedema may have progressed to frank oedema in MA zones, occurring together with a marked alteration in tissue morphology, hyperplasia of epithelial cells and an increase in interstitial pressure similar to that reported for other oedematous tissues, such as solid tumours and brain oedema [12,13]. One cannot exclude that in the lung the increase in tissue pressure might also reflect an increase in alveolar pressure (auto-PEEP) that should not exceed 1-2 cmH 2 O.…”
Section: Discussionmentioning
confidence: 63%
See 1 more Smart Citation
“…Hypoxia may indeed induce matrix fragmentation by activation of tissue metalloproteases [1]. Therefore, initial interstitial oedema may have progressed to frank oedema in MA zones, occurring together with a marked alteration in tissue morphology, hyperplasia of epithelial cells and an increase in interstitial pressure similar to that reported for other oedematous tissues, such as solid tumours and brain oedema [12,13]. One cannot exclude that in the lung the increase in tissue pressure might also reflect an increase in alveolar pressure (auto-PEEP) that should not exceed 1-2 cmH 2 O.…”
Section: Discussionmentioning
confidence: 63%
“…The increase in tissue pressure was likely to impact on pulmonary capillaries that represent a network of parallel thin-walled, collapsible channels whose patency depends upon the pressure existing in their perimicrovascular environment, a mechanical behaviour referred to as ''Starling resistor'' [14]. Thus, it seems reasonable to hypothesise that the increase in peri-microvascular interstitial pressure may represent an important factor to decrease CVI in MA regions; the corresponding increase in regional flow resistance would then divert blood flow towards other zones, similarly to what occurs in oedematous ischaemic brain regions [12]. Moreover, in high-altitude pulmonary oedema (HAPE)-sensitive subjects exposed to hypoxia, a blood shift was found from basal towards the apical regions [15], the former being characteristically more exposed to oedema formation in humans.…”
Section: Discussionmentioning
confidence: 99%
“…A potential explanation can be found in the so-called ‘cerebral venous steal’ hypothesis [23]. In the core of the cerebral infarction, local interstitial brain tissue pressures rise producing a collapse of venules and capillaries in and around the infarcted tissue [24].…”
Section: Discussionmentioning
confidence: 99%
“…12 Venous collapse in the ischemic core and peripheral displacement of blood volume caused by venous diversion have also been studied. 13 The decline in local cerebral blood volume (CBV) and venous collapse results in increased downstream resistance that further aggravates the marginal inflow pressure of arterial collaterals. Progressive ischemia after initial increases in CBV may be explained by this moving wavefront of hemodynamic instability originating in the core and moving toward the boundary of what has been termed benign oligemia (Fig 2).…”
Section: Hemodynamicsmentioning
confidence: 99%