A Starling resistor regulates cerebral venous outflow in dogs

Luce, J. M.; Huseby, Jon S.; Kirk, W.; Butler, J

doi:10.1152/jappl.1982.53.6.1496

Cited by 102 publications

(84 citation statements)

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“…It has been demonstrated that the cerebral venous pressure (CVP) increases in parallel with the CSFP and it is always kept slightly higher than the CSFP. Parallel modifications in CSFP and CVP can be induced by the inflation of intracranial balloons or by the modification of the PaCO2 (Yada et al, 1973;Luce et al, 1982;Wiig and Reed, 1983). Thus, the increase in the CVP of the vessels draining the tumour could lead to a further increase in the tumour MVP and IFP.…”

Section: Discussionmentioning

confidence: 99%

Interstitial fluid pressure in intracranial tumours in patients and in rodents

Boucher

Salehi²,

Witwer³

et al. 1997

Br J Cancer

172

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Summary Fluid transport parameters in intracranial tumours influence the delivery of therapeutic agents and the resolution of peritumoral oedema. The tumour and cortex interstitial fluid pressure (IFP) and the cerebrospinal fluid pressure (CSFP) were measured during the growth of brain and pial surface tumours [R3230AC mammary adenocarcinoma (R3230AC) and F98 glioma (F98)] in rats. Intratumoral and intracranial pressures were also measured in rodents and patients treated with dexamethasone, mannitol and furosemide (DMF), and hypocapnia. The results show that (1) for the R3230AC on the pial surface, IFP increased with tumour volume and CSFP increased exponentially for tumours occupying a brain volume of 5% or greater; (2) in F98 with volumes of approximately 10 mm3, IFP decreased from the tumour to the cortex, whereas for tumour volumes > 16 mm3 IFP equilibrates between F98 and the cortex; (3) DMF treatment reduced the IFP of intraparenchymal tumours significantly and induced a pressure gradient from the tumour to the cortex; and (4) in 11 patients with intracranial tumours, the mean IFP was 2.0 ± 2.5 mmHg. In conclusion, the IFP gradient between intraparenchymal tumours and the cortex decreases with tumour growth, and treatment with DMF can increase the pressure difference between the tumour and surrounding brain. The results also suggest that antioedema therapy in patients with brain tumours is responsible in part for the low tumour IFP.Keywords: interstitial fluid pressure; microvascular pressure; brain tumours in rodents; intracranial tumours in patients; antioedema therapy Studies from our group and other investigators have shown that the interstitial fluid pressure (IFP) of human tumours in situ is significantly elevated compared with normal tissues Roh et al, 1991;Gutmann et al, 1992;Less et al, 1992;Curti et al, 1993;Arbit et al, 1994;Nathanson and Nelson, 1994). In most normal tissues the IFP is around 0 mmHg while for the different carcinoma types measured to date the mean IFPs vary between 14 and 30 mmHg. In general, in human and experimental tumours the IFP increases with tumour size (Jain, 1987a;Boucher et al, 1990Boucher et al, , 1991Boucher et al, , 1995Gutmann et al, 1992;Lee et al, 1992;Nathanson and Nelson, 1994). However, in other studies, the IFP was found to be independent of the tumour volume (Less et al, 1992;Curti et al, 1993;Boucher et al, 1995;Tufto and Rofstad, 1995;Znati et al, 1996). Measurements in experimental tumours have demonstrated that (1) the IFP is uniform throughout the centre of tumours and drops steeply in the tumour periphery or in the normal tissue surrounding the tumour (Boucher et al, 1990;Boucher and Jain, 1992;DiResta et al, 1993) and (2) that the hydrostatic and oncotic pressures in the vascular and interstitial space are at or close to equilibrium Jain, 1989, Boucher andStohrer et al, 1995). The similarity in hydrostatic pressures between the microvascular and interstitial space is thought to be a major mechanism limiting the convective delivery of large therapeut...

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Section: Discussionmentioning

confidence: 99%

Interstitial fluid pressure in intracranial tumours in patients and in rodents

Boucher

Salehi²,

Witwer³

et al. 1997

Br J Cancer

172

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“…2 When calculating the CPP, the mean arterial pressure (MAP) is commonly used as effective upstream pressure and the intracranial pressure (ICP) as effective downstream pressure (EDP) of the cerebral circulation, because of a Starling resistor phenomenon located at the level of cerebral veins. 3 However, another major component of the EDP is the critical closing pressure (CCP), which cannot be directly measured in patients with spontaneous circulation. It has been proven that in vivo pressure-flow relationships are linear for many vascular beds, including the cerebral vessels.…”

Section: Introductionmentioning

confidence: 99%

Carbon Dioxide Induced Changes in Cerebral Blood Flow and Flow Velocity: Role of Cerebrovascular Resistance and Effective Cerebral Perfusion Pressure

Grüne

Kazmaier

Stolker

et al. 2015

J Cereb Blood Flow Metab

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In addition to cerebrovascular resistance (CVR) zero flow pressure (ZFP), effective cerebral perfusion pressure (CPPe) and the resistance area product (RAP) are supplemental determinants of cerebral blood flow (CBF). Until now, the interrelationship of PaCO 2 -induced changes in CBF, CVR, CPPe, ZFP, and RAP is not fully understood. In a controlled crossover trial, we investigated 10 anesthetized patients aiming at PaCO 2 levels of 30, 37, 43, and 50 mm Hg. Cerebral blood flow was measured with a modified Kety-Schmidt-technique. Zero flow pressure and RAP was estimated by linear regression analysis of pressure-flow velocity relationships of the middle cerebral artery. Effective cerebral perfusion pressure was calculated as the difference between mean arterial pressure and ZFP, CVR as the ratio CPPe/CBF. Statistical analysis was performed by one-way RM-ANOVA. When comparing hypocapnia with hypercapnia, CBF showed a significant exponential reduction by 55% and mean V MCA by 41%. Effective cerebral perfusion pressure linearly decreased by 17% while ZFP increased from 14 to 29 mm Hg. Cerebrovascular resistance increased by 96% and RAP by 39%; despite these concordant changes in mean CVR and Doppler-derived RAP correlation between these variables was weak (r = 0.43). In conclusion, under general anesthesia hypocapnia-induced reduction in CBF is caused by both an increase in CVR and a decrease in CPPe, as a consequence of an increase in ZFP.

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“…2. The existence of a subdural venous collapse was demonstrated already in 1928 (26), but its physiological role or its role in various pathophysiological conditions for brain circulation has not until recently received any scientific attention (20,27,28).…”

Section: General Physiological and Physical Principlesmentioning

confidence: 99%

Mechanisms behind postspinal headache and brain stem compression following lumbar dural puncture – a physiological approach

Grände

2005

Acta Anaesthesiol Scand

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Mechanisms behind postspinal headache and brain stem compression following lumbar dural puncture -a physiological approach.Grände, Per-Olof 619-626. DOI: 10.1111619-626. DOI: 10. /j.1399619-626. DOI: 10. -6576.2004 General rights Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights.• Users may download and print one copy of any publication from the public portal for the purpose of private study or research.• You may not further distribute the material or use it for any profit-making activity or commercial gain • You may freely distribute the URL identifying the publication in the public portal Methods: Hydrostatic effects of distal opening of the dural sac towards the atmosphere are described and applied to the normal brain and the brain with disrupted BBB. Analogue analyses from an isolated skeletal muscle enclosed in a rigid shell were applied to the brain in an attempt to simulate and verify haemodynamic effects of distal opening of the spinal canal. Results Conclusion:The present study strongly suggest that post-spinal headache and brain stem compression and other LP-related effects are predictable following LP, without involving CSF leakage, and can be explained by hydrostatic effects triggered by distal opening of the normally closed dural space to the atmosphere.

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A Starling resistor regulates cerebral venous outflow in dogs

Cited by 102 publications

References 0 publications

Interstitial fluid pressure in intracranial tumours in patients and in rodents

Interstitial fluid pressure in intracranial tumours in patients and in rodents

Carbon Dioxide Induced Changes in Cerebral Blood Flow and Flow Velocity: Role of Cerebrovascular Resistance and Effective Cerebral Perfusion Pressure

Mechanisms behind postspinal headache and brain stem compression following lumbar dural puncture – a physiological approach

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