scholarly journals Intracranial Pressure Elevation Reduces Flow through Collateral Vessels and the Penetrating Arterioles they Supply. a Possible Explanation for ‘Collateral Failure’ and Infarct Expansion after Ischemic Stroke

2015 ◽  
Vol 35 (5) ◽  
pp. 861-872 ◽  
Author(s):  
Daniel J Beard ◽  
Damian D McLeod ◽  
Caitlin L Logan ◽  
Lucy A Murtha ◽  
Mohammad S Imtiaz ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Occlusion ◽  
Vessel Diameter ◽  
Experimental Stroke ◽  
Collateral Flow ◽  
Intracranial Pressure Elevation ◽  
Infarct Expansion ◽  
Flow Through ◽  
Collateral Vessels

Recent human imaging studies indicate that reduced blood flow through pial collateral vessels (‘collateral failure’) is associated with late infarct expansion despite stable arterial occlusion. The cause for ‘collateral failure’ is unknown. We recently showed that intracranial pressure (ICP) rises dramatically but transiently 24 hours after even minor experimental stroke. We hypothesized that ICP elevation would reduce collateral blood flow. First, we investigated the regulation of flow through collateral vessels and the penetrating arterioles arising from them during stroke reperfusion. Wistar rats were subjected to intraluminal middle cerebral artery (MCA) occlusion (MCAo). Individual pial collateral and associated penetrating arteriole blood flow was quantified using fluorescent microspheres. Baseline bidirectional flow changed to MCA-directed flow and increased by 4450% immediately after MCAo. Collateral diameter changed minimally. Second, we determined the effect of ICP elevation on collateral and watershed penetrating arteriole flow. Intracranial pressure was artificially raised in stepwise increments during MCAo. The ICP increase was strongly correlated with collateral and penetrating arteriole flow reductions. Changes in collateral flow post-stroke appear to be primarily driven by the pressure drop across the collateral vessel, not vessel diameter. The ICP elevation reduces cerebral perfusion pressure and collateral flow, and is the possible explanation for ‘collateral failure’ in stroke-in-progression.

Abstract W P211: Investigating the Cause for “Collateral Failure” in Stroke-in-Progression: Intracranial Pressure Elevation Reduces Flow Through Collateral Vessels

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Daniel Beard ◽  
Damian McLeod ◽  
Neil J Spratt
Keyword(s):  
Intracranial Pressure ◽  
Flow Velocity ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Minor Stroke ◽  
Collateral Flow ◽  
Mca Occlusion ◽  
Intracranial Pressure Elevation ◽  
Flow Through ◽  
Collateral Vessels

Background: Adequacy of the collateral circulation is a major determinant of outcome in stroke patients. Recent human imaging data indicates that collateral failure, rather than reperfusion-reocclusion is the most common cause for early progression in minor stroke. Our previous experimental data shows that intracranial pressure (ICP) rises transiently 24 h after even minor stroke. Herein, we investigated the effect of ICP manipulation on blood flow through collateral vessels during MCA occlusion. Methods: We developed and validated a method to quantify flow velocity and vessel diameter of anterior-middle cerebral artery (ACA-MCA) leptomeningeal collaterals in rats during stroke, using fluorescent microspheres. BIood flow velocity and diameter was quantified in individual collateral vessels and used to calculate absolute flow during MCA occlusion and reperfusion (n = 6). In separate experiments, ICP was increased after MCA occlusion by fluid infusion into the lateral ventricles and effects on relative collateral flow were determined (n = 4). Results: In vitro validation indicated accurate flow quantification (R 2 = 0.99, P<0.0001). Collateral flow was seen to switch from bidirectional to unidirectional flow (toward occluded vessel) and increase by 595 ± 134 % within 10 min of vessel occlusion. Direction and flow changes were variable after MCA reperfusion, however there was a mean flow reduction of 52 ± 15 % by 5 mins. Artificially elevating ICP during MCA occlusion caused a reduction of cerebral perfusion pressure which was strongly correlated with collateral flow reduction (R 2 = 0.90, p<0.0001). Discussion: Our method permits real time quantification of flow through individual collateral vessels during stroke and reperfusion. Intracranial pressure elevation reduced collateral flow, proportional to its effect on cerebral perfusion pressure. Coupled with our previous data indicating significant ICP elevation after even minor stroke, this suggests that transient ICP elevation is the possible cause of the collateral failure recently described in patients with stroke-in-progression.

scholarly journals Cerebral Blood Flow in Patients with Intracranial Pressure Elevation due to Traumatic Brain Edema

1976 ◽  
Vol 3 (1) ◽  
pp. 35-37 ◽  
Author(s):  
W. A. Tweed ◽  
Jørn Overgaard
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Brain Edema ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Monitoring And Control ◽  
Intracranial Pressure Elevation ◽  
Flow Through ◽  
And Control

SUMMARY:The object of this study was to determine if traumatic brain edema (BE) and increased intracranial pressure (ICP) reduce cerebral blood flow (CBF). Two groups of patients were studied, one with slight BE and ICP less than 20 mm Hg., the other with pronounced BE and ICP over 20 mm Hg. Although ICP was higher and cerebral perfusion pressure lower in pro-nounced edema there was only a small and non-significant reduction in CBF and no difference in cerebro-vascular resistance. Since traumatic BE does not increase resistance to blood flow through the brain, cerebral perfusion can be maintained if an adequate perfusion pressure is established. This in turn, demands the monitoring and control of ICP.

scholarly journals Effects of Adenosine and 2-Chloroadenosine on Cerebral Collateral Vessels

1995 ◽  
Vol 15 (6) ◽  
pp. 1075-1081 ◽  
Author(s):  
Michael G. Muhonen ◽  
Christopher M. Loftus ◽  
Donald D. Heistad
Keyword(s):  
Blood Flow ◽  
Cerebral Artery ◽  
Topical Application ◽  
Collateral Circulation ◽  
Arterial Occlusion ◽  
Collateral Flow ◽  
Cortical Layers ◽  
Area At Risk ◽  
Collateral Vessels ◽  
Cerebral Vasodilator

Adenosine is a potent cerebral vasodilator. We tested the hypothesis that dilatation of collateral vessels in cerebrum, in response to topical adenosine and 2-chloroadenosine (2-CAD), would increase blood flow to collateral-dependent cerebrum. In dogs anesthetized with halothane, a branch of the middle cerebral artery (MCA) was occluded proximally and cannulated distally. The collateral-dependent area at risk for infarction was perfused from a reservoir with microsphere-free blood, and blood flow to normal cerebrum and to cerebrum dependent on collateral flow was measured with radioactive microspheres injected into the left ventricle through a femoral artery catheter. Perfusion through the cannulated MCA branch was stopped, and flow to normal and collateral-dependent cerebrum was measured after adenosine (10−2 M) or 2-CAD (10−4 M) was added to the superfusate over the cerebrum. In normal cerebrum, topical application of adenosine increased flow to outer but not inner layers. Topical application of adenosine had little effect on flow to collateral-dependent tissue. In normal cerebrum, 2-CAD increased flow to outer layers, whereas flow to inner layers tended to increase. During 2-CAD, flow to outer cortical layers of collateral-dependent cerebrum increased from 140 ± 20 ml/100 g/min (mean ± SD) to 231 ± 68, whereas flow to the inner collateral-dependent tissue did not change. The findings indicate that, after occlusion of a cerebral artery, topical 2-CAD increases blood flow to outer layers of collateral-dependent and normal cerebrum. The findings suggest also that, after arterial occlusion, collateral circulation to cerebrum has dilator reserve, and flow to tissues that are dependent on collaterals may be augmented.

Naftidrofuryl (praxilene) in peripheral vascular disease

1979 ◽  
Vol 17 (21) ◽  
pp. 81.2-84
Keyword(s):  
Blood Flow ◽  
Muscle Pain ◽  
Arterial Occlusion ◽  
Collateral Flow ◽  
Rest Pain ◽  
Peripheral Vascular ◽  
Skin Changes ◽  
Flow Through ◽  
Arterial Insufficiency ◽  
Vascular Beds

Arterial insufficiency in the leg usually presents as muscle pain on exercise (intermittent claudication). Blood flow through the narrowed major arteries may be adequate to meet resting needs but not the increased requirements of exercise. When collateral flow is also impaired or there is further major arterial occlusion then rest pain in the foot, trophic skin changes and eventually gangrene result. Medical treatment has been largely unsuccessful. Systemically acting vasodilators are often given but may actually reduce blood flow in ischaemic areas by diverting it to healthy responsive vascular beds.1 2

Abstract TP146: Impaired Acute Collateral Flow Dynamics Experimental Stroke In Type 2 Diabetic Mice

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Yosuke Akamatsu ◽  
Chih C Lee ◽  
Ruikang K Wang ◽  
Jialing Liu
Keyword(s):  
Blood Flow ◽  
Neurologic Deficit ◽  
Flow Dynamics ◽  
Collateral Flow ◽  
Doppler Flowmetry ◽  
Collateral Arteries ◽  
Significant Difference ◽  
Blood Flow Dynamics ◽  
Collateral Vessels

Introduction: Type 2 diabetes mellitus (T2DM) is a major risk factor for stroke, yet it is unclear whether T2DM associated-poor outcome after stroke is related to unfavorable cerebral blood flow dynamics. The current study aimed to investigate the effect of T2DM on acute blood flow dynamics and stroke outcome. Methood: Adult male db/db and db/+ mice (8-9 weeks of age) were subjected to permanent distal middle cerebral artery occlusion (pMCAo). Neurologic deficit was assessed with a 5-point scoring system (0 to 4) and infarction volume was determined at 48 hours after pMCAo by TTC staining. Hemodynamics was evaluated by laser doppler flowmetry. The number of connecting collateral vessels, functional microvascular network morphology, and vessel area density of the ischemic hemisphere were determined by DiI-labeling, and optical coherence tomography (OCT), respectively. Results: db/db mice had a higher baseline blood glucose level (341±39.7 vs. 172±26.5 mg/dl, p <0.01) and a larger infarct volume after pMCAO compared to db/+ mice (69.5±5.4 vs. 51.0±3.1 mm 3 , p <0.01). Neurologic deficit did not differ between groups at 2 hours after pMCAO, but was significantly worse in the db/db at 24 hours after pMCAo compared to db/+ mice (1.9±0.1 vs. 1.4±0.2, p <0.05), correlated with lower rCBF in the core of the MCA territory at 24 and 48 hours (10.9%±1.1 vs. 14.4%±0.8, p <0.05 and 9.5%±1.0 vs. 14.1%±1.2, p =0.01). Ipsilateral functional microvascular density as detected by OCT did not differ between groups at one hour after occlusion but was significantly lower in the db/db mice at 24 hr after pMCAo ( p <0.05). However, we did not observe a significant difference in the number of connecting collateral arteries between groups at 48 hours after pMCAo in this age group. Conclusion: Our results demonstrate that T2DM is associated with lower rCBF and lower density of functional blood vessels during the acute phase of pMCAo, which might in part, contribute to the observed worse outcome in the db/db mice. Ongoing experiments will investigate whether T2DM affects the flow dynamics in individual collateral following MCA occlusion and outward remodeling of the collateral vessels.

Major and collateral components of blood flow to pregnant sheep uterus

1975 ◽  
Vol 229 (2) ◽  
pp. 279-285 ◽  
Author(s):  
EO Fuller ◽  
PM Galletti ◽  
T Takeuchi
Keyword(s):  
Blood Flow ◽  
Balloon Catheter ◽  
Vessel Diameter ◽  
Pressure Curve ◽  
Collateral Flow ◽  
In Situ Perfusion ◽  
Uterine Arteries ◽  
Pregnant Sheep ◽  
Near Term

In vivo measurements of vessel diameter, latex injections, and acrylic-cast studies indentified the middle uterine arteries as the main source of blood supply to the pregnant sheep uterus. Collateral circulation stemmed from the dorsal uterine arteries, and the ovarian arteries, and small cervical branches derived from the external iliac arteries (in decreasing order of importance). These morphological observations were related to estimates of collateral flow obtained during isolated, in situ perfusion of the pregnant sheep uterus carried out through the cannulated middle uterine arteries. Collateral blood flow was estimated from the shift of the flow-pressure curve produced by inflation of a balloon catheter advanced into the aorta below the renal arteries. Middle uterine artery flow to one horn increased from 162 +/- 23 ml/min in midgestation to 323 +/- 44 ml/min near term. Collateral uterine blood flow did not change significantly: 82 +/- 15 ml/min in midterm, 74 +/- 9 ml/min near term. Collateral flow consituted a larger fraction of inflow to the horn containing the fetus in 9 of 10 single pregnancies.

Normal cerebrovascular physiology and vascular anatomy

2019 ◽  
pp. 539-558
Author(s):  
Diederik O. Bulters ◽  
Andrew Durnford
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Cerebral Perfusion ◽  
Vascular Anatomy ◽  
Vessel Diameter ◽  
Cerebral Veins ◽  
Deep Cerebral Veins ◽  
Neurovascular Anatomy ◽  
Arterial Anatomy

The first part of this chapter describes normal neurovascular anatomy including its embryology, histology, and normal arterial variants. It includes angiographic arterial anatomy and also the structures and territories supplied by specific vessels. The anatomy of the venous sinuses and both the superficial and deep cerebral veins are described. The second part details normal cerebral neurophysiology, including autoregulation and the control of cerebral perfusion. It covers the myogenic, metabolic, and neurogenic mechanisms of cerebral blood flow and vessel diameter regulation. Finally, the role and influence of mannitol on cerebral blood flow is described, and how although it acutely reduces cerebral volume and intracranial pressure, its exact mechanism of action remains unclear.

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