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.

Studies of collateral perfusion to canine middle cerebral artery territory

1990 ◽  
Vol 259 (2) ◽  
pp. H560-H566 ◽  
Author(s):  
C. M. Loftus ◽  
G. M. Greene ◽  
K. N. Detwiler ◽  
G. L. Baumbach ◽  
D. D. Heistad
Keyword(s):  
At Risk ◽  
Blood Flow ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Autologous Blood ◽  
Base Line ◽  
Collateral Flow ◽  
Area At Risk ◽  
Risk Area ◽  
Anatomical Basis

Previous studies of intracranial collateral circulation have not distinguished between true "collateral" blood flow (flow to a region that occurs only when a primary artery is occluded) and "overlap" flow (flow to a region that is present under both normal and demand conditions). These experiments had three purposes: 1) to identify tissues that were truly collateral dependent, 2) to determine potential for true collateral flow in the absence of overlap flow, and 3) to determine whether an anatomical basis for overlap flow could be demonstrated. Branches (700-900 microns) of the dog middle cerebral artery (MCA) were perfused with autologous blood. The perfused region, which was the area at risk, was identified by intravenous injection of neutral red dye. Microspheres were used to measure regional cerebral blood flow (rCBF). Overlap flow was determined by perfusion of the artery with microsphere-free blood. True collateral flow (total rCBF minus overlap flow) was determined by analysis of rCBF to the risk area after cessation of vessel perfusion. Most of the risk area had substantial levels of overlap flow (about one-third of base line). In the center of the area at risk, the true collateral-dependent area was identified [mean overlap flow 4 +/- 1 (mean +/- SE) ml.min-1.100 g-1], which had high levels of perfusion from collateral vessels (102 +/- 14) within 30 s of vascular occlusion. Microfil injection into two adjacent MCA branches showed discrete borders between vascular territories, with no overlapping vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

Abstract 2716: Patients with Leukoaraiosis Have Poor Recruitment of Collaterals After Middle Cerebral Artery Occlusion

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Ethem Murat Arsava ◽  
Osman Melih Topcuoglu ◽  
Erhan Akpinar ◽  
Kader K Oguz ◽  
Mehmet Akif Topcuoglu
Keyword(s):  
Blood Flow ◽  
Ischemic Stroke ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Collateral Circulation ◽  
Artery Occlusion ◽  
Poor Recruitment ◽  
Collateral Vessels ◽  
Cerebral Artery Occlusion

Background: Previous studies have shown reduced penumbral salvage in ischemic stroke patients with higher leukoaraisosis (LA) volume. Although unproven, decreased cerebral vessel density and diminished capacity of cerebral vessels to dilate in response to reduced blood flow in severe LA, are considered among the factors that might explain the association between LA burden and infarct growth in ischemic stroke. Both of these factors, in theory, might negatively affect the extent of collateral blood flow, an important predictor of tissue and clinical outcome in patients with acute ischemic stroke. In this study, we therefore analyzed whether extent of LA adversely affected the degree of collateral circulation in a cohort of patients presenting with middle cerebral artery occlusion. Methods: We retrospectively analyzed a consecutive series of patients admitted with a diagnosis of middle cerebral artery occlusion. Computed tomography angiography source images (CTA-SI) were used to assess the degree of collateral circulation, based on a previously validated scoring system which grades collateral vessels in the sylvian fissure and leptomeningeal convexity separately on a scale from 1 to 5, with 1 being the worst and 5 the best. The extent of LA was determined on FLAIR images by using the Fazekas scale. Multivariate analysis was used to explore the relationship between extent of LA and degree of collateral circulation, adjusted for other covariates like age, gender, vascular risk factors and time from symptom onset to CTA imaging. Results: A total of 51 patients (31 female, 20 male) were included into the study. LA severity was significantly and negatively correlated with the degree of collateral supply (r=-0.31, p=0.03). LA severity (OR 5.9, 95%CI 1.5-24.0) and history of prior stroke (OR 7.8, 95%CI 1.0-59.3) were the only significant variables associated with insufficient collaterals (defined as a combined sylvian and lepotmeningeal collateral score of 5 or less) in the multivariate logistic regression analysis. Conclusion: Patients with higher LA burden have a poor recruitment of collateral vessels after middle cerebral artery occlusion. This association might contribute to reduced penumbral salvage and increased susceptibility to infarct growth observed in patients with severe LA.

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.

scholarly journals Augmenting Collateral Blood Flow during Ischemic Stroke via Transient Aortic Occlusion

2013 ◽  
Vol 34 (1) ◽  
pp. 61-71 ◽  
Author(s):  
Ian R Winship ◽  
Glenn A Armitage ◽  
Gomathi Ramakrishnan ◽  
Bin Dong ◽  
Kathryn G Todd ◽  
...  
Keyword(s):  
Blood Flow ◽  
Ischemic Stroke ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Collateral Circulation ◽  
Aortic Occlusion ◽  
Collateral Flow ◽  
Collateral Blood Flow ◽  
Flow Through ◽  
Transient Aortic Occlusion

Collateral circulation provides an alternative route for blood flow to reach ischemic tissue during a stroke. Blood flow through the cerebral collaterals is a critical predictor of clinical prognosis after stroke and response to recanalization, but data on collateral dynamics and collateral therapeutics are lacking. Here, we investigate the efficacy of a novel approach to collateral blood flow augmentation to increase collateral circulation by optically recording blood flow in leptomeningeal collaterals in a clinically relevant model of ischemic stroke. Using high-resolution laser speckle contrast imaging (LSCI) during thromboembolic middle cerebral artery occlusion (MCAo), we demonstrate that transiently diverting blood flow from peripheral circulation towards the brain via intra-aortic catheter and balloon induces persistent increases in blood flow through anastomoses between the anterior and middle cerebral arteries. Increased collateral flow restores blood flow in the distal middle cerebral artery segments to baseline levels during aortic occlusion and persists for over 1 hour after removal of the aortic balloon. Given the importance of collateral circulation in predicting stroke outcome and response to treatment, and the potential of collateral flow augmentation as an adjuvant or stand-alone therapy for acute ischemic stroke, this data provide support for further development and translation of collateral therapeutics including transient aortic occlusion.

Effects of serotonin on cerebral circulation after middle cerebral artery occlusion

1997 ◽  
Vol 87 (2) ◽  
pp. 301-306 ◽  
Author(s):  
Michael G. Muhonen ◽  
Scott C. Robertson ◽  
Jeffrey S. Gerdes ◽  
Christopher M. Loftus
Keyword(s):  
Blood Flow ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Perfusion Pressure ◽  
Cerebral Arteries ◽  
Area At Risk ◽  
Systemic Injection ◽  
Content Type ◽  
Vessel Resistance ◽  
Collateral Vessels

✓ Serotonin (5-HT) produces constriction of peripheral collateral blood vessels. Using an animal model, the authors tested the hypothesis that 5-HT constricts collateral vessels in the cerebrum. A branch of the middle cerebral artery (MCA) was occluded proximally and cannulated distally in anesthetized dogs. Blood flow to the area at risk for infarction was detected by perfusing the cannulated MCA branch with microsphere-free blood during systemic injection of radioactive microspheres (shadow flow technique). Blood flow to collateral-dependent and normal cerebrum was measured during intravenous infusion of 5-HT (10 and 40 mg/kg/minute). Serotonin produced a dose-related reduction of blood flow to collateral-dependent cerebrum, increased collateral vessel resistance in large cerebral arteries and collateral vessels, and decreased cerebral artery perfusion pressure. In contrast, blood flow to normal cerebrum was not altered because a decrease in small vessel resistance effectively compensated for a decrease in MCA perfusion pressure. These findings indicate that 5-HT produces constriction of collateral vessels in the cerebrum. This response is clearly different from normal small cerebral vessels, which dilate during 5-HT infusion.

scholarly journals Acetaminophen and myocardial infarction in dogs

2004 ◽  
Vol 287 (5) ◽  
pp. H1913-H1920 ◽  
Author(s):  
Gary F. Merrill ◽  
Tyler H. Rork ◽  
Norell M. Spiler ◽  
Roseli Golfetti
Keyword(s):  
Myocardial Infarction ◽  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Infarct Size ◽  
Blood Gases ◽  
Left Ventricular ◽  
Collateral Flow ◽  
Area At Risk ◽  
Developed Pressure

The hypothesis that acetaminophen can reduce necrosis during myocardial infarction was tested in male dogs. Two groups were studied: vehicle- ( n = 10) and acetaminophen-treated ( n = 10) dogs. All dogs were obtained from the same vendor, and there were no significant differences in their ages (18 ± 2 mo), weights (24 ± 1 kg), or housing conditions. Selected physiological data, e.g., coronary blood flow, nonspecific collateral flow, epicardial temperature, heart rate, systemic mean arterial pressure, left ventricular developed pressure, the maximal first derivative of left ventricular developed pressure, blood gases, and pH, were collected at baseline and during regional myocardial ischemia and reperfusion. There were no significant differences in coronary blood flow, nonspecific collateral flow, epicardial temperature, heart rate, systemic mean arterial pressure, or blood gases and pH between the two groups at any of the three time intervals, even though there was a trend toward improved function in the presence of acetaminophen. Infarct size, the main objective of the investigation, was markedly and significantly reduced by acetaminophen. For example, when expressed as a percentage of ventricular wet weight, infarct size was 8 ± 1 versus 3 ± 1%( P < 0.05) in vehicle- and acetaminophen-treated hearts, respectively. When infarct size was expressed as percentage of the area at risk, it was 35 ± 3 versus 13 ± 2% ( P < 0.05) in vehicle- and acetaminophen-treated groups, respectively. When area at risk was expressed as percentage of total ventricular mass, there were no differences in the two groups. Results reveal that the recently reported cardioprotective properties of acetaminophen in vitro can now be extended to the in vivo arena. They suggest that it is necessary to add acetaminophen to the growing list of pharmaceuticals that possess cardioprotective efficacy in mammals.

Abstract T P83: Strain Differences In Leptomeningeal Collateral Flow Dynamics Correlate With Differences In Stroke Outcome

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Yasuo Nishijima ◽  
Yosuke Akamtsu ◽  
Chih Cheng Lee ◽  
Jialing Liu
Keyword(s):  
Blood Flow ◽  
Acute Phase ◽  
Collateral Circulation ◽  
Artery Occlusion ◽  
Flow Dynamics ◽  
Mouse Strains ◽  
Collateral Flow ◽  
Doppler Flowmetry ◽  
Collateral Arteries ◽  
Retrograde Filling

Introduction: Emerging evidences suggest that the collateral circulation plays a key role in the risk of stroke and the severity of infarction. The current study aimed to investigate the effect of the brain collateral circulation in acute phase of stroke and outcome in two inbred mouse strains that differ markedly in anatomical collateralization. Methods: Male C57BL/6 and Balb/C mice were subjected to permanent unilateral common carotid artery occlusion (CCAO) or temporary distal middle cerebral artery occlusion (dMCAo). Regional cerebral blood flow (rCBF) was assessed by laser doppler flowmetry. In vivo imaging of collateral blood flow and flow velocity was evaluated by doppler optical coherence tomography (DOCT). Infarct size and motor function was assessed at 24 hours and 1 week after dMCAo, respectively. DiI-labeling was used to reveal anastomoses and to determine vessel diameter. Results: The diameters of the ICA and ACA on the ischemic side in both strains markedly decreased at 24 hours after CCAO but recovered at 7 days, although the diameters of ICA, MCA and ACA are larger in the Balb/C compared to the C57BL/6 strain before and after CCAO. Balb/C mice exhibited significantly less leptomeningeal connecting collateral arteries compared to C57BL/6 (0.6±0.3 vs 11.3±0.4, p<0.001), coincided with a larger infarction and worse neurological outcomes after dMCAo compared to C57BL/6. During the acute phase of occlusion of the CCA or MCA, C57BL/6 mice also demonstrated a much more robust retrograde filling of several distal branches of the MCA from ACA compared to Balb/C mice. Conclusion: Our results demonstrate that anatomical insufficiency of the leptomeningeal collateralization is associated with an impaired collateral flow dynamics, resulting in reduced rCBF during the acute phase of MCA stroke, which might in part, contribute to the larger infarction observed in the Balb/C strain.

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.

Effect of nitroglycerin on myocardial collateral conductance in awake dogs

1988 ◽  
Vol 254 (4) ◽  
pp. H751-H755
Author(s):  
S. Brazzamano ◽  
J. C. Rembert ◽  
J. C. Greenfield
Keyword(s):  
Blood Flow ◽  
Pressure Gradient ◽  
Collateral Circulation ◽  
Coronary Occlusion ◽  
Mean Value ◽  
Coronary Collateral Circulation ◽  
Control Value ◽  
Coronary Pressure ◽  
The Mean ◽  
Collateral Vessels

Conductance of the coronary collateral circulation during the course of two abrupt circumflex coronary occlusions (pre- and posttreatment with nitroglycerin) was measured in awake dogs approximately 2 wk after collateral vessels were stimulated to develop. The pressure gradient from the central aorta to the distal circumflex coronary artery was measured, and myocardial blood flow was determined by 9-microns radioactive microspheres at 30 s and 4 min after coronary occlusions. Collateral conductance was calculated as mean collateral blood flow divided by the mean aorta-coronary pressure gradient. Before nitroglycerin, collateral conductance increased in all eight dogs from 30 s to 4 min by a mean value of 0.006 +/- 0.003 ml.min-1.g-1.mmHg-1. After nitroglycerin administration, the conductance at 30 s increased from the prenitroglycerin control value of 0.009 +/- 0.008 to 0.014 +/- 0.012 ml.min-1.g-1.mmHg-1, P less than 0.03. The mean change in conductance from 30 s to 4 min postnitroglycerin 0.003 +/- 0.003 ml.min-1.g-1.mmHg-1 was significantly less than during prenitroglycerin (P = 0.01). These data indicate that an increase in conductance during coronary occlusion occurs even in the immature collateral circulation. This effect presumably takes place in the arterial smooth muscle at the origin of the collateral vasculature.

scholarly journals Modeling of the Human Cerebral Collateral Circulation: Evaluation of the Impact on the Cerebral Perfusion in Case of Ischemic Stroke

2019 ◽  
Vol 5 (1) ◽  
pp. 533-536
Author(s):  
Lorena Krames ◽  
Rosa Daschner ◽  
Yannick Lutz ◽  
Axel Loewe ◽  
Olaf Dössel ◽  
...  
Keyword(s):  
Blood Flow ◽  
Ischemic Stroke ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Collateral Circulation ◽  
Treatment Method ◽  
Developed Countries ◽  
Extended Model ◽  
Flow Through ◽  
The Impact

AbstractStroke is the third-most cause of death in developed countries. A new promising treatment method in case of an ischemic stroke is selective intracarotid blood cooling combined with mechanical artery recanalization. However, the control of the treatment requires invasive or MRI-assisted measurement of cerebral temperature. An auspicious alternative is the use of computational modeling. In this work, we extended an existing 1D hemodynamics model including the characteristics of the anterior, middle and posterior cerebral artery. Furthermore, seven ipsilateral anastomoses were additionally integrated for each hemisphere. A potential stenosis was placed into the M1 segment of the middle cerebral artery, due to the highest risk of occlusion there. The extended model was evaluated for various degrees of collateralization (“poor”, “partial” and “good”) and degrees of stenosis (0%, 50%, 75% and 99.9%). Moreover, cerebral autoregulation was considered in the model. The higher the degree of collateralization and the degree of stenosis, the higher was the blood flow through the collaterals. Hence, a patient with a good collateralization could compensate a higher degree of occlusion and potentially has a better outcome after an ischemic stroke. For a 99.9% stenosis, an increased summed mean blood flow through the collaterals of +97.7% was predicted in case of good collateralization. Consequently, the blood supply via the terminal branches of the middle cerebral artery could be compensated up to 44.4% to the physiological blood flow. In combination with a temperature model, our model of the cerebral collateral circulation can be used for tailored temperature prediction for patients to be treated with selective therapeutic hypothermia.

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