SEARCH · PubMed Health

Results for “Collateral Circulation”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,801 records · Page 100Linked to original sources

PubMed2002

Exogenous application of transforming growth factor beta 1 stimulates arteriogenesis in the peripheral circulation.

Increased expression of transforming growth factor beta1 (TGF-beta1) during collateral artery growth, as well as its numerous effects on monocytes/macrophages and the smooth muscle cell cycle and differentiation, suggest a modulating role for this growth factor during arteriogenesis. We studied the effects of exogenously applied TGF-beta1 on arteriogenesis as well as its interactions with monocytes, endothelial cells, and smooth muscle cells. In a New Zealand White (NZW) rabbit model of femoral artery ligation, increased expression of active TGF-beta1 was found around proliferating arteries in NZW rabbits. The exogenous application of TGF-beta1 led to an increase in both the number of visible collateral arteries as well as the conductance of the collateral circulation (4.0 +/- 0.5 ml/min/100 mmHg vs. 28.9 +/- 3.7 ml/min/100 mmHg, P<0.05). Fluorescence activated cell sorting analysis showed an increase in the expression of the MAC-1 receptor in both rabbit and human monocytes after treatment with TGF-beta1 (control: 91.2 +/- 4.2/482 +/- 21.7; TGF-beta1 200 ng/ml 193.9 +/- 6.7/ 675.5 +/- 25.7, P<0.05 for all differences). TGF-beta1 treated monocytes showed an increased endothelial adhesion and transmigration in transendothelial migration assays (5.75 +/- 0.63 x 10(5) vs. 10.11 +/- 0.04 x 10(5), P<0.05). TGF-beta1 had no direct pro-angiogenic effect on human umbilical vein endothelial cells in a spheroid model of angiogenesis and inhibited the angiogenic effects of vascular endothelial growth factor.

Animals↗

PubMed2004

Regional angiographic grading system for collateral flow: correlation with cerebral infarction in patients with middle cerebral artery occlusion.

BACKGROUND AND PURPOSE: Collateral flow plays an important role in maintaining tissue viability in proximal large vessel occlusion. We developed and tested a regional angiographic collateral grading system for patients with angiographically confirmed acute symptomatic middle cerebral artery occlusion to predict regional infarction. METHODS: A subset of 42 patients was selected from 180 patients enrolled in the Prolyse in Acute Cerebral Thromboembolism II (PROACT II) trial. Readers evaluated baseline cerebral angiograms in a blinded fashion for the degree of regional collateral circulation, which was graded on a 4-point scale in each of 15 anatomic regions. Regional and total collateral flow scores were compared with the presence or absence of infarction on 7- to 10-day follow-up computed tomography (CT), as well as clinical outcome as assessed by National Institute of Health Stroke Scale (NIHSS) scores. RESULTS: The collateral flow score on baseline angiography accurately predicted infarction, demonstrating a receiver operating characteristic curve of 0.87 (95% CI: 0.83 to 0.91) for all regions. Collateral grades on baseline angiography correlated moderately with infarct volume on follow-up CT scan at 7 to 10 days (R=0.61; P=0.0001). Collateral grades also correlated with follow-up NIHSS scores for patients who received thrombolysis (R=0.36 to 0.49, P<0.05), but not for control patients. CONCLUSIONS: An angiographic grading system for regional collateral flow accurately predicts the extent and location of cerebral infarction. This study corroborates the correlation between the presence of collateral flow, infarction volume, and clinical outcome, and it reinforces the need to control for collateral flow in clinical trials.

Cerebral Angiography↗

PubMed1982

Regional cerebral blood flow in patients with vertebrobasilar disease.

We have investigated the changes in regional cerebral blood flow (rCBF) in patients with occlusive vertebrobasilar disease. Fifty patients who showed severe stenosis or occlusion of the vertebrobasilar artery territory were studied by angiography. Lesions in 13 of these patients were limited to the vertebrobasilar artery (limited VB group), and 37 patients showed combined vertebrobasilar/carotid artery lesions (combined VB-C group). Measurements of rCBF in the group of 50 patients using the intravenous xenon 133 technique showed that there was a significant decrease in the mean rCBF (47.5 +/- 1.4 ml/100 gm/min) as compared with 19 age-matched normal subjects (54.9 +/- 1.8 ml/100 gm/min. There was also a significant difference in mean rCBF between the combined VB-C group (45.6 +/- 1.5 ml/100 gm/min) and a group of 153 patients with limited carotid artery lesions (C group, 49.8 +/- 1.0 ml/100 gm/min). However, no significant difference in mean rCBF was found between the limited VB group and normal subjects. There were no differences in rCBF when evaluated according to the presence or absence of angiographic collateral circulation via the posterior communicating artery (Pcom). Good correlation was found between mean rCBF and direction of collateral flow via the Pcom (p less than 0.05). The value of hemispheric rCBF of patients with carotid system transient ischemic attacks (TIAs) was significantly lower than that of patients with vertebrobasilar system TIAs (p less than 0.02). In cerebral autoregulation tests of 24 patients with occlusive vertebrobasilar disease (7 patients from the limited VB group and 17 patients from the combined VB-C group), 13 of these 24 patients (54%) showed an impairment of autoregulation.

Aged↗

PubMed2005

[Organ-saving method of treatment of spleen disruption].

Based on 102 X-ray and 73 anatomic examinations, the scheme of arterial circulation of the pancreas and spleen, features of their collateral circulation are analyzed. Optimal level of spleen artery ligation at proximal part as the main stage of organ-saving surgical treatment in traumatic disruption of the spleen is substantiated.

Adolescent↗

PubMed1989

Large animal model of left ventricular aneurysm.

In 28 Dorsett sheep, ligation of the distal homonymous (equivalent to human left anterior descending) and second diagonal coronary arteries produced a constant transmural infarct of 22.9% +/- 2.5% (mean +/- standard deviation) of the left ventricular mass. Serial left ventriculograms showed that within four hours the infarct segment expands, wall thickness decreases, and aneurysmal dilatation occurs and progresses over the next 60 days in all sheep. Epicardial ventricular point references indicated that adjacent noninfarcted myocardium participates in the formation of the aneurysm. Anatomy of the coronary vasculature was studied in 22 excised sheep hearts. In sheep, coronary arterial anatomy is remarkably constant. The left coronary artery provides all of the blood supply to the left ventricle and septum and only a small rim of both the anterior and posterior right ventricles. Cardiac veins from the left ventricle drain into the coronary sinus, which also receives the left azygos vein. Right ventricular veins drain separately. The essentially separate coronary circulations to the two ventricles, the paucity of coronary collateral circulation, and the consistent evolution of left ventricular infarcts into aneurysms are important advantages of the ovine model for both metabolic and ventricular mechanical studies of acute myocardial infarction and left ventricular aneurysm.

Animals↗

PubMed1999

Transmyocardial laser induces coronary hyperemia and reduces ischemia-related arrhythmias, but fails to delay development of myocardial necrosis after coronary artery occlusion in pigs.

BACKGROUND: Several investigators have reported that transmyocardial revascularization (TMR) prior to acute coronary artery occlusion improves regional myocardial function and reduces the infarct size in animals with significant coronary collateral circulation. Whether the protective effect of TMR is due to perfusion through the laser-made channels, increased collateral flow or other mechanisms remains unresolved. The aim of this study was to investigate whether TMR performed prior to acute coronary artery occlusion could offer protection from ischemic injury in the pig, an animal with limited native collateral coronary circulation. METHODS: In one group (n=4), TMR was performed in the anterior wall of the left ventricle 30 minutes prior to occlusion of the proximal LAD for 45 minutes. The other group (n=6) was subjected to transient ischemia of the same duration without previous TMR. Area at risk and infarct size were determined after sacrifice. RESULTS: No significant difference was found in the infarct size between the two groups (69+/-2% in the TMR group versus 62+/-4% in the control group). However, the arrhythmic index during the period of ischemia was significantly lower in the TMR group (1.0+/-0.3 vs 8.3+/-2.2, p<0.001). Blood flow in LAD increased to a maximum of 135+/-6% of baseline level three minutes after the end of the TMR procedure. CONCLUSIONS: TMR failed to reduce the infarct size following acute coronary artery occlusion in the pig, an animal with a small collateral coronary flow capacity, but reduced ischemia-related arrhythmias and increased coronary flow transiently.

Animals↗

PubMed1988

Effect of internal carotid artery occlusion on intracranial hemodynamics. Transcranial Doppler evaluation and clinical correlation.

Neurologic deficits that occur simultaneously with or subsequent to internal carotid artery occlusion may be influenced by the adequacy of the intracerebral collateral circulation. Transcranial Doppler ultrasonography was used to evaluate mean middle cerebral artery blood velocity and blood flow in major collateral arteries in 78 patients, including 39 patients with 40 internal carotid artery occlusions and 39 control patients with less severe extracranial cerebrovascular disease, matched for age and sex distribution. Middle cerebral artery blood velocity was 38.9 +/- 17.9 cm/sec ipsilateral to an occlusion, 50.9 +/- 18.3 cm/sec contralateral to an occlusion (p less than 0.01), and 56.8 +/- 14.4 cm/sec in the controls (p less than 0.01). Pulsatility index ipsilateral to an occlusion (0.86 +/- 0.32) was reduced compared with contralateral and control pulsatility indexes (1.05 +/- 0.33 and 1.03 +/- 0.18) respectively; p less than 0.05). Major intracerebral collateral arteries were detectable in 94.9% of occlusion patients and in 53.8% of controls (p less than 0.01). A posterior communicating artery was demonstrated ipsilateral to an occlusion in 80.0% of the patients and contralateral to an occlusion in 39.5% (p less than 0.01). An ipsilateral posterior communicating artery was identified in all 10 asymptomatic occlusions and in 75.8% of the symptomatic ones. Pulsatility index was 1.02 +/- 0.34 for asymptomatic occlusions and 0.76 +/- 0.30 for symptomatic occlusions (p less than 0.01). Transcranial Doppler ultrasonography permits noninvasive quantification of the cerebral hemodynamic consequences of internal carotid artery occlusion and direct evaluation of the collateral blood supply, which can be correlated with symptomatology.

Aged↗

PubMedDate not supplied

Correlation between arteriographic and electrocardiographic features during spasm in the left anterior descending coronary artery.

BACKGROUND: The clinical role of collateral vessels, which are transiently augmented during coronary artery spasm, remains controversial. OBJECTIVE: To examine the correlation between coronary arteriographic and electrocardiographic features during spasm in the left anterior descending artery (LAD). METHODS: We studied 45 patients in whom LAD spasms were induced by administration of acetylcholine or ergonovine maleate into the left coronary artery, or in whom spontaneous LAD spasms were documented during diagnostic cardiac catheterization. RESULTS: During spasm, only three patients had transient appearance or augmentation of collateral flow opacifying the LAD. In these three patients, electrocardiograms obtained from anterior precordial chest leads during LAD spasm showed ST-segment depression, ST-segment elevation followed by ST-segment depression, and only T-wave change, respectively. Except for these three patients, ST-segment elevations were observed in all other patients (31 of 34) with main-branch spasm of the LAD. However, ST-segment elevation was observed in only two of 11 patients in whom spasm of the diagonal branch alone was induced. CONCLUSIONS: Our observations suggest that the electrocardiographic changes during spasm are not always a sensitive indicator of LAD side branch spasm or LAD main-branch spasm associated with collateral circulation. From consideration of the angiographic features of the collaterals in the three patients with LAD main-branch spasm, we speculate that the balance of tonus of both the recipient and donor arteries, and the degree of organic stenosis of the recipient artery, may have important roles in the mechanism responsible for the change in the appearance of collaterals in patients with coronary spasm.

Acetylcholine↗

PubMed2005

Collaterals in acute stroke: beyond the clot.

Collateral circulation is a fundamental determinant of stroke pathophysiology. Distal arterial embolism and hypoperfusion resulting from severe proximal arterial stenosis may be offset by collateral flow. Collaterals influence whether or not infarction results. The detection and characterization of arterial deoxygenation and other consequences of collateral perfusion depend on neuroimaging techniques. Imaging advances will further the understanding of clinical correlates, including collateral sustenance and collateral failure, and possibly promote the development of collateral therapeutics. Refinements of perfusion imaging protocols may quantify the delay and dispersion of collateral flow more accurately. This review explores the role of collateral flow in acute ischemic stroke and describes the imaging modalities used to investigate phenomena "beyond the clot."

Blood Coagulation↗

PubMed1999

Larger anastomoses in angiotensinogen-knockout mice attenuate early metabolic disturbances after middle cerebral artery occlusion.

Abnormalities in the homeostasis of the renin-angiotensin system have been implicated in the pathogenesis of vascular disorders, including stroke. The authors investigated whether angiotensinogen (AGN) knockout mice exhibit differences in brain susceptibility to focal ischemia, and whether such differences can be related to special features of the collateral circulation. Wild-type and AGN-knockout mice were submitted to permanent suture occlusion of the middle cerebral artery (MCA). The collateral vascular system was visualized by systemic latex infusion, and the ischemic lesions were identified by cresyl-violet staining. The core and penumbra of the evolving infarct were differentiated by bioluminescence and autoradiographic imaging of ATP and protein biosynthesis, respectively. In wild-type mice, mean arterial blood pressure was 95.0 +/- 8.6 mm Hg, and the diameter of fully relaxed anastomotic vessels between the peripheral branches of the anterior and middle cerebral arteries 26.6 +/- 4.0 microm. In AGN knockouts, mean arterial blood pressure was significantly lower, 71.5 +/- 8.5 mm Hg (P < .01), and the anastomotic vessels were significantly larger, 29.4 +/- 4.6 microm (P < .01). One hour after MCA occlusion, AGN-knockout mice exhibited a smaller ischemic core (defined as the region of ATP depletion) but a larger penumbra (the area of disturbed protein synthesis with preserved ATP). At 24 hours after MCA occlusion, this difference disappeared, and histologically visible lesions were of similar size in both strains. The observations show that in AGN-knockout mice the more efficient collateral blood supply delays ischemic injury despite the lower blood pressure. Pharmacologic suppression of angiotensin formation may prolong the therapeutic window for treatment of infarcts.

Acute Disease↗

PubMed2004

Collateral therapeutics for cerebral ischemia.

Current therapeutic strategies for acute ischemic stroke focus on vessel recanalization or penumbral neuroprotection without consideration of collaterals. Collateral circulation defines the extent of the ischemic penumbra, providing blood flow to tissues at risk of infarction downstream from an occluded artery. Therefore, leptomeningeal collaterals are a principal delivery route for oxygen, nutrients and potential therapeutic agents. Understanding of collateral anatomy and physiology is essential for the development of effective stroke treatments. Diagnostic imaging modalities may illustrate the penumbra from the collateral perspective, defining regions of relative ischemic vulnerability. Although specific collateral therapeutics are unrealized, insight may be gleaned from subtle details of prior stroke studies. Future advances will result from nascent research in therapeutic arteriogenesis and gene therapy adapted to the specific features of the cerebral circulation.

Brain Ischemia↗

PubMed1977

Surgical and embolic treatment of cerebral arteriovenous malformations.

Twenty-eight cases of cerebral arteriovenous malformations in which the treatment consisted of embolization and/or surgical excision are reviewed. Embolization was considered an adjuvant procedure; carried out to reduce the size of the malformation or eliminate the deep arterial supply to it prior to excision. In sixteen of the cases the combined treatment was carried out with one death and one significant postoperative deficit. In the other twelve cases surgical operation or embolization alone was carried out. The anatomy of the lesion determined the applicability of embolization. Although embolization has a high degree of safety, certain pitfalls must be avoided. Changing patterns in the cerebral circulation following embolization and operation as well as the role of collateral circulation to cerebral arteriovenous malformations are discussed.

Adult↗

PubMed2001

Impaired collateral vessel development in diabetes: potential cellular mechanisms and therapeutic implications.

The formation of coronary collateral vessels is a compensatory mechanism secondary to repetitive or chronic myocardial ischemia. During the past three decades the functional and prognostic benefit of such collateral vessels has been established. There are large interindividual differences in the number and extent of collateral vessels that may be explained by differences in the anatomic situation or by differences in the individual capacity to develop functional collateral vessels. Diabetes mellitus has recently been identified as one of the first negative predictors of collateral vessel formation. Novel molecular approaches have helped to improve our understanding of the process of collateral vessel formation in recent years. Besides the process of true angiogenesis, i.e. the formation of new capillaries out of preexisting ones, the formation of a collateral circulation is largely based on the growth of preexisting arterioles (collateral vessels or anastomoses) named arteriogenesis. One important feature of arteriogenesis is the infiltration of monocytes into the growing collateral vessel. Our group shows that the ability of monocytes to migrate towards a gradient of VEGF-A is severely impaired in diabetic individuals, and this impaired response seems to be secondary to a signal transduction defect within the monocyte. In this review the pathophysiology of diabetes-related monocyte dysfunction and the potential role of VEGF-A in collateral vessel formation are discussed.

Aged↗

PubMed1985

Hypertrophy and coronary and collateral vascularity in dogs with severe chronic anemia.

The purpose of this study was to determine 1) whether a severe hypoxic stimulus could produce an increase in coronary and collateral vascularization and 2) whether minimal coronary resistance, which increases with hypertension-induced hypertrophy, decreases when hypoxia is superimposed on volume load hypertrophy. Data were obtained on 11 dogs rendered anemic to a hematocrit of 11 +/- 0.2 vol% and maintained at this level for 4 wk. Eighteen dogs with a hematocrit of 42 +/- 0.02 vol% were used as controls. After chronic anemia the coronary and collateral flows were quantitated in a beating, vasodilated, isolated heart preparation perfused solely with blood from two normal donor dogs. The following variables were significantly increased in anemia-exposed hearts compared with controls: coronary flow per gram myocardium for the left anterior descending, the circumflex, the right, and the septal arteries; ratio of total coronary flow of each vessel to body weight; and the collateral flows to each coronary vessel. Both the right and left ventricles were hypertrophied. We conclude that severe chronic anemia produces a dissociation between hypertrophy and increased minimal coronary resistance. Severe chronic anemia appears to increase vascularization of both coronary and collateral circulation probably due to tissue hypoxia. In this model coronary collateral vascularity seems to increase in the absence of a pressure difference across collaterals.

Anemia↗

PubMed1990

Functional anatomical site of intramural collaterals in dogs.

The objectives of the present study were to determine quantitatively whether the retrograde flow measurement reflects the total flow from collateral vessels or overestimates or underestimates collateral flow, and to determine the functional anatomical origin of intramural collaterals in the native dog heart. In an isolated heart preparation, three experimental procedures were used. 1) The left circumflex coronary artery was embolized with microspheres of different sizes; then retrograde flows and the peripheral coronary pressures were measured. 2) Epicardial collaterals were cauterized, and retrograde flows were measured before and after cautery. 3) Epicardial collaterals were cauterized followed by embolization of the circumflex coronary artery with different size spheres. We found that 1) the retrograde flow measurement underestimates the total collateral flow to the circumflex coronary artery by approximately 25%, 2) intramural collateral flow constitutes 58 +/- 3.5% of the retrograde flow measurement, 3) the antegrade component of blood flow that is not measured during a retrograde flow measurement is from the intramural collateral circulation, and 4) the functional site of origin of intramural collaterals is greater than 25 microns but less than 80 microns in diameter. We conclude that, in our preparation, retrograde flow underestimates total collateral flow, and that intramural collateral flow is a major component of retrograde flow in the native dog heart.

Animals↗

PubMed1995

Time dependency of the acetazolamide effect on cerebral hemodynamics in patients with chronic occlusive cerebral arteries. Early steal phenomenon demonstrated by [15O]H2O positron emission tomography.

BACKGROUND AND PURPOSE: The acetazolamide effect is thought to reach a maximum at 10 to 20 minutes after administration. However, we sometimes encountered patients who showed a transient deterioration of ischemic symptoms several minutes after acetazolamide administration. We therefore considered that a steal phenomenon may occur before the acetazolamide effect reaches a maximum. We evaluated the time dependency of the acetazolamide effect on cerebral hemodynamics in patients with severe stenosis or occlusion of the unilateral internal carotid artery. METHODS: The subjects consisted of 13 patients with severe stenosis or occlusion of the unilateral internal carotid artery. Regional cerebral blood flow was measured at the resting state and at 5 and 20 minutes after the intravenous administration of 1 g acetazolamide by the use of the [15O]H2O bolus-injection method and positron emission tomography. The steal phenomenon was interpreted as positive when the regional cerebral blood flow values decreased by more than 10% after the administration of acetazolamide in more than one region of interest. RESULTS: A steal phenomenon was observed in 5 of 13 patients at 5 minutes after acetazolamide administration on the occlusive side, whereas it was observed in only 1 patient at 20 minutes. Thus, this phenomenon was observed more frequently in the early phase of the acetazolamide test. It was also observed more frequently in patients with poorly developed collateral circulation. CONCLUSIONS: Our acetazolamide [15O]H2O positron emission tomography study revealed an early steal phenomenon at 5 minutes after intravenous administration of acetazolamide, which may be a cause of the transient deterioration of ischemic symptoms during the acetazolamide test.

Acetazolamide↗

PubMedDate not supplied

Cerebral arterial revascularization: the value of repeated angiography in selection of patients for operation.

Three patients with occlusive cerebrovascular disease were evaluated for possible extracranial-intracranial arterial anastomosis. Cerebral angiography repeated at a later date revealed disappearance of the initial vascular stenosis or occlusion and development of extensive collateral circulation. It was concluded in these cases that surgical revascularization would not improve upon natural revascularization. Repeated angiography provides information of value to the physician who must make a decision about such surgical treatment.

Carotid Artery Diseases↗

PubMed1993

Graft flow and reactive hyperemia immediately following coronary artery bypass surgery.

Graft flow rates and reactive hyperemia (RH) were measured in 166 patients undergoing coronary artery bypass graft surgery. A wide range of graft flow rates was found within 273 grafts: the left anterior descending (LAD) arterial graft flow rate was the highest; the left circumflex (LCX) arterial graft flow rate was the lowest; and the right coronary (RCA) arterial graft flow rate was in between. There was no relation between the severity of coronary stenosis and basal graft flow. In LAD and RCA grafts, there was a higher percentage of positive RH (> 10%) in vessels with severe obstruction (grades 4 and 5). No correlation was demonstrated between graft flow and RH in patients with or without myocardial infarction. In addition, RH increased in patients with good coronary arterial collateral circulation (p < 0.05). Our data support the theory that coronary collaterals do not provide sufficient blood flow to the myocardium supplied by a stenotic coronary artery.

Adult↗

Refine your search to explore more results.