Characterization of segmental collateral blood flow in the small intestine

1985 ◽  
Vol 249 (2) ◽  
pp. G228-G235 ◽  
Author(s):  
G. B. Bulkley ◽  
W. A. Womack ◽  
J. M. Downey ◽  
P. R. Kvietys ◽  
D. N. Granger
Keyword(s):  
Blood Flow ◽  
Reactive Hyperemia ◽  
Arterial Occlusion ◽  
Control Flow ◽  
Collateral Flow ◽  
Collateral Blood Flow ◽  
Donor Segment ◽  
Capillary Bed ◽  
Adjacent Segments

Collateral blood flow and the pressures and resistances determining that flow were measured between two adjacent segments of canine jejunum following acute occlusion of the arterial branch perfusing one of the segments (the “recipient” segment). Collateral flow was approximately 55% of control flow in the recipient segment. This flow was provided by an equal increment in arterial flow to the nonischemic (“donor”) segment, such that pressures, resistances, and flows in the donor segment were not affected. Virtually all of the total collateral flow was derived from precapillary channels and was therefore available to the capillary bed of the recipient segment. Collateral flow was adequate to maintain the recipient segment in a nonischemic state, as indicated by the absence of a reactive hyperemia following release of the arterial occlusion. Selective occlusions of intramural or extramural collateral channels indicate that about two-thirds of the total collateral flow is derived from the extramural (marginal) vessels, while the remainder is supplied by intramural collaterals. For the most part collateral flow between adjacent segments is determined simply by the pressure gradient between connecting collateral channels.

scholarly journals Failure of Collateral Blood Flow is Associated with Infarct Growth in Ischemic Stroke

2013 ◽  
Vol 33 (8) ◽  
pp. 1168-1172 ◽  
Author(s):  
Bruce CV Campbell ◽  
Søren Christensen ◽  
Brian M Tress ◽  
Leonid Churilov ◽  
Patricia M Desmond ◽  
...  
Keyword(s):  
Blood Flow ◽  
Ischemic Stroke ◽  
Arterial Occlusion ◽  
Perfusion Magnetic Resonance Imaging ◽  
Lesion Volume ◽  
Collateral Flow ◽  
Collateral Blood Flow ◽  
Collateral Vessel ◽  
Magnetic Resonance Imaging Mri ◽  
Simultaneous Assessment

Changes in collateral blood flow, which sustains brain viability distal to arterial occlusion, may impact infarct evolution but have not previously been demonstrated in humans. We correlated leptomeningeal collateral flow, assessed using novel perfusion magnetic resonance imaging (MRI) processing at baseline and 3 to 5 days, with simultaneous assessment of perfusion parameters. Perfusion raw data were averaged across three consecutive slices to increase leptomeningeal collateral vessel continuity after subtraction of baseline signal analogous to digital subtraction angiography. Changes in collateral quality, Tmax hypoperfusion severity, and infarct growth were assessed between baseline and days 3 to 5 perfusion-diffusion MRI. Acute MRI was analysed for 88 patients imaged 3 to 6 hours after ischemic stroke onset. Better collateral flow at baseline was associated with larger perfusion-diffusion mismatch (Spearman's Rho 0.51, P < 0.001) and smaller baseline diffusion lesion volume (Rho − 0.70, P < 0.001). In 30 patients without reperfusion at day 3 to 5, deterioration in collateral quality between baseline and subacute imaging was strongly associated with absolute ( P = 0.02) and relative ( P < 0.001) infarct growth. The deterioration in collateral grade correlated with increased mean Tmax hypoperfusion severity (Rho − 0.68, P < 0.001). Deterioration in Tmax hypoperfusion severity was also significantly associated with absolute ( P = 0.003) and relative ( P = 0.002) infarct growth. Collateral flow is dynamic and failure is associated with infarct growth.

Peak calf blood flow estimates are higher with Dohn than with Whitney plethysmograph

1996 ◽  
Vol 81 (3) ◽  
pp. 1418-1422 ◽  
Author(s):  
D. N. Proctor ◽  
J. R. Halliwill ◽  
P. H. Shen ◽  
N. E. Vlahakis ◽  
M. J. Joyner
Keyword(s):  
Blood Flow ◽  
Reactive Hyperemia ◽  
Arterial Occlusion ◽  
Venous Occlusion ◽  
Calf Blood Flow ◽  
Absolute Flow ◽  
Wide Range ◽  
Before And After ◽  
The Mean ◽  
Highly Correlated

Estimates of calf blood flow with venous occlusion plethysmography vary widely between studies, perhaps due to the use of different plethysmographs. Consequently, we compared calf blood flow estimates at rest and during reactive hyperemia in eight healthy subjects (four men and four women) with two commonly used plethysmographs: the mercury-in-silastic (Whitney) strain gauge and Dohn air-filled cuff. To minimize technical variability, flow estimates were compared with a Whitney gauge and a Dohn cuff on opposite calves before and after 10 min of bilateral femoral arterial occlusion. To account for any differences between limbs, a second trial was conducted in which the plethysmographs were switched. Resting flows did not differ between the plethysmographs (P = 0.096), but a trend toward lower values with the Whitney was apparent. Peak flows averaged 37% lower with the Whitney (27.8 +/- 2.8 ml.dl-1.min-1) than with the Dohn plethysmograph (44.4 +/- 2.8 ml.dl-1.min-1; P < 0.05). Peak flow expressed as a multiple above baseline was also lower with the Whitney (10-fold) than with the Dohn plethysmograph (14.5-fold; P = 0.02). Across all flows at rest and during reactive hyperemia, estimates were highly correlated between the plethysmographs in all subjects (r2 = 0.96-0.99). However, the mean slope for the Whitney-Dohn relationship was only 60 +/- 2%, indicating that over a wide range of flows the Whitney gauge estimate was 40% lower than that for the Dohn cuff. These results demonstrate that the same qualitative results can be obtained with either plethysmograph but that absolute flow values will generally be lower with Whitney gauges.

Differences in reactive hyperemia between the intestinal mucosa and muscularis

1984 ◽  
Vol 247 (6) ◽  
pp. G617-G622
Author(s):  
A. P. Shepherd ◽  
G. L. Riedel
Keyword(s):  
Blood Flow ◽  
Metabolic Rate ◽  
Laser Doppler Velocimetry ◽  
Reactive Hyperemia ◽  
Arterial Occlusion ◽  
Oxygen Demand ◽  
Laser Doppler ◽  
Doppler Velocimetry ◽  
Total Blood ◽  
Total Blood Flow

In a previous study of regional intestinal blood flow by laser-Doppler velocimetry, we noted that the mucosa displayed reactive hyperemia following arterial occlusion but that the muscularis did not. Therefore, to determine whether this observation is generally valid, we compared responses of the mucosa and muscularis externa to arterial occlusion. We measured total blood flow to isolated loops of canine small bowel with an electromagnetic flow probe on the supply artery; blood flow either in the mucosa or in the muscularis was measured by laser-Doppler velocimetry. Mucosal and total blood flow consistently showed reactive hyperemia in response to a 60-s occlusion, but the muscularis did not. To determine whether metabolic rate influenced reactive hyperemia, we increased enteric oxygen uptake by placing 5% bile and transportable solutes in the lumen; these agents increased oxygen consumption by 36%. After a 60-s occlusion, the durations of both total and mucosal reactive hyperemia were significantly prolonged by increased metabolic rate. Similarly, the payback-to-debt ratios in both total and mucosal blood flows were significantly increased at elevated metabolic rate. These data support the conclusions that reactive hyperemia occurs more frequently and has a greater magnitude in the mucosa compared with the muscularis and both total and mucosal reactive hyperemia are strongly influenced by the preocclusive oxygen demand. These findings therefore constitute further evidence that metabolic factors contribute to reactive hyperemia in the intestinal circulation.

Effects of time on volume and distribution of coronary collateral flow

1976 ◽  
Vol 230 (2) ◽  
pp. 279-285 ◽  
Author(s):  
ML Marcus ◽  
RE Kerber ◽  
J Ehrhardt ◽  
FM Abboud
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Coronary Occlusion ◽  
Marked Decrease ◽  
Relative Proportion ◽  
Collateral Flow ◽  
Coronary Vascular Resistance ◽  
Collateral Blood Flow ◽  
Coronary Collateral Flow ◽  
Hemodynamic Measurements

Changes in the volume and distribution of collateral blood flow were studied during the 1st h after coronary occlusion in nine open-chest dogs. Labeled microspheres (7-10 mum) were injected into the left atrium prior to and 20 s, 5 min, and 60 min after acute occlusion of the midcircumflex coronary artery so that myocardial perfusion to small segments of the entire left ventricle could be measured. The segmental perfusions were classified as normally perfused, severely hypoperfused, moderately hypoperfused, and borderline hypoperfused. Standard hemodynamic measurements were obtained and relative coronary vascular resistance to the normally perfused and hypoperfused zones was calculated. The principal conclusions of the study are as follows: 1) during the 1st h after coronary occlusion the collateral flow to the hypoperfused myocardium increases substantially; 2) the increase in collateral flow is distributed fairly evenly to various hypoperfused zones and is associated with a marked decrease in coronary vascular resistance; and 3) as a result of this influx in collateral flow the size of the hypoperfused area decreases and the relative proportion of severely hypoperfused segments within the hypoperfused area decreases.

Characteristics of reactive hyperemia in the cerebral circulation

1984 ◽  
Vol 246 (1) ◽  
pp. H52-H58 ◽  
Author(s):  
J. K. Gourley ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
White Matter ◽  
Cerebral Ischemia ◽  
Gray Matter ◽  
Cerebral Circulation ◽  
Time Course ◽  
Reactive Hyperemia ◽  
Arterial Occlusion ◽  
Maximal Peak ◽  
Minimal Resistance

Reactive hyperemia has been characterized in many vascular beds, but little is known about quantitative characteristics of reactive hyperemia in the cerebral circulation. We measured velocity of blood flow and pial artery diameter to characterize the time course of reactive hyperemia and used microspheres to study regional blood flow in the brain. Cerebral ischemia was produced by raising intracranial pressure or by arterial occlusion with a cuff around the neck. Five seconds of ischemia produced virtually maximal peak reactive hyperemia, and 30 s of ischemia produced maximal peak reactive hyperemia. During reactive hyperemia after 30 s of cerebral ischemia, there was a three- to fourfold increase in cerebral blood flow. The magnitude of reactive hyperemia was greater in gray matter than in white matter. Minimal resistance during reactive hyperemia, after ischemia produced by arterial occlusion, is similar to minimal resistance during seizures or hypercapnia, which suggests that reactive hyperemia produces maximal vasodilatation. Oxygen saturation of cerebral venous blood increased almost twofold during reactive hyperemia, which indicates that factors in addition to venous (and presumably tissue) oxygen are important determinants of reactive hyperemia. In summary, 1) we have characterized the time course of reactive hyperemia in the cerebral circulation; 2) reactive hyperemia after arterial occlusion produces maximal cerebral vasodilatation; and 3) there is marked heterogeneity of the response, with much larger increases in flow in cortical gray matter than white matter.

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.

scholarly journals Relationship between haemodynamic impairment and collateral blood flow in carotid artery disease

2017 ◽  
Vol 38 (11) ◽  
pp. 2021-2032 ◽  
Author(s):  
Nolan S Hartkamp ◽  
Esben T Petersen ◽  
Michael A Chappell ◽  
Thomas W Okell ◽  
Maarten Uyttenboogaart ◽  
...  
Keyword(s):  
Blood Flow ◽  
Carotid Artery ◽  
Carotid Artery Disease ◽  
Tissue Level ◽  
Cerebrovascular Reactivity ◽  
Collateral Flow ◽  
Collateral Blood Flow ◽  
Ischaemic Damage ◽  
Before And After ◽  
Artery Disease

Collateral blood flow plays a pivotal role in steno-occlusive internal carotid artery (ICA) disease to prevent irreversible ischaemic damage. Our aim was to investigate the effect of carotid artery disease upon cerebral perfusion and cerebrovascular reactivity and whether haemodynamic impairment is influenced at brain tissue level by the existence of primary and/or secondary collateral. Eighty-eight patients with steno-occlusive ICA disease and 29 healthy controls underwent MR examination. The presence of collaterals was determined with time-of-flight, two-dimensional phase contrast MRA and territorial arterial spin labeling (ASL) imaging. Cerebral blood flow and cerebrovascular reactivity were assessed with ASL before and after acetazolamide. Cerebral haemodynamics were normal in asymptomatic ICA stenosis patients, as opposed to patients with ICA occlusion, in whom the haemodynamics in both hemispheres were compromised. Haemodynamic impairment in the affected brain region was always present in symptomatic patients. The degree of collateral blood flow was inversely correlated with haemodynamic impairment. Recruitment of secondary collaterals only occurred in symptomatic ICA occlusion patients. In conclusion, both CBF and cerebrovascular reactivity were found to be reduced in symptomatic patients with steno-occlusive ICA disease. The presence of collateral flow is associated with further haemodynamic impairment. Recruitment of secondary collaterals is associated with severe haemodynamic impairment.

Forearm Vasoreactivity in Type I Diabetic Subjects

2001 ◽  
Vol 26 (1) ◽  
pp. 34-43 ◽  
Author(s):  
Jason D. Allen ◽  
Michael Welsch ◽  
Nikki Aucoin ◽  
Robert Wood ◽  
Matt Lee ◽  
...  
Keyword(s):  
Risk Factors ◽  
Blood Flow ◽  
Vascular Function ◽  
Forearm Blood Flow ◽  
Reactive Hyperemia ◽  
Arterial Occlusion ◽  
Type I ◽  
Handgrip Exercise ◽  
Blood Flows

This study compared forearm vasoreactivity in 15 Type 1 diabetic subjects with 15 healthy controls. The groups were matched for age, exercise capacity, and the absence of other cardiovascular risk factors. Vasoreactivity was measured using strain gauge plethysmography, at rest, after arterial occlusion (OCC), and following OCC coupled with handgrip exercise (ROCC). Forearm blood flows were significantly elevated between conditions 2.58 ± 0.37 ml/100mltissue at rest to 26.80 ± 6.56 after OCC and 32.80 ± 8.26ml/100mltissue following ROCC in Type 1 diabetic subjects. There were no differences in forearm blood flow between groups for any of the conditions. These data indicate the degree of forearm blood flow is directly related to the intensity of the vasodilatory stimulus. However, our study did not reveal evidence of impaired vasodilatory capacity in Type 1 diabetic subjects compared to controls in the absence of other risk factors. Key words: IDDM, vascular function, exercise, fitness, and reactive hyperemia

Changes in the myocardial area at risk, infarct size, and collateral flow following nicardipine infusion in dogs

1991 ◽  
Vol 69 (12) ◽  
pp. 1789-1796
Author(s):  
Reena Sandhu ◽  
George P. Biro
Keyword(s):  
At Risk ◽  
Blood Flow ◽  
Infarct Size ◽  
Blue Dye ◽  
Collateral Flow ◽  
Collateral Blood Flow ◽  
Area At Risk ◽  
Arterial Blood ◽  
Myocardial Area ◽  
Size Limitation

The area at risk of infarction after an acute occlusion of the left anterior descending coronary artery was defined in anesthetized dogs using the distribution of 99mTc-labelled albumin microaggregates and Monastral blue dye. In thirteen dogs, it was determined that these two particulate labels identified identical areas of unperfused myocardium. In a second group of dogs (n = 12), the risk areas determined at 10 (99mTc-labelled macroaggregates) and at 180 min (Monastral blue dye) were found to be identical, with no change in collateral blood flow, indicating the absence of a spontaneous change in underperfused myocardium over this time. In a third group of dogs (n = 17) nicardipine was infused (10 μg∙kg−1∙min−1 for 5 min, followed by 8 μg∙kg−1∙min−1 for 165 min). This resulted in a significant and sustained fall (32 ± 4 mmHg; 1 mmHg = 133.32 Pa) in mean arterial blood pressure but no significant change in collateral blood flow was found, except for a marginal increase in the center of the ischemic zone. Area at risk and infarct sizes were also not significantly different between the latter two groups (18.2 ± 4.1 vs. 21.6 ± 4.0% of left ventricle). In this model, the magnitude of the area at risk appears to be determined early after a coronary occlusion and appears to be unmodified by treatment with nicardipine begun after the occlusion.Key words: area at risk, nicardipine, collateral flow, risk region, risk zone, infarct size limitation.

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