Changes In Collateral Blood Flow Research Articles

Is There a Role for the Vascular Laboratory in Supporting Home-Based Vascular Rehabilitation Programs?

A pilot study assessing the efficacy of a nonsupervised exercise program for intermittent claudication is described, and case descriptions of 4 patients are presented. The ankle/brachial index (ABI) has long been the standard for evaluating lower limb perfusion; however, the ABI is not reliable with noncompressible arteries. Pedal acceleration time (PAT), a novel technique that quantifies perfusion using duplex ultrasound by measuring the acceleration time of the arterial waveform, has been found to be more reliable. When considering only ABI, nonsupervised exercise is not sufficient management of claudication in peripheral arterial disease (PAD), but PAT may be more sensitive to changes in collateral blood flow developed by exercise. We initiated a pre-post study from a single institution over 6 weeks that included a walking program for patients with claudication with modified resistance band exercises for amputees. Changes in symptoms, smoking, and the perfusion markers of resting ABI and anterior pedal and posterior pedal PAT were monitored. Of the 4 patients described, 3 noted symptomatic improvement with categorical improvement in PAT. Compliant patients do report success with at-home exercise regimens. Patients who are unsuccessful may benefit from supervised vascular rehabilitation. PAT, in comparison with ABI, may offer a better approach to monitor this progression and offer a stepwise approach to the management of PAD.

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

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.

Laser Speckle Contrast Imaging of Collateral Blood Flow during Acute Ischemic Stroke

Collateral vasculature may provide an alternative route for blood flow to reach the ischemic tissue and partially maintain oxygen and nutrient support during ischemic stroke. However, much about the dynamics of stroke-induced collateralization remains unknown. In this study, we used laser speckle contrast imaging to map dynamic changes in collateral blood flow after middle cerebral artery occlusion in rats. We identified extensive anastomatic connections between the anterior and middle cerebral arteries that develop after vessel occlusion and persist for 24 hours. Augmenting blood flow through these persistent yet dynamic anastomatic connections may be an important but relatively unexplored avenue in stroke therapy.

Phase contrast MR imaging to measure changes in collateral blood flow after stenting of recurrent aortic coarctation: Initial experience

To assess the feasibility of using phase contrast magnetic resonance (PC-MR) imaging to measure the change in collateral blood flow early after stenting of aortic coarctation. A total of 10 consecutive patients with coarctation of the aorta underwent MR imaging, X-ray angiography, and stent placement. PC-MR at two sites in the descending aorta was performed before and early after stenting in order to estimate collateral inflow to the descending thoracic aorta. The collateral flow and collateral flow percentage before and after stent placement were compared. Before stenting, the mean proximal aortic flow = 43.9 +/- 14.6 mL/second; mean distal flow = 54.2 +/- 10 mL/second; collateral flow = 10.2 +/- 6.8 mL/second; and collateral flow percentage = 30.1 +/- 27.9%. After stenting, the mean proximal aortic flow = 62.1 +/- 17.9 mL/second; mean distal flow = 60 +/- 19 mL/second; collateral flow = -1.9 +/- 3.7 mL/second; and collateral flow percentage = -3.3 +/- 6.8%. PC-MR can be used to measure changes in collateral circulation after stent treatment of coarctation of the aorta.

Time course of changes in collateral blood flow and isolated vessel size and gene expression after femoral artery occlusion in rats.

The objectives of this study were to assess the time course of enlargement and gene expression of a collateral vessel that enlarges following occlusion of the femoral artery and to relate these responses to the increases in collateral-dependent blood flow to the calf muscles in vivo. We employed exercise training to stimulate collateral vessel development. Rats were exercise trained or kept sedentary for various times of up to 25 days postbilateral occlusion (n=approximately 9/time point). Collateral blood flow to the calf muscles, determined with microspheres, increased modestly over the first few days to approximately 40 ml.min(-1).100 g(-1) in sedentary animals; the increase continued over time to approximately 80 ml.min(-1).100 g(-1) in the trained animals. Diameters of the isolated collateral vessels increased progressively over time, whereas an increased vessel compliance observed at low pressures was similar across time. These responses were greater in the trained animals. The time course of upregulation of vascular endothelial growth factor and placental growth factor, and particularly endothelial nitric oxide synthase and fms-like tyrosine kinase 1, mRNAs in the isolated collateral vessel implicates these factors as integral to the arteriogenic process. Collateral vessel enlargement and increased compliance at low pressures contribute to the enlarged circuit available for collateral blood flow. However, modulation of the functioning collateral vessel diameter, by smooth muscle tone, must occur to account for the observed increases in collateral blood flow measured in vivo.

Angiographic methods to assess human coronary angiogenesis

It is unclear how agents designed to promote angiogenesis in the human heart affect the arteriographic appearance of the collateral circulation. Possible changes in collateral vessels include new collateral vessels arising from epicardial arteries, new branches emanating from existing collateral vessels, wider or longer collateral vessels, and higher dye transit rates that result in improved recipient vessel filling. Given the multiple mechanisms by which these new agents may improve myocardial perfusion, a rigorous, systematic, and comprehensive analysis of coronary arteriograms is required to discern the true mechanism of benefit. The method of analysis must account for potential changes in collateral blood flow, number, branching pattern, and length as well as changes in recipient vessel filling. The ability to detect differences between intricate networks of vessels in an angiographic study is dependent on maintaining consistency in cinefilming as well as the core laboratory methods between time points. In this report, we describe the methodology our angiographic core laboratory has found to be most effective to evaluate these very complex angiograms and attempt to capture all the possible modalities of angiogenesis. (Am Heart J 1999;137:169-79.)

The Antioxidant, N-(2-mercaptopropionyl)-glycine (MPG), Does Not Reduce Myocardial Infarct Size in an Acute Canine Model of Myocardial Ischemia and Reperfusion.

Oxygen radical generation can be measured when blood flow is restored to previously ischemic tissue. Although several studies have suggested oxygen radicals contribute to lethal injury of myocardium after ischemia, other studies have failed to confirm this implication. Antioxidants, such as N-(2-mercaptoptopionyl)-glycine (MPG) and superoxide dismutase, have had inconsistent effects on lethal myocardial injury in animal models of ischemia and reperfusion. Many variables influence lethal myocardial injury in these models: time of ischemia, time of reperfusion, dose of antioxidant, myocardial oxygen demand, area at risk, collateral blood flow, and body core temperature. The purpose of this study is to test the effects of infusion of MPG on lethal reperfusion injury in a canine model of ischemia and reperfusion with these variables tightly controlled. The left anterior descending coronary artery of anesthetized dogs was ligated for 90 minutes and reperfused for 4 hours. MPG was infused (100 mg/kg/h) 15 minutes before the end of ischemia and throughout reperfusion. Core body temperature was closely monitored, and infarct size was adjusted to transmural myocardial blood flow during ischemia. MPG had no effect on infarct size or infarct size adjusted for changes in collateral blood flow. These data reinforce a general difficulty in demonstrating the effects of antioxidant therapies on lethal injury, even when closely monitoring covariates known to impact infarct size.

Effects of intracoronary cromakalim on postischaemic contractile function and action potential duration.

The effects of intracoronary cromakalim (1 microgram.kg-1 x min-1) on postischaemic contractile function and monophasic action potential duration at the 95% repolarisation level (APD95) were assessed in a canine model of stunned myocardium. Animals (n = 24) were anaesthetised, subjected to a left thoracotomy, and the left anterior descending coronary artery was isolated. Measurements of segmental shortening and monophasic action potential were taken before drug, after drug, during a 15 min occlusion, and at times following reperfusion. Cromakalim significantly improved reperfusion recovery of function. Both preischaemic and postischaemic myocardial blood flows were increased with cromakalim, although there was no significant change in collateral blood flow during ischaemia relative to vehicle. In the absence of ischaemia, cromakalim reduced APD95 by 8%. There was no change in APD95 with vehicle alone. During coronary occlusion, cromakalim significantly reduced APD95 by 27% as compared with 8% in the vehicle group. APD95 values returned to preocclusion levels within minutes of reperfusion and remained there throughout reperfusion (30 min). Glyburide (3.0 mg.kg-1 intravenously), a blocker of ATP sensitive potassium channels, abolished the APD95 effects of cromakalim. One out of six animals given glyburide survived through reperfusion. In contrast, four out of five of the glyburide+cromakalim treated animals survived through reperfusion. Cardioprotection with cromakalim is likely to be mediated through activation of ATP sensitive potassium channels, measured as a decrease in action potential duration. Shortening of action potential duration with cromakalim was shown to be augmented in the presence of ischaemia. It is suggested that a possible interrelationship between cardioprotection and action potential duration shortening may exist such that the cardioprotective effects of cromakalim may be selective for ischaemic conditions.

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

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 micrograms.kg-1.min-1 for 5 min, followed by 8 micrograms.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.

Progressive change in collateral blood flow after coronary occlusion in conscious dogs.

This study used a retrospective analysis of infarcted and salvaged tissue samples to determine the patterns of blood flow changes (radioactive microsphere technique) that occur within the area at risk during the first 24 h after coronary artery occlusion (CAO) in conscious dogs. With the triphenyl tetrazolium chloride (TTC) technique, individual samples were selected and included in either the infarcted (TTC-negative) or salvaged (TTC-positive) group. The infarcted and salvaged samples were paired according to blood flow levels of 0.1-0.2, 0.2-0.3, or 0.3-0.4 ml.min-1.g-1 at either 5 min, 1 h, 3 h, or 6 h after CAO. In tissue samples that were salvaged, blood flow rose progressively, i.e., from 5 min to 1 h, from 1 to 3 h, from 3 to 6 h, and from 6 to 24 h. Blood flow to infarcted tissue rose only in the longest interval, from 6 to 24 h after CAO. When blood flow levels were less than 0.1 ml.min-1.g-1, virtually all the samples were infarcted, whereas corresponding lesser amounts of infarction were observed with increasing blood flow levels after CAO. Thus, in the conscious dog, blood flow rises progressively to salvaged but not infarcted tissue within the area at risk. Except for myocardium with blood flow levels less than 0.1 ml.min-1.g-1, the blood flow levels at any of the time points after CAO could not be used to predict necrosis.

Topographic Correspondence of Contrast Echocardiographic Perfusion Mapping and Myocardial Infarct Extent After Varying Durations of Coronary Occlusion

After acute coronary occlusion, the extent of dysfunction exceeds the extent of infarction by a variable amount. Contrast echocardiography has been shown to be a good predictor of the extent of acute infarction after permanent occlusion. We used hydrogen peroxide contrast echocardiography to study the temporal and topographic relationship between contrast enhancement and tissue viability during acute myocardial infarction in 32 dogs undergoing 1, 2, 3, or 4 hours of circumflex occlusion before reperfusion. To account for changes in collateral blood flow, contrast studies were performed by aortic root injection immediately before reperfusion. The area, circumference, and transmural extent of the region at risk in vivo by contrast echocardiography were statistically unchanged regardless of the duration of occlusion before reperfusion. Echo contrast defect analysis of the risk region predicted the area, circumference, and transmural extent of infarcts reperfused at 2 or more hours (r = 0:81, 0.84, 0.71, respectively). For the 1-hour occlusion group, contrast defect analysis predicted the circumference at risk but markedly overestimated the area and transmural extent of infarction. These data indicate that the circumferential extent of infarction can be identified by contrast echo and is fixed by 1 hour of occlusion. Infarction progression transmurally within the circumferential boundaries had nearly reached the transmural contrast extent by 2 hours of occlusion in this model. Assuming the development of a similar high contrast agent safe for human injection, aortic root contrast echocardiography could be useful to predict myocardium at risk of infarction early after occlusion. Late after occlusion it could be of value to predict the presence of still viable myocardial layers within the dysfunctional infarct region.

Early changes in collateral blood flow to ischemic myocardium and their influence on bimodal vulnerability during the first 30 min of acute coronary artery occlusion in dogs.

Coronary collateral blood flow and its changes during the first 30 min of acute coronary artery occlusion were studied in 34 anesthetized dogs to clarify its influence on the vulnerability of the heart in this first arrhythmic phase. Collateral flow was determined with 9-micron tracer microspheres (TM) injected at 1, 10 and 30 min after acute proximal occlusion of the left circumflex (LCX, n = 30) or left anterior descending (LAD, n = 4) coronary artery. The post-mortem selective retrograde coronary angiography was used to evaluate the functional extent of preexisting coronary collaterals. After acute LCX occlusions collateral flow increased significantly (p less than 0.05) from 17.8 +/- 2.7 ml.(min.100 g)-1 (mean +/- SE; n = 13) at 1 min to 29.3 +/- 5.1 ml . (min . 100 g)-1 at 30 min of occlusion in animals with well-formed preexisting coronary collaterals (group 1), whereas it was very low (4.7 +/- 0.6 ml . (min . 100 g)-1; n = 13) and changed only slightly in dogs with poor collaterals (group 2). Most of these animals died by ventricular fibrillation (VF) before a second measurement could be carried out. In four dogs with poor collaterals but an unusually small LCX area (group 3), flow remained almost constant (11.0 +/- 4.7 versus 11.0 +/- 4.4 ml . (min . 100 g)-1) during this period. Similar results were obtained in animals with acute LAD occlusion (group 4). Ventricular extrasystoles (VES) mainly developed in animals with poor collaterals and respective low and almost unchanging collateral flow (group 2,3,4) while none or only a few VES occurred in dogs in which flow initially was clearly higher and increased significantly (group 1). The animals of group 1, 3 and 4 all survived the first arrhythmic phase, whereas all the animals of group 2 died by VF, either in the arrhythmic subphase Ia (n = 7) or Ib (n = 6). The results of the present study show that only the initial magnitude of flow is decisive for the development of VES and VF during the first arrhythmic phase, whereas the subsequent increase in flow is of no importance to the bimodal vulnerability in the first arrhythmic phase (subphases Ia and Ib). The in vivo measured critical minimal collateral flow of about 5 ml . (min . 100 g)-1 corresponds well with the survival limit (border between collateral state III and IV) previously determined by post-mortem retrograde coronary angiography.

Effects of inotropic and chronotropic stimuli on acute myocardial ischemic injury. II. Studies with dopamine and ouabain in the barbiturate-anesthetized dog.

To test the hypothesis that selective increases in inotropic state without concomitant acceleration of heart rate would not augment acute ischemic injury in the non-failing heart of the anesthetized dog, we carried out studies in 16 dogs subjected to serial 10-min occlusions of the left anterior descending coronary artery. The severity of ischemic injury was determined by mass spectrometric measurement of the rise in intramural carbon dioxide tension (delta PmCO2) in the ischemic zone, and inotropic stimulation was provided by either dopamine or ouabain. In Group I dogs (n = 9), dopamine [4 +/- 1 (SD) micrograms/kg/min] was infused before the final occlusion to increase left ventricular (LV) dP/dt without changing heart rate; delta PmCO2 was not significantly different between control (64 +/- 21 mm Hg) and postdopamine (67 +/- 22 mm Hg) occlusions. In Group II dogs (n = 7), ouabain (0.03 mg/kg) was administered 15 min before the final occlusion, resulting in a significant increase in LV dP/dt and a slight decrease in heart rate (average 13 beats/min); delta PmCO2 was slightly decreased in the occlusion after ouabain (60 +/- 12 mm Hg) compared with the preceding occlusion without inotropic stimulation (67 +/- 13 mm Hg), p less than 0.05. Throughout the studies in both groups, there were no significant changes in collateral blood flow to the central ischemic zone, or in heart rate-systolic arterial pressure product, an estimate of myocardial oxygen consumption. Analyses of individual responses revealed that when LV dP/dt increased by 50% or more after dopamine or ouabain, ischemia was more likely to intensify.(ABSTRACT TRUNCATED AT 250 WORDS)

Early changes in collateral blood flow during myocardial infarction in conscious dogs.

We studied the early changes in collateral blood flow (CBF) after acute coronary artery occlusion and the relation of these changes to subsequent necrosis. We measured CBF with 7--9 microns radioactive microspheres before and at various times after circumflex artery occlusion in 42 conscious dogs that were killed 48 h later. CBF increased from 20 s postocclusion to later measurements (5 min, 15 min, 1 h, or 6 h) and did so in both necrotic and nonnecrotic areas of the occluded bed. However, the increase in CBF over time was not gradual, but appeared to occur between 20 s and 5 min, with no further changes for up to 6 h. There was a gradation of CBF in the occluded bed, from periphery to center and subepicardium to subendocardium. Central and subendocardial regions with CBF less than 0.40 ml-min-1-g-1 at 5--15 min postocclusion subsequently showed necrosis whereas epicardial and lateral regions with CBF greater than 0.50 ml/min did not. Thus CBF increases very early throughout the occluded coronary bed, and the level of CBF by 5 min appears to determine whether necrosis ultimately occurs.

Effects of intracoronary potassium chloride on electrograms of canine Purkinje fibers in six-hour- to four-week-old myocardial infarcts. An indication of time-dependent changes in collateral blood flow.

HomeCirculation ResearchVol. 44, No. 3Effects of intracoronary potassium chloride on electrograms of canine Purkinje fibers in six-hour- to four-week-old myocardial infarcts. An indication of time-dependent changes in collateral blood flow. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAbstractPDF/EPUBEffects of intracoronary potassium chloride on electrograms of canine Purkinje fibers in six-hour- to four-week-old myocardial infarcts. An indication of time-dependent changes in collateral blood flow. K H Dangman, H H Wang and A L Wit K H DangmanK H Dangman Search for more papers by this author , H H WangH H Wang Search for more papers by this author and A L WitA L Wit Search for more papers by this author Originally published1 Mar 1979https://doi.org/10.1161/01.RES.44.3.392Circulation Research. 1979;44:392–405 Previous Back to top Next FiguresReferencesRelatedDetailsCited By Wit A (2017) Basic Electrophysiologic Mechanisms of Sudden Cardiac Death Caused by Acute Myocardial Ischemia and Infarction, Cardiac Electrophysiology Clinics, 10.1016/j.ccep.2017.07.004, 9:4, (525-536), Online publication date: 1-Dec-2017. PATTERSON E, SCHERLAG B and LAZZARA R (1992) Ectopic Ventricular Beats Originating in Ischemically-Injured Left Ventricular Epicardium, 24 Hours Following Coronary Artery Occlusion in the Dog, Journal of Cardiovascular Electrophysiology, 10.1111/j.1540-8167.1992.tb00977.x, 3:4, (315-333), Online publication date: 1-Aug-1992. JANSE M and KLÉBER A (1992) Propagation of Electrical Activity in Ischemic and Infarcted Myocardium as the Basis of Ventricular Arrhythmias, Journal of Cardiovascular Electrophysiology, 10.1111/j.1540-8167.1992.tb01098.x, 3:1, (77-87), Online publication date: 1-Feb-1992. Wit A (1989) The Time Course of Occurrence of Ventricular Arrhythmias After Experimental Myocardial Ischemia Adrenergic System and Ventricular Arrhythmias in Myocardial Infarction, 10.1007/978-3-642-74317-7_23, (275-296), . Sugi K, Karagueuzian H, Fishbein M, Mandel W and Peter T (1987) Cellular electrophysiologic characteristics of surviving subendocardial fibers in chronically infarcted right ventricular myocardium susceptible to inducible sustained ventricular tachycardia, American Heart Journal, 10.1016/0002-8703(87)90753-8, 114:3, (559-569), Online publication date: 1-Sep-1987. Karagueuzian H, Sugi K, Ohta M, Fishbein M, Mandel W and Peter T (1986) Inducible sustained ventricular tachycardia and ventricuar fibrillation in conscious dogs with isolated right ventricular infarction: Relation to infarct structure, Journal of the American College of Cardiology, 10.1016/S0735-1097(86)80347-3, 7:4, (850-858), Online publication date: 1-Apr-1986. Karagueuzian H, Sugi K, Ohta M, Meesmann M, Takeshi I, Peter T and Mandel W (1986) The efficacy of cibenzoline and propafenone against inducible sustained and nonsustained ventricular tachycardias in conscious dogs with isolated chronic right ventricular infarction: A comparative study with procainamide, American Heart Journal, 10.1016/0002-8703(86)90346-7, 112:6, (1173-1183), Online publication date: 1-Dec-1986. Sugi K, Karagueuzian H, Fishbein M, McCullen A, Sato Y, Ganz W, Mandel W and Peter T (1985) Spontaneous ventricular tachycardia associated with isolated right ventricular infarction, one day after right coronary artery occlusion in the dog: Studies on the site of origin and mechanism, American Heart Journal, 10.1016/0002-8703(85)90589-7, 109:2, (232-244), Online publication date: 1-Feb-1985. Wilber D, Walton J, O’neill W, Laufer N and Pitt B (1984) Effects of reperfusion on complete heart block complicating anterior myocardial infarction, Journal of the American College of Cardiology, 10.1016/S0735-1097(84)80156-4, 4:6, (1315-1321), Online publication date: 1-Dec-1984. March 1, 1979Vol 44, Issue 3 Advertisement Article InformationMetrics Copyright © 1979 by American Heart Associationhttps://doi.org/10.1161/01.RES.44.3.392 Originally publishedMarch 1, 1979 PDF download Advertisement

Redistribution of collateral blood flow from necrotic to surviving myocardium following coronary occlusion in the dog.

Early changes in collateral blood flow after acute coronary occlusion may be critical for survival of ischemic myocardium. We used 15-mum radioactive microspheres to study myocardial blood flow in thoracotomized dogs 10 minutes and 24 hours after occlusion of the left anterior descending coronary artery (LAD). The ischemic area was delineated by dye injected into the distal artery, and indentification of potentially ischemic samples was confirmed by a newly developed technique in which microspheres were excluded from the normally perfused LAD. Layers were separated into necrotic or normal as defined by gross inspection and confirmed by histological examination and creatine phosphokinase assay. Infarction always involved endocardial layers and extended toward the epicardium. Average myocardial blood flow in 48 necrotic samples from 16 dogs either remained low (less than 0.05 ml/min g-1) or declined, falling from 0.11 +/-0.02(SE) at 10 minutes to 0.05 +/-0.01 ml/min g-1 at 24 hours (P less than 0.001). In contrast, in the 32 normal-appearing samples which were ischemic at 10 minutes, flow increased from 0.24 +/-0.03 to 0.39 +/-0.04 ml/min g-1 (P less than 0.001). Flow in control myocardium was 1.43 +/-0.12 and 1.04 +/-0.07 ml/min g-1, respectively. Peripheral mean coronary arterial pressure increased from 26 +/- 3 to 35 +/- 3 mm Hg, largely because of enlargement of collateral vessels; collateral conductance calculated from retrograde flow in 14 dogs increased from 0.023 +/- 0.005 after occlusion to 0.051 +/- 0.009 ml/min mm Hg-1 24 hours later (P less than 0.001). Thus, coronary collateral blood flow is redistributed from necrotic endocardial layers to surviving epicardial ones. In combination with a developing collateral supply this process may be essential for sparing myocardium after coronary occlusion.