Effects Of Coronary Occlusion Research Articles

Effect of coronary occlusion during percutaneous transluminal angioplasty in humans on left ventricular chamber stiffness and regional diastolic pressure-radius relations

The effect of repeated (3 to 10 second) and transient (15 to 75 second) abrupt coronary occlusion on the global and regional chamber stiffness was studied in nine patients undergoing angioplasty of a single proximal left anterior descending coronary artery stenosis. The left ventricular high fidelity pressure and volume relation was obtained before and after the procedure as well as during coronary occlusion, after 20 seconds (n = 9) and after 50 seconds (n = 5). During ischemia, there was an upward shift of the pressure-volume relation. The nonlinear simple elastic constant of chamber stiffness increased from 0.0273 +/- 0.017 before angioplasty (mean +/- SD) to 0.0621 +/- 0.026 after 20 seconds of occlusion (p less than 0.05) and 0.0605 +/- 0.015 after 50 seconds of occlusion (p less than 0.01). In five patients, the postangioplasty value remained higher than the control value, but at the group level the mean value (0.0529 +/- 0.037) was not statistically different. The regional stiffness was determined from the changes in the length of six segmental radii during diastole, from the lowest diastolic to the end-diastolic pressure. The regional constant of elastic stiffness was unaffected in the nonischemic zone. In the adjacent and ischemic zones, the regional stiffness was increased during occlusion (p less than 0.05). These regional abnormalities in diastolic function persisted at the time of postangioplasty measurements, 12 minutes after the end of the procedure. This suggests that recovery of normal diastolic function after repeated ischemic injuries is delayed after restoration of normal blood flow and systolic function.

Evaluation of “ischemia at a distance”: Effects of coronary occlusion on a remote area of left ventricle

The effect of coronary occlusion on blood flow and function in a remote zone of the left ventricle was studied in 21 open-chest dogs. Group A consisted of 6 dogs not undergoing left circumflex (LC) coronary artery cannulation. The other 15 dogs underwent cannulation of the LC artery followed by partial occlusion to 40 mm Hg diastolic perfusion pressure. Of these dogs, 7 with constant perfusion pressure (group B) were separately evaluated from 8 with declining perfusion pressure (group C). Sequentially more proximal left anterior descending (LAD) occlusions were performed in each group. Blood flow in the LC zone remained unchanged in group A after sequential LAD occlusions, whereas in groups B and C distal and proximal LAD occlusions caused progressive reduction in LC flow. Although in group A segment shortening improved in the LC zone after distal LAD occlusion, in groups B and C progressive impairment in segmental shortening was observed in the LC zone after distal and proximal LAD occlusions. Thus, in the setting of critical coronary stenosis in a zone, total occlusion in another coronary artery can initiate a series of events leading to decreased blood flow in the territory of the stenotic coronary artery, resulting in ischemia and impaired segmental function.

Effects of coronary occlusion on flow in the distribution of a neighboring stenotic coronary artery in the dog

The effect of left anterior descending coronary artery (LAD) occlusion on flow through a severely stenotic left circumflex artery (LC) was studied in 19 openchest dogs. In 8 dogs (Group 1) aortic pressure, distal circumflex pressure, circumflex flow, and heart rate were measured. In the absence of an LC stenosis, LAD occlusion resulted in an increase in LC flow from 32 ± 3 to 41 ± 5 ml/min (p < 0.001). In the presence of a severe LC stenosis produced with a snare, LAD occlusion resulted in a decrease in distal LC pressure (54 ± 2 to 30 ± 1 mm Hg; p < 0.001), an increase in resistance across the LC stenosis (1.8 ± 0.2 to 3.5 ± 0.4 units; p < 0.001) and a decrease in flow through the LC (24 ± 2 to 20 ± 2 ml/min; p < 0.001). Aortic pressure did not change significantly (94 ± 3 to 93 ± 3 mm Hg) and heart rate increased slightly (90 ± 5 to 104 ± 5 beats/ min; p < 0.001). LAD occlusion, therefore, increased the severity of the LC stenosis and resulted in a decrease in LC flow. The decrease in intraluminal pressure distal to the LC stenosis, and thus in the stenotic segment itself, may have resulted in passive narrowing of the stenotic segment, which may have been responsible for the decrease in flow. In 11 dogs (Group 2) the LC stenoses were produced so that anterograde flow through the stenotic LC artery did not change significantly after LAD occlusion. However, LAD occlusion resulted in a decrease in flow (measured with radioactive microspheres) to the area supplied by the stenotic LC artery (0.62 ± 0.02 to 0.50 ± 0.09 ml/min/g; p < 0.05), possibly because collateral flow from the LAD to the LC-dependent myocardium was interrupted. In addition, LAD occlusion resulted in selective underperfusion of the subendocardial layers of the LC-dependent area (endocardial/epicardial flow ratio from 0.89 ± 0.07 to 0.40 ± 0.10; p < 0.005), possibly because of a combination of a decrease in perfusion pressure distal to the stenoses (54 ± 4 to 39 ± 3 mm Hg; p < 0.005) and an increase in left ventricular end-diastolic pressure (from 6 ± 1 to 13 ± 2 mm Hg; p < 0.005). The results of these studies demonstrate mechanisms by which myocardial ischemia may occur in the area supplied by a stenotic coronary artery if a neighboring coronary artery becomes occluded.

Effect of coronary occlusion on arrhythmias and conduction in the ovine heart.

The proximal left circumflex coronary artery was occluded for 1 h in 16 open-chest sheep anesthetized with pentobarbital sodium. Epicardial conduction was monitored at three or four sites within the ischemic zone and one site in the normal zone. Eight of the sheep developed ventricular fibrillation within the first 15 min of occlusion; the remaining sheep survived the 1-h observation period. In the sheep that developed spontaneous ventricular fibrillation, the circumflex perfused a significantly greater amount of the left ventricle (44 +/- 3 vs. 39 +/- 3%; P = 0.008). The occurrence of spontaneous ventricular fibrillation was invariably preceded by a period of sustained (0.5-4 min) ventricular tachycardia. Six of the surviving sheep developed episodes of sustained (2-10 min) tachycardia that were self-terminating. The ischemic zone electrograms showed continuous fractionated electrical activity during both self-terminating tachycardias and tachycardias ending in fibrillation. The continuous epicardial electrical activity did not appear to cause the tachycardias but rather occurred as a result of the tachycardias. The genesis of ventricular tachycardia and fibrillation in this model may involve mechanisms different from ischemia-induced ventricular tachycardia and fibrillation in canine and porcine hearts.

Effects of coronary occlusion and norepinephrine on the myocardium of alloxan-diabetic dogs

The aim of this study was to clarify the role of altered diabetic vascular reactivity in ischaemic heart disease. In diabetic condition, the necrotic area of myocardial infarction was significantly extended and myocardial oedema failed to develop after administration of norepinephrine 2 or 48 hours after ligation of the left anterior descending coronary artery. In metabolically healthy dogs the necrotic area of myocardial infarction was considerably smaller and an increase in myocardial water content, in myocardial thiocyanate space, in microscopically demonstrable permeability and in diastolic stiffness of left ventricular wall occurred when norepinephrine was administered 2 or 48 hours after coronary infarction. A close correlation was demonstrable between enhanced water content, thiocyanate space and diastolic stiffness in metabolically healthy animals, whereas in diabetic condition diastolic stiffness was primarily increased, and decreased when norepinephrine was infused after coronary ligation. Therefore, the altered vascular reactivity in diabetes is supposed to be responsible for the lack of oedema in the nonischaemic part of myocardium after norepinephrine infusion as well as for the size and severity of myocardial infarction.

Effects of physical training on myocardial vascularity and perfusion.

Physical training is thought to be a stimulus for coronary vascular growth and coronary collateral development. This report is a summary of knowledge in the area. Studies in experimental animals with normal hearts indicate that physical training promotes increased myocardial capillary density and also causes enlargement of the surface coronary vessels. The physiologic effect of these changes on coronary vascular reserve and protection of segments of the heart against myocardial ischemia has not been established. Physically trained dogs and pigs do not appear to be protected against the effects of coronary occlusion, in that the ischemic area appears to be as large in trained animals as in untrained animals for any given coronary lesion. One study in physically trained rats appears to show protection against myocardial infarction, but whether this is related to coronary vascular changes has not been established. Experiments in dogs subjected to chronic narrowing or gradual occlusion demonstrate that physical training in these models does promote collateral blood flow as measured by retrograde flow in open-chest experiments. Studies using the microsphere technique in closed-chest animals confirms increased collateral flow to ischemic areas in some animals, but the magnitude of the increases appears to be small and varies greatly from animal to animal. Studies in athletes suggest that myocardial blood flow is lower at any submaximal level of training in athletes than in sedentary persons. Studies in patients with coronary artery disease have generally failed to show an increase in coronary blood flow or in perfusion of ischemic areas after physical training programs, but the techniques used might not have been sensitive enough to detect changes. The evidence in the experimental animals is sufficiently promising to indicate that the search should be continued to define physical training programs that will most stimulate myocardial vascularity and coronary collaterals in humans.

Effect of coronary occlusion on arterial baroreflex control of heart rate.

To determine whether the baroreflex control of heart rate is altered during acute myocardial ischaemia, the baroreflex slope was measured at the control state, during coronary occlusion, and at the recovery phase in nine conscious dogs. The baroreflex slope was obtained by relating the R-R interval to the preceding systolic pressure during phenylephrine-induced transient hypertension. The baroreflex slope was reduced during coronary occlusion (18.8 +/- 3.8 ms.kPa-1, mean +/- SE) compared with that at the control state (41.4 +/- 6.0 ms.kPa-1). This reduction in the baroreflex slope during coronary occlusion was also present after propranolol, which suggests that this reduction of the slope during myocardial ischaemia is not due to a simultaneous increase in beta-adrenergic activity. These results suggest that the reflex originating from the cardiac receptors may modulate heart rate response to arterial baroreceptor stimulation.

Effects of coronary occlusion on early ventricular diastolic events in conscious dogs.

ARTICLESEffects of coronary occlusion on early ventricular diastolic events in conscious dogsT. Kumada, J. S. Karliner, H. Pouleur, K. P. Gallagher, K. Shirato, and J. Ross JrT. Kumada, J. S. Karliner, H. Pouleur, K. P. Gallagher, K. Shirato, and J. Ross JrPublished Online:01 Nov 1979https://doi.org/10.1152/ajpheart.1979.237.5.H542MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByLeft Ventricular Systolic Asynchrony is Induced Even in the Normal Heart During Increases in Afterload: A Study With Angiotensin II Stress Pulsed Tissue Doppler ImagingJournal of Echocardiography, Vol. 5, No. 2Magnetic resonance stress tagging in ischemic heart diseaseIngo Paetsch*, Daniela Föll*, Adam Kaluza, Roger Luechinger, Matthias Stuber, Axel Bornstedt, Andreas Wahl, Eckart Fleck, and Eike Nagel1 June 2005 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 288, No. 6Diastolic time fraction as a determinant of subendocardial perfusionDirk S. Fokkema, Jurgen W. G. E. VanTeeffelen, Simone Dekker, Isabelle Vergroesen, Johannes B. Reitsma, and Jos A. E. Spaan1 May 2005 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 288, No. 5Prolonged Diastolic Time Fraction Protects Myocardial Perfusion When Coronary Blood Flow Is ReducedCirculation, Vol. 100, No. 1Does Diltiazem protect the ischemic myocardium during PTCA? More from this issue > Volume 237Issue 5November 1979Pages H542-H549 Copyright & PermissionsCopyright © 1979 the American Physiological Societyhttps://doi.org/10.1152/ajpheart.1979.237.5.H542PubMed495759History Published online 1 November 1979 Published in print 1 November 1979 Metrics

Effects of a cardiac glycoside in combination with propranolol on the ischemic heart of conscious dogs.

The effects of coronary occlusion and of subsequent propranolol and ouabain administration were examined in 12 conscious dogs. Overall left ventricular (LV) function was assessed by measurement of LV pressure and dP/dt, and regional myocardial function was assessed by measurements of segment length (SL), velocity of SL shortening and regional myocardial "work," i.e., pressure-length loops in normal and moderately and severely ischemic zones. Regional intramyocardial electrograms were measured at the same sites as function along with regional myocardial blood flow as determined by the radioactive microsphere technique. Coronary occlusion resulted in graded loss of function from the normal to severely ischemic zones, along with graded flow reductions and graded elevation of the ST segment. Propranolol, 1 mg/kg, depressed overall LV function and function in the normal zone more than in ischemic zones. Propranolol reduced flow to the normal zone and increased flow to ischemic zones, while not affecting ST-segment elevation significantly. In the presence of occlusion and propranolol, ouabain, 20 microgram/kg, improved overall LV function as well as regional function in the normal, moderately ischemic and severely ischemic zones. In addition, ouabain reduced ST elevation and increased blood flow further in moderately and severely ischemic zones. Most strikingly, ouabain returned normal systolic shortening to eight severely ischemic segments which were previously akinetic.

Effects of propranolol on regional myocardial function, electrograms, and blood flow in conscious dogs with myocardial ischemia.

The effects of coronary occlusion and of subsequent propranolol administration were examined in 18 conscious dogs. Overall left ventricular (LV) function was assessed by measurements of LV pressure and dP/dt, and regional myocardial function was assessed by measurements of segment length (SL), velocity of SL shortening and regional myocardial "work", i.e., pressure-length loops in normal, moderately, and severely ischemic zones. Regional intra-myocardial electrograms were measured from the same sites along with regional myocardial blood flow as determined by the radioactive microsphere technique. Coronary occlusion resulted in graded loss of function from the normal to severely ischemic zones with graded flow reduction and graded elevation of the ST segment. Propranolol depressed overall LV function, function in the normal zone (work fell by 17+/-4%), and in the majority of moderately ischemic segments (work fell by 7+/-3%). In severely ischemic segments the extent of paradoxical motion and post-systolic shortening was reduced by propranolol. After propranolol regional myocardial blood flow fell in the normal zone (11+/-2%) and rose in the moderately (15+/-4%) and severely (63+/-10%) ischemic zones. Thus, in the conscious dog with regional myocardial ischemia, propranolol induces a redistribution of myocardial blood flow, with flow falling in normal zones and rising in moderately and severely ischemic zones. The improvement in perfusion of ischemic tissue was associated with slight but significant depression of shortening, velocity, and work in the moderately ischemic zones and of paradoxical bulging and post-systolic shortening in the severely ischemic zone.

Effects of isoproterenol on regional myocardial function, electrogram, and blood flow in conscious dogs with myocardial ischemia.

The effects of coronary occlusion and of subsequent isoproterenol infusion were examined in conscious dogs. Left ventricular (LV) function was assessed by measurements of LV diameter, pressure, velocity and dP/dt/P, and regional myocardial function was assessed by measurements of segment length (SL) and velocity of SL shortening in normal, border, and ischemic zones. Regional myocardial function was measured from the same sites, along with intramyocardial electrograms and regional myocardial blood flow as determined by radioactive microspheres. Coronary occlusion resulted in graded loss of function from the normal to severely ischemic zones with graded flow reductions and graded increases in ST segment elevation. Isoproterenol improved overall LV function, and function in the normal zone. Isoproterenol also improved function in 19 of 21 border-zone segments and in all moderately ischemic segments, while elevating further the ST segments. These changes were accompanied by increases in myocardial blood flow. In contrast, in severely ischemic segments, isoproterenol resulted in a deterioration of function, in that paradoxical motion occurred in segments previously akinetic during systole, while paradoxical motion was intensified in those segments in which it was already present. These changes were accompanied by further ST segment elevation but not by concurrent increases in blood flow. In addition, in 2 of 21 border zone segments, myocardial blood flow fell and these segments responded to isoproterenol with complete loss of function; paradoxical motion developed. Thus, in the conscious dog, a strong inotropic agent can improve function, even in the ischemic myocardium, as long as the required additional blood flow can be provided wither through primary or collateral channels.

The pumping ability of the left heart and the effect of coronary occlusion.

In an isolated preparation of cat heart we studied the pumping capacity of the left heart while left atrial filling pressure was kept constant. We used the source impedance concept to quantify the pumping capacity. In this source impedance concept the relation between left ventricular output and left ventricular pressure is given by the formula (see article) where Zs = source impedance, Plv = left ventricular pressure, Iao = flow in the ascending aorta, and omega = 2pif, f being frequency.. The pressure obtained at zero flow is called the hydromotive pressure (HMP). Only the mean values of pressure and flow were studied. We studied the behavior of 10 hearts in three different experimental situations and in the following sequence: (1) control conditions, (2) after ligating a part of the left coronary arterial system, and (3) after restoring left ventricular output to control level by raising left atrial filling pressure. It was found that source resistance was not significantly different in the three situations but that mean hydromotive pressure (HMP) was significantly lower after ligation of a part of the left coronary arterial system. It was concluded that the decrease in pumping capacity of the left heart after infarction can be compensated for almost completely by an increase in left atrial filling pressure. This compensating mechanism therefore seems to be very efficient.

Electrophysiologic effects of nitroglycerin during experimental coronary occlusion.

Previous studies have shown that nitroglycerin (TNG) exerts beneficial electrophysiological effects in the setting of acute myocardial ischemia. To investigate the basis for these actions, the effects of TNG during coronary occlusion were studied in 19 anesthetized mongrel dogs. Refractory periods (obtained by extrastimulus method) and conduction times measured from local electrograms were determined in potentially ischemic and nonischemic areas prior to and after varying periods of occlusion of the left anterior descending coronary artery and following administration of TNG (300-400 mug intravenous bolus followed by an infusion titrated to reduce systolic blood pressure by 20 mm Hg). Following 15 minutes of occlusion, refractory periods in the ischemic zones shortened to 83% of control (P less than 0.001) resulting in a difference between refractory periods in the nonischemic and ischemic zones of 17.7%. After TNG administration this difference was decreased to 10.0% (P less than 0.001). However, with periods of occlusion of 60-90 min TNG did not significantly affect the difference of refractory periods. TNG had no significant effects on conduction times in nonischemic or ischemic areas. In six dogs, the effects of coronary occlusion and TNG on ventricular automaticity were examined by induction of complete heart block. The idioventricular rate and ventricular escape intervals after cessation of ventricular overdrive were used as indices of automaticity. Control idioventricular rates (62.5 +/- 3.7 beats/min) remained unchanged following both coronary occlusion (62.0 +/- 3.9) and TNG administration (60.7 +/- 3.2). Similarly, mean control escape intervals (1.84 +/- 0.2 sec) did not change after occlusion (1.78 +/- 0.3 sec) or TNG administration (1.86 +/- 0.2 sec). In conclusion, these observations suggest that 1) TNG enhances the electrical stability of the acutely ischemic myocardium by decreasing the difference of refractory periods between nonischemic and ischemic areas in the immediate period following occlusion, 2) since TNG has no significant effects on ventricular automaticity, its beneficial effects might be limited in suppression of arrhythmias of re-entrant origin.

急性虚血心における虚血部収縮曲線と循環諸量の関係

急性虚血心における虚血部収縮曲線と循環諸量の関係

Therapy in Acute Coronary Care.

Perhaps "Therapy in Units for Intensive Care of Patients With Acute Myocardial Infarction" would be a more appropriate title for this monograph, written for nurses, paramedical personnel, and physicians concerned with such well-equipped individual units as are illustrated on the cover and in two frontispieces. The glossary will be of great value to nurses and lay attendants in the unit. The 233 items in the bibliography can guide physicians to recent literature on the acute effects of coronary occlusion and management in units designed for intensive care of myocardial infarction patients or those recovering from surgical intervention for heart disease. Part 1 (57 pages) of the text is devoted to concise sound reviews of the physiology and pathophysiology of the heart and vascular bed. There are sections on arrhythmias, shock, and other complications of coronary occlusion. Part 2 (67 pages) provides thorough discussion of the pharmacology, clinical value, and

Determination of interarterial coronary anastomosis by radioactive spherules. Effect of coronary occlusion and hypoxemia

1. 1. Experiments using radioactive spherules demonstrate that the coronary interarterial collateral circulation is not functional in the normal dog's heart. Hypoxemia can activate some coronary interarterial anastomosis. 2. 2. Three weeks after coronary occlusion the interarterial anastomosis is at least 35 μ in diameter, and at 12 weeks is even more extensive.

Some factors affecting ouabain-induced ventricular arrhythmia in the reserpine-treated cat.

Some factors affecting ouabain-induced ventricular arrhythmia in the reserpine-treated cat.

Circulatory adaptations in hypoxia.

ArticlesCirculatory Adaptations in HypoxiaP. I. KornerP. I. KornerPublished Online:01 Oct 1959https://doi.org/10.1152/physrev.1959.39.4.687MoreSectionsPDF (7 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByIn-flight angina pectoris; an unusual presentation5 April 2018 | BMC Cardiovascular Disorders, Vol. 18, No. 1Renal responses to acute reflex activation of renal sympathetic nerve activity and renal denervation in secondary hypertensionRoger G. Evans, Sandra L. Burke, Gavin W. Lambert, and Geoffrey A. Head1 September 2007 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 293, No. 3Adenosine contributes to hypoxia-induced forearm vasodilation in humansUrs A. Leuenberger, Kris Gray, and Michael D. Herr1 December 1999 | Journal of Applied Physiology, Vol. 87, No. 6Effects of acute exposure to altitude (3,460 m) on blood pressure response to dynamic and isometric exercise in men with systemic hypertensionThe American Journal of Cardiology, Vol. 70, No. 18A central role for adenosine in the hypotension elicited by hypoxia in anesthetized ratsBrain Research Bulletin, Vol. 23, No. 1-2Vascular response to hypoxia in humans.Circulation, Vol. 62, No. 6Cellular basis for increased sensitivity of vascular smooth muscle in spontaneously hypertensive rats.Circulation Research, Vol. 38, No. 6Effects of chronic anemia on the coronary and coronary collateral vasculature in dogs.Circulation Research, Vol. 38, No. 6Experimental myocardial infarctionThe American Journal of Cardiology, Vol. 34, No. 7Studies on circulatory response to hypoxia in the denervated transplanted human heartThe American Journal of Medicine, Vol. 56, No. 4Comparison of the effects of two anesthetic agents on the production of hypoxic pulmonary hypertension in dogsAmerican Heart Journal, Vol. 84, No. 2Alteration of Glucose and Insulin Metabolism in Congenital Heart DiseaseCirculation, Vol. 46, No. 2Acclimation to simulated altitude in the lizard Dipsosaurus dorsalisComparative Biochemistry and Physiology Part A: Physiology, Vol. 42, No. 2Effect of CO2 on O2, transport, O2;, uptake and blood lactate in hypoxia of anesthetized dogRespiration Physiology, Vol. 10, No. 1Determination of interarterial coronary anastomosis by radioactive spherules. Effect of coronary occlusion and hypoxemiaAmerican Heart Journal, Vol. 79, No. 2Effects of arterial hypoxemia and hyperoxia on oxygen availability for myocardial metabolismThe American Journal of Cardiology, Vol. 24, No. 2Cardiovascular Function in Children with Severe AnemiaCirculation, Vol. 39, No. 6Effect of ‘100%’ Oxygen Breathing on Mixed Venous Oxygen Pressures25 June 2016 | Scottish Medical Journal, Vol. 10, No. 5Effect of Prolonged Hypoxia Upon Granularity of Renal Juxtaglomerular CellsCirculation Research, Vol. 16, No. 1General and regional circulatory alterations in cirrhosis of the liverThe American Journal of Medicine, Vol. 37, No. 4Effect of Posthemorrhagic Anemia on the Renal Circulation of the Unanesthetized RabbitCirculation Research, Vol. 14, No. 5Life at High AltitudesThe Lancet, Vol. 276, No. 7166Effects of Anoxia on the Vascular Resistance of the Dog's Hind LimbCirculation Research, Vol. 8, No. 3 More from this issue > Volume 39Issue 4October 1959Pages 687-730 Copyright & PermissionsCopyright © 1959 the American Physiological Societyhttps://doi.org/10.1152/physrev.1959.39.4.687PubMed14411079History Published online 1 October 1959 Published in print 1 October 1959 Metrics

Coronary interarterial anastomoses in young pigs and mongrel dogs.

Interarterial anastomoses in young pigs have been compared with those in mongrel dogs by direct flow measurements during life and by injections after death. Results indicate that pigs have minimal functional collaterals in comparison with dogs and that injection studies roughly predict the Degrees of collateral function. The data indicate that the extent of collateral development in dogs is independent of dog or heart weight and hence offers more protection against the effects of coronary occlusion in small hearts than in large hearts. Other studies indicate that coronary flow, myocardial oxygen consumption and coronary vasomotor responses in pigs are similar to those in dogs.

STUDIES ON THE CORONARY CIRCULATION. VI. LOSS OF MYOCARDIAL CONTRACTILITY AFTER CORONARY ARTERY OCCLUSION

Excerpt INTRODUCTION It is well known clinically and experimentally that an ischemic portion of myocardium may bulge or "balloon" out during systole.1This remarkable phenomenon, which is of diagnos...