Coronary Venous Plasma Research Articles

Evidence for partial sympathetic cardiac reinnervation following cardiac transplantation.

Heart transplantation causes total cardiac denervation. Measurements of plasma concentrations of the main presynaptic noradrenal metabolite, dihydroxyphenylglycol (DOPEG, exclusively neuronal in origin), were used to examine the possibility of sympathetic reinnervation of the transplanted human heart. We determined arterial and coronary-venous plasma concentrations of DOPEG in 15 heart transplant recipients (28-68 years of age at the time of transplantation with the transplant ageing from 0.5 to 4 years at the time of investigation) and in nine control patients (45-75 years of age). In each of the control patients the DOPEG concentration was higher in coronary venous plasma than in arterial plasma (mean arteriovenous increment: 60 +/- 10%; P < 0.001). In the heart transplant recipients nine patients showed an arteriovenous increment in plasma DOPEG. For the mean group results it was found that the ratio of the coronary-venous to arterial DOPEG concentration was positively correlated with the time after transplantation (r = 0.92; n = 5; P < 0.05). Thus, our data provide neurochemical evidence for partial sympathetic reinnervation in some of the heart transplants. Moreover, it is suggested that the time after transplantation is unlikely to be the only determinant for the occurrence and extent of sympathetic reinnervation.

Cardiac noradrenergic function one year following cardiac transplantation.

Controversy exists whether or not cardiac nerves regrow into a human transplanted heart. The present study examined cardiac noradrenergic function one year following cardiac transplantation. Eight male cardiac transplant recipients having standard triple immunosuppressive treatment were catheterized diagnostically one year after heart transplantation. They had normalized cardiac hemodynamics and showed no histological rejection in biopsies. A second study group, with intact cardiac innervation, consisted of 19 patients with stable angina pectoris class I to III. Cardiac sympathetic nerve activity was assessed by measurements of cardiac noradrenaline (NA) extraction and spillover, using infusion of tritium-labelled NA (3H-NA). To further characterize cardiac noradrenergic function (synthesis and metabolism) arterial and coronary venous plasma concentrations of the NA precursor, dihydroxyphenylalanine (DOPA), the dopamine metabolite, dihydroxyphenylacetic acid (DOPAC), and the intra-neuronal NA metabolite, dihydroxyphenylglycol (DHPG), were also examined. In transplant recipients, cardiac sympathetic function was also examined before and during supine bicycle exercise and after administration of desipramine to block neuronal uptake. Significant dilution of 3H-NA with endogenous NA from arterial to coronary venous plasma in cardiac transplant patients indicated detectable spillover of NA into plasma from transplanted hearts. However, cardiac spillover of NA in heart transplant patients was only a quarter of that observed in angina patients. Also, transplanted hearts showed no production of DOPA, DOPAC, DHPG or 3H-labelled DHPG, whereas there were positive arterial-venous plasma gradients in all these catechols across the hearts of angina patients. Cardiac fractional extraction of NA was 74% in the angina patients, but only 13% in transplant patients. In transplant patients, cardiac spillover of NA and extraction of 3H-NA were not affected by desipramine or exercise. The present study shows little evidence of any functional activity of cardiac sympathetic nerves in the transplanted heart, as assessed by biochemical indices of release, reuptake, metabolism and synthesis of NA. This argues against cardiac reinnervation of functional importance, at least within the first postoperative year.

Cardiac microdialysis measurement of extracellular adenine nucleotide breakdown products during regional ischemia and reperfusion in canine heart: protective effect of propranolol against reperfusion injury.

Using cardiac microdialysis, we studied release of the adenine nucleotide breakdown products (ANBP) adenosine (ADS), inosine (INS), and hypoxanthine (HYP) into the interstitium of canine myocardium during 20- and 40-min occlusion of the anterior descending coronary artery and reperfusion. Dialysate ANBP concentrations reached maximum values not at the end of ischemia but in the first 10 min of reperfusion. The effect was more pronounced after 20-min ischemia. Further reperfusion led to an ANBP decrease that was more prolonged after 40-min ischemia. Pretreatment with DL-propranolol (0.5 mg/kg, intravenously, i.v.) given 40 min before coronary occlusion had no effect on adenine nucleotide catabolism rate during 20- and 40-min ischemia, but it facilitated washout of ANBP from ischemic zone immediately after the start of reperfusion. A similar effect was elicited by a D-stereoisomer of propranolol with no beta-adrenoceptor blocking activity. Results suggest that the reperfusion injury and probably the no-reflow phenomenon were the cause of enhanced adenine nucleotide catabolism at the beginning of reperfusion and prolonged ANBP washout from the ischemic zone. Reduction of reperfusion injury by propranolol could be related to the membrane stabilizing and antioxidant activity of this agent. Examination of DL-propranolol kinetics in arterial and coronary venous blood plasma showed that drug accumulation in the myocardium was almost maximum at the start of ischemia; therefore, the efficiency of cardio-protection with DL-propranolol was not limited by pharmacokinetic causes. Insertion of an additional microdialysis probe in the myocardium allowed monitoring of extracellular propranolol concentrations.

Coronary venous lipid peroxide concentrations after coronary angioplasty: correlation with biochemical and electrocardiographic evidence of myocardial ischaemia.

Raised lipid peroxide concentrations in coronary venous plasma have been reported after coronary angioplasty in humans. This may reflect increased free radical activity after myocardial ischaemia and reperfusion. If so, it may be possible to correlate lipid peroxide concentrations with the degree of myocardial ischaemia produced during angioplasty. 15 patients (age range 42-70; 12 men) with stable angina pectoris undergoing angioplasty of a proximal left anterior descending coronary artery stenosis were studied. Plasma lipid peroxide and lactate concentrations were measured in sequential blood samples taken from the great cardiac vein before and immediately after one to five serial 60 second balloon inflations. The maximum ST segment shift during each balloon inflation was also measured. Lipid peroxide concentrations in coronary venous plasma were raised from pre-angioplasty values by more than 2 SDs of the relevant measurement error after 27 out of 46 (59%) balloon inflations. Lactate concentrations were raised after 43 out of 46 (93%) balloon inflations. No significant difference was found between the peak percentage change of either lipid peroxide or lactate concentrations after any of the first three serial inflations. The maximum ST segment shift after each of the first three serial inflations was also similar. Coronary venous lactate concentrations after balloon inflation correlated positively with the maximum ST segment shift, but did not correlate with lipid peroxide concentrations. Raised lipid peroxide concentrations in coronary venous plasma can be detected in humans after balloon angioplasty. There is no positive correlation between lipid peroxide concentrations in coronary venous plasma after angioplasty and the degree of preceding myocardial ischaemia as assessed by either ST segment shift or lactate production. These indices showed that one to three serial 60 second balloon inflations each produce a similar degree of myocardial ischaemia. The origin of the raised lipid peroxide concentrations in coronary venous plasma after angioplasty remains unknown.

Simultaneous measurements of cardiac noradrenaline spillover and sympathetic outflow to skeletal muscle in humans.

1. Muscle sympathetic nerve activity (MSA) was recorded in the peroneal nerve at the knee by microneurography in ten healthy subjects and determinations were made simultaneously of intra-arterial blood pressure, and whole-body and cardiac noradrenaline spillover to plasma. Measurements were made at rest, during isometric handgrip at 30% of maximum power and during stress induced by forced mental arithmetic. 2. At rest there were significant positive correlations between spontaneous MSA (expressed as number of sympathetic bursts min-1) and both spillover of noradrenaline from the heart and concentration of noradrenaline in coronary sinus venous plasma. 3. Both isometric handgrip and mental arithmetic led to sustained increases of blood pressure, heart rate and MSA. Plasma concentrations of noradrenaline and spillover of noradrenaline (total body and cardiac) increased. In general the effects were more pronounced during handgrip than during stress. 4. When comparing effects during handgrip and stress the ratio between the fractional increases of MSA and cardiac noradrenaline spillover were significantly greater during handgrip. 5. The data suggest (a) that there are proportional interindividual differences in the strength of resting sympathetic activity to heart and skeletal muscle which are determined by a common mechanism and (b) that handgrip and mental stress are associated with differences in balance between sympathetic outflows to heart and skeletal muscle.

Xanthine oxidase inhibition does not limit canine infarct size.

Evidence supporting the role of xanthine oxidase in myocardial reperfusion injury is based on studies with pharmacological interventions used to inhibit enzyme function. Controversy exists, however, regarding the true role of xanthine oxidase in reperfusion injury. This study was performed to determine whether xanthine oxidase inhibition limits myocardial injury due to coronary artery occlusion and reperfusion. Anesthetized dogs underwent coronary artery occlusion (90 minutes) and reperfusion (6 hours). Oxypurinol (28 mg/kg) or amflutizole (30 mg/kg), chemically unrelated inhibitors of xanthine oxidase, or vehicle was infused intravenously 15 minutes before and 3 hours after reperfusion. Regional myocardial blood flow was determined with radiolabeled microspheres. Infarct size was determined with the tetrazolium method. Myocardial infarct size (percent of risk region) was less in oxypurinol-treated dogs, 32 +/- 16%, compared with that of the control group, 46 +/- 15%. Infarct size for the amflutizole-treated dogs, 40 +/- 21%, was not significantly different from that of the control group. There were no differences in rate-pressure product or collateral blood flow to account for differences in infarct size. Uric acid concentration in the coronary venous plasma increased after reperfusion in the dogs treated with vehicle but not in the drug-treated dogs. Xanthine oxidase inhibition was demonstrated in each of the drug treatment groups, but only oxypurinol limited the extent of myocardial injury. Previously reported cardioprotective effects of allopurinol, noted to occur only when the drug was administered chronically, may be related to a property of oxypurinol, a major metabolite of allopurinol. The beneficial effect of oxypurinol is unrelated to inhibition of superoxide formation during xanthine oxidase-catalyzed oxidation of xanthine and hypoxanthine.

Stimulation of Prostacyclin Synthesis by Defibrotide

Prostacyclin (PGI2) improves regional contractility of postischemically dysfunctional ("stunned") myocardium. We determined whether defibrotide, a fraction of mammalian DNA known to stimulate endogenous formation of PGI2, also improves contractile recovery of stunned myocardium. Anesthetized, open-chest minipigs were subjected to coronary occlusion of 5 min (left anterior descending branch, LAD) followed by 120 min of reperfusion. The animals were treated with defibrotide (32 mg x kg-1 x h-1, intravenously, i.v.) or vehicle throughout the experimental period. Defibrotide improved regional contractility in the ischemic reperfused area from 30 (vehicle) to 78% of the preischemic control without altering the contractility of nonischemic myocardium. Transcardiac PGI2 formation, determined from the difference between coronary venous and arterial plasma concentrations, was elevated from 437 (preischemic control) to 869 pmol x l-1 in defibrotide-treated animals, but was unchanged in the vehicle-treated and a sham-operated group. Thromboxane A2 (TXA2) release was not modified. Defibrotide reduced ischemia-induced formation of platelet aggregates but did not affect the activity of polymorphonuclear neutrophil granulocytes. The data demonstrate an improvement of contractile recovery from stunning by defibrotide that may be related to an inhibition of ischemia-induced platelet activation and (or) membrane protection owing to enhanced transcardiac formation of PGI2.

Effects of Peptide 6A on Coronary Blood Flow Dynamics in Canine Coronary Thrombosis

Intracoronary thrombi resulting in acute myocardial ischemia can often be lysed by thrombolytic agents. We examined the potential of a fibrin(ogen)-degradation product pentapeptide 6A (Ala-Arg-Pro-Ala-Lys), which increases coronary blood flow partly by stimulation of prostacyclin release, in reestablishing coronary blood flow in dogs with experimentally induced thrombus. An occlusive thrombus in the circumflex coronary artery was created by electrical stimulation of the endothelial surface. After the occlusive thrombus was stable without electrical current for at least 15 min, peptide 6A (5 mumol/min for 20 min intracoronary) or tissue-plasminogen activator (t-PA) [10 micrograms/kg/min for 20 min intravenously (i.v.)] was randomly administered. Peptide 6A administration reestablished coronary blood flow (peak 16 +/- 2 ml/min, mean +/- SE) in 6 of 12 animals with occlusive coronary thrombus. Mean time to blood flow reestablishment was 5.3 +/- 2.2 min, but the reflow was short lived (mean duration of reflow: 15.7 +/- 1.6 min). t-PA reestablished coronary blood flow (peak 19 +/- 3 ml/min) in 4 of 10 animals. The time of flow reestablishment was 12.0 +/- 3.9 min and the reflow persisted for 22.0 +/- 3.1 min. Peptide 6A administration was associated with an increase in coronary venous plasma 6-keto-PGF1 alpha, indicating stimulation of prostacyclin release. This study demonstrates the potential of peptide 6A in reestablishing coronary blood flow in a canine model of coronary thrombosis. This transient effect is associated with release of prostacyclin, which may be beneficial because of its vasodilator and platelet inhibitory effects.

Adenosine's role in coronary vasodilation induced by atrial pacing and norepinephrine.

If adenosine (ADO) mediates metabolic vasodilation in the heart, increases in interstitial ADO (ISF[ADO]) must accompany increases in coronary vascular conductance. We tested this using ADO release, defined as the difference in [ADO] in coronary venous and arterial plasma multiplied by coronary plasma flow, as an index of ISF[ADO]. Pentobarbital-anesthetized dogs received intravenous norepinephrine or left atrial pacing, and the resulting changes in coronary blood flow (delta CBF), conductance (delta C), myocardial oxygen consumption (delta VO2), and ADO release (delta RADO) were measured. If ISF[ADO] and C are coupled, the ratio delta RADO/delta C should be greater than zero. For dogs receiving atrial pacing, the ratios delta RADO/delta C, delta RADO/delta CBF, and delta RADO/delta VO2 equal -2.4 +/- 2.2 nmol . mmHg-1 . ml-1, -0.022 +/- 0.020 nmol/ml, and -0.13 +/- 0.12 nmol/ml, respectively. These values do not differ from zero. For dogs receiving norepinephrine, delta RADO/delta C, delta RADO/delta CBF, and delta RADO/delta VO2 equal 9.7 +/- 1.8, 0.051 +/- 0.017, and 0.44 +/- 0.13, respectively. These values are greater than zero (P less than 0.05). These differences between atrial pacing and norepinephrine infusion rate observed despite similar changes in C, CBF, and VO2. We conclude that ADO may mediate the vasodilation induced by norepinephrine, but not atrial pacing.

Effects of clonidine, prazosin and phentolamine on heart rate and coronary sinus catecholamine concentration during cardioaccelerator nerve stimulation in spinal dogs.

1 In spinal dogs, continuous electrical stimulation of the cardioaccelerator nerve produced a transient rise in aortic blood pressure and a sustained increase in both heart rate and coronary sinus blood flow. The latter effects were accompanied by a significant elevation in the coronary sinus plasma noradrenaline concentration without significant changes in the levels of dopamine and adrenaline. The concentrations of the three catecholamines in thoracic aorta plasma were not significantly changed by cardioaccelerator nerve stimulation.2 Clonidine (20 mug/kg, i.v.), given during cardioaccelerator nerve stimulation, increased both mean aortic blood pressure and coronary sinus blood flow and decreased heart rate and coronary sinus venous plasma noradrenaline overflow.3 Phentolamine (0.3 mg/kg, i.v.) completely antagonized these effects of clonidine. Prazosin (0.3 mg/kg, i.v.) inhibited by only 43 and 38% the respective reductions in heart rate and noradrenaline overflow elicited by clonidine.4 On termination of cardioaccelerator stimulation (about 10 min after either prazosin or phentolamine), heart rate and coronary sinus noradrenaline overflow returned to control prestimulation levels.5 Phentolamine or prazosin, administered alone during stimulation of the cardioaccelerator nerve, increased heart rate and noradrenaline overflow into the coronary sinus plasma. However, intravenous phentolamine and prazosin, in contrast to desipramine (0.3 mg/kg, i.v.) or tyramine (1.0 mg, i.a.), failed to change the tachycardia resulting from the local administration of noradrenaline into the sinus node artery (i.a.).6 These results show that in spinal dogs the clonidine-induced reduction in heart rate (elevated by electrical stimulation of the cardioaccelerator nerve) is accompanied by a fall in the quantity of noradrenaline overflowing into the coronary sinus plasma. The latter effect is presumably the result of an action of clonidine on cardiac presynaptic alpha-adrenoceptors, the activation of which is followed by a reduction in the release of noradrenaline per nerve impulse. Phentolamine and prazosin are both antagonists of cardiac presynaptic alpha-adrenoceptors in spinal dogs, as suggested by their action against clonidine and by their positive chronotropic effect when administered during stimulation of the cardioaccelerator nerve.

Myocardial extraction of cyclic AMP during pacing-induced angina

The application of cyclic AMP as a marker of myocardial ischemia in humans with coronary artery disease has been investigated during pacing-induced angina. Cyclic AMP was determined by a radioimmunoassay. In 15 patients myocardial lactate extraction at rest (20 +/- 12%) converted to production levels (-30 +/- 23%) during angina (p less than 0.0005). Insignificant changes occurred in coronary venous plasma cyclic-AMP levels. The mean myocardial cyclic-AMP extraction at rest (0.3 +/- 8.7%) converted to small release values (-6.0 +/-11%) during angina (= n.s.). No significant correlation was found between myocardial lactate and cyclic-AMP uptake or release. Therefore, cyclic AMP is an insensitive marker in the evaluation of myocardial ischemia.

Effects of DC electric countershock on ventricular function, cation balance and endogenous norepinephrine in the dog heart.

Effects of DC electric countershock on cardiac function in thoracotomized dogs were evaluated from recordings of ECG, aortic pressure, left ventircular pressure and its first derivative, and coronary sinus flow. Samples of arterial and coronary venous plasma and left ventricular myocardium obtained before and after countershock at times corresponding to post-shock arrhythmias and recovery were analyzed for Mg++, K+ and Ca++, and norepinephrine. At 1 min after countershock, ECG changes included transient cardiac arrhythmias and ST segment alterations, accompanied by depressed ventricular function and decreased myocardial Ca++ concentration. At 5 min postshock, coronary venous Mg++ and K+ concentrations had risen and ventricular function was still depressed. Function recovered within 10-20 min. There was no evidence of consistent loss of endogenous myocardial norepinephrine.

Myocardial: blood purine nucleoside concentration ratios in canine myocardium.

Adenosine is a potent coronary vasodilator which may play an important role in the regulation of coronary blood flow (2). According to this hypothesis, adenosine is produced when adenosine triphosphate is breaking down in response to an increased demand for energy. The resulting increment of adenosine is thought to diffuse out of the myocardial cells and pass through the extracellular fluid to the coronary myocytes where it produces relaxation resulting in vasodilatation and increased flow to establish a new steady state. Increased adenosine content1 is felt to be dissipated by washout into coronary venous blood (7). The concentration of adenosine in coronary venous plasma and in pericardial fluid has been used for indirect estimates of the adenosine content of the myocardium (11, 12); such estimates imply that adenosine is readily diffusible across biological membranes. Because estimates of the myocardial concentration of adenosine from its concentration in coronary sinus plasma (12) are some 30-fold lower than estimates derived from analysis of heart muscle extracts (9), studies of myocardial: blood and myocardial: pericardial fluid concentration ratios were undertaken. The experiments reported below indicate that there may be significant barriers to the diffusion of adenosine out of canine myocardium and that washout of adenosine by coronary blood flow may not be an important mechanism in the regulation of tissue levels of this nucleoside.

Electrolyte changes in heart tissue and coronary arterial and venous plasma following coronary occlusion.

When coronary sinus and arterial plasma samples obtained during a period of ventricular tachycardia 8 to 11 hours after coronary ligation were analyzed for electrolyte concentrations, it was found that there was an increase in K and Mg and a decrease in Ca and Na. By comparison, when blood samples were taken from sham dogs 8 to 11 hours after the ligatures had simply been placed under the artery, no significant change in plasma cation concentrations over control values was observed. Infarcted ventricular tissue, as compared with noninfarcted tissue, contained an average of 5.1 mEq./100 Gm. wet weight more Na, 4.0 mEq./100 Gm. wet weight less K, and 1.12 mEq./100 Gm. wet weight less Mg.

Magnesium sulfate and chloride in suppression of ectopic ventricular tachycardia accompanying acute myocardial infarction.

ArticleMagnesium Sulfate and Chloride in Suppression of Ectopic Ventricular Tachycardia Accompanying Acute Myocardial InfarctionA. Sidney Harris, Antonio Estandía, Herbert T. Smith, Roy W. Olsen, Tedroe J. Ford JR., and Rex F. TillotsonA. Sidney HarrisFrom the Departments of Physiology, Louisiana State University School of Medicine New Orleans, Louisiana and Baylor University College of Medicine, Houston, Texas, Antonio EstandíaFrom the Departments of Physiology, Louisiana State University School of Medicine New Orleans, Louisiana and Baylor University College of Medicine, Houston, Texas, Herbert T. SmithFrom the Departments of Physiology, Louisiana State University School of Medicine New Orleans, Louisiana and Baylor University College of Medicine, Houston, Texas, Roy W. OlsenFrom the Departments of Physiology, Louisiana State University School of Medicine New Orleans, Louisiana and Baylor University College of Medicine, Houston, Texas, Tedroe J. Ford JR.From the Departments of Physiology, Louisiana State University School of Medicine New Orleans, Louisiana and Baylor University College of Medicine, Houston, Texas, and Rex F. TillotsonFrom the Departments of Physiology, Louisiana State University School of Medicine New Orleans, Louisiana and Baylor University College of Medicine, Houston, TexasPublished Online:31 Dec 1952https://doi.org/10.1152/ajplegacy.1952.172.1.251MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Download PDF FiguresReferencesRelatedInformation Cited ByIntravenous magnesium sulfate for acute termination of sustained monomorphic ventricular tachycardia associated with coronary artery diseaseThe American Journal of Cardiology, Vol. 86, No. 11Magnesium — Electrophysiological Effects, Antiarrhythmic Properties and Clinical ApplicationsMagnesium and the heart: Antiarrhythmic therapy with magnesiumClinical Cardiology, Vol. 16, No. 11Magnesium and cardiovascular diseaseProgress in Cardiovascular Diseases, Vol. 35, No. 4Magnesium Therapy in Ventricular ArrhythmiasPacing and Clinical Electrophysiology, Vol. 13, No. 7Quinidine-Induced Early Afterdepolarizations and Triggered Activity28 June 2008 | Journal of Electrophysiology, Vol. 3, No. 5Quinidine-induced action potential prolongation, early afterdepolarizations, and triggered activity in canine Purkinje fibers. Effects of stimulation rate, potassium, and magnesium.Circulation, Vol. 79, No. 3Effects of magnesium on ischemic and reperfusion arrhythmias in the rat heart and electrophysiologic effects of hypermagnesemia in the anesthetized dogCardiovascular Drugs and Therapy, Vol. 2, No. 5The ionic basis of the anti-ischemic and anti-arrhythmic properties of magnesium in the heart.Journal of the American College of Nutrition, Vol. 6, No. 1Management of acute myocardial infarction with natural physiological agentsMedical Hypotheses, Vol. 11, No. 4MAGNESIUM DEFICIENCY: ROLE IN ARRHYTHMIAS COMPLICATING ACUTE MYOCARDIAL INFARCTION?1 April 1981 | Medical Journal of Australia, Vol. 1, No. 7THE CLINICAL SIGNIFICANCE OF MAGNESIUM DEPLETION IN THALASSEMIAAnnals of the New York Academy of Sciences, Vol. 344, No. 1 Fourth CooleyChanges in plasma and urine magnesium following Subcutaneous insulin7 August 2008 | Current Medical Research and Opinion, Vol. 4, No. 4Magnesium interrelationships in ischemic heart disease: a reviewThe American Journal of Clinical Nutrition, Vol. 27, No. 1Time course of vulnerability to fibrillation after experimental coronary occlusionThe American Journal of Cardiology, Vol. 27, No. 6Antiarrhythmic CompoundsThe effect of the magnesium-disodium salt of EDTA on experimental ventricular arrhythmias in dogsBulletin of Experimental Biology and Medicine, Vol. 54, No. 5Die Mg++-L�hmung des isolierten Froschmyokards Ein Beitrag zur Frage der Beziehung zwischen Aktionspotential und KontraktionPfl�gers Archiv f�r die Gesamte Physiologie des Menschen und der Tiere, Vol. 275, No. 5Electrolyte Changes in Heart Tissue and Coronary Arterial and Venous Plasma Following Coronary OcclusionCirculation Research, Vol. 8, No. 4Mineralstoffwechsel und KreislaufMineralstoffwechsel und KreislaufArrhythmic and Antiarrhythmic Effects of Sodium, Potassium, and Calcium Salts and of Glucose Injected into Coronary Arteries of Infarcted and Normal HeartsCirculation Research, Vol. 6, No. 5ARRHYTHMIAS FOLLOWING EXPERIMENTAL CORONARY OCCLUSION AND THEIR RESPONSE TO DRUGSAnnals of the New York Academy of Sciences, Vol. 64, No. 4 More from this issue > Volume 172Issue 1December 1952Pages 251-258 Copyright & PermissionsCopyright © 1952 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1952.172.1.251History Received 30 June 1952 Published online 31 December 1952 Published in print 31 December 1952 Metrics