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Arrhythmias Arising in Atrioventricular Node There is both experimental and clinical evidence11 that extrasystoles and tachycardia originating in the atrioventricular node often cannot be different...

H OUSSAY, Taquini, and their co-workers1 have made certain observations which are of fundamental importance in the study of experimental hypertension. They were able to demonstrate that transplantation of the ischemic kidneys of dogs with Goldblatt hypertension’ caused an almost immediate rise in the blood pressure of the recipient animal after anastomosis of the renal and carotid-jugular vessels. A msore pronounced rise took place if the animals into which the transplantation was made had been previously nephrectomized. An attempt to confirm these results on another animal appeared to be of sufficient importance to justify the experiments reported in this paper. The rabbit was chosen because, like the dog, it lends itself to the production of hypertension by means of artificial renal ischemia.3 The hypertension in this animal appears to be identical with that in the dog; furthermore, it can be extremely severe, to the extent of attaining the so-called malignant phase, with widespread, neerotizing arteriolitis.4

In our studies on the effects of broncho-constricting drugs on intrapleural pressure,1 we noted that whereas a more positive intrapleural pressure on expiration developed following the administrati...

Although many of its effects have not been clarified, it is well known that the carotid sinus reflex has a profound influence on the cardiovascular system. The purpose of this paper is to investigate the effect of the carotid sinus reflex on the canine heart.The present experiments were performed on the in situ canine heart: 1) during sinus rhythm, 2) during electrically driven rhythm, and 3) during electrically driven rhythm after the administration of atropine. Before and during carotid sinus stimulation, the intracellular and surface electrograms, standard lead II electrocardiograms and aortic blood pressure were simultaneously recorded. The intracellular and surface electrograms were obtained from the epicardial surfaces of the right atrium and the left ventricle.Atrium. The duration of the membrane action potential (MAP) shortened during sinus rhythm and electrically driven rhythm. There were no significant changes in the amplitude of the MAP and the membrane resting potential (MRP). The PQ interval in the standard lead II electrocardiogram became significantly prolonged during both types of rhythm. The P amplitudes decreased during sinus rhythm. The shortening of the duration of the MAP was almost entirely inhibited by atropine.Ventricle. The duration of the MAP during sinus rhythm showedsignificant widening. The ST segment in the surface electrogram became significantly elevated during sinus rhythm and during electrically driven rhythm. The QT interval in the standard lead II electrocardiogram prolonged significantly during sinus rhythm, but less so during electrically driven rhythm. The RR interval became significantly prolonged during sinus rhythm. After atropine, the duration of the MAP widened very slightly during electrically driven rhythm.The following possibilities are discussed: Electrical behavior in atrial muscle is mainly mediated by the cholinergic nervous system. The response of the sinoatrial node is caused by cholinergic activity as well as by the decrease in adrenergic activity.The effect of carotid sinus stimulation on intracellular electrograms is more apparent in atrial muscle and in the sinoatrial node than in ventricular muscle.

In 1938, Taquini 1 reported that, when the kidney of a dog is made completely ischemic, re-establishment of the renal circulation is followed by a rise in blood pressure. In a previous study, 2 it was found that the expected rise in blood pressure did not occur in rabbits following the termination of complete renal ischemia which had lasted four to six hours. At that time, the only way to account for the difference in the response of dogs and rabbits was to assume a species variation. Because of the negative response in rabbits, it seemed desirable to extend these observations to other animals; in this communication we are reporting the effects upon the blood pressure of re-establishment of the circulation of ischemic kidneys in cats, dogs, and rats.

Seven clinical cases with electrocardiographic patterns of constant or variable short P-R interval are reported. The QRS complex was either normal or aberrant. These abnormalities were reproduced experimentally in dogs by the injection of various drugs into the region of the A-V node. The theories advanced to explain these phenomena are discussed. The results indicate that accelerated A-V nodal conduction is responsible for the short P-R interval. The form of the ventricular complex may be dependent upon synchronous or asynchronous activity of the A-V node. A classification of A-V nodal dysfunction is presented.

1. 1. Increase in the R wave and decrease in the S wave have been clinically observed with myocardial infarction and during episodes of the variant form of angina pectoris. 2. 2. The same changes have been reproduced in experiments with animals by acute ischemia. 3. 3. The electrocardiographic changes were most marked from the center of the ischemic area, where ischemia is most severe, and became progressively smaller as recorded toward the periphery. 4. 4. The term “giant R” wave has been used to describe this marked increase in amplitude of the R wave. 5. 5. The giant R wave has been demonstrated during severe attacks of the variant form of angina pectoris. As pain subsided, the R wave gradually returned to the preattack level. These findings are similar to those observed in experiments on animals after ligation of a large coronary artery and release of the ligation. 6. 6. Hemorrhagic hypotension following coronary occlusion resulted in increased severity of ischemia. There was an additional increase in the R wave and the S wave receded or disappeared. These changes were reversed with return to normal systemic pressure by transfusion. 7. 7. In ischemia with S-T depression due to hemorrhagic hypotension, a decrease in the R wave and an increase in the S wave sometimes occur. This is similar to findings in severe classic angina pectoris. R and S wave changes in ischemia with S-T depression are opposite to those seen in ischemia with S-T elevation. 8. 8. Injection of potassium and sodium in various concentrations directly into a coronary artery produced characteristic R and S changes under nonischemic conditions. High concentration potassium or low concentration sodium resulted in increased amplitude of R waves and decreased amplitude of S waves. Low concentration potassium or high concentration sodium resulted in reduced amplitude of R waves and increased amplitude of S waves. Five per cent glucose in water injected directly into the coronary artery produced a large increase in the amplitude of the R wave and a marked receding or disappearance of the S wave, together with the appearance of S-T depression. 9. 9. Among the explanations for these changes in the R and S waves, the possible role of the membrane action potential, of electrical conductivity of the extracellular medium and of the propagation process have been discussed. 10. 10. Increases in the R wave and decreases in the S wave are noted in severe acute ischemia and may have great clinical significance. When decrease in the R wave and increase in the S wave occur, ischemia probably is less severe in that particular part of the heart. 11. 11. Similar changes in the R and S waves can occur with electrolyte alterations without ischemia.

1. (1) For many decades the treatment of acute myocardial infarction has routinely included many weeks of rest, regardless of the severity of the attack. 2. (2) Modern technics made it possible to classify most cases of acute myocardial infarction into three categories—“mild,” “moderate,” and “severe.” Some cases are unclassifiable since there is no sharp line of demarcation between these groups. 3. (3) In the typical “mild” case, the patient is young or middle-aged, usually has pain of short duration and looks and feels well 24 to 48 hours after the attack. There is no associated hypertension or previous heart disease. Fever is slight or absent. Leukocytosis is mild and transaminase levels only slightly elevated. Shock, heart failure, gallop rhythm, cardiac enlargement and other serious phenomena do not occur in these cases. 4. (4) In our series of 200 cases of acute myocardial infarction, the “mild” cases constituted 15 per cent of the total number but it is believed that this is a falsely low figure. 5. (5) A review of 400 cases of fatal acute myocardial infarction observed over a six and one-half year period, failed to reveal any patient with a “mild” case who died during or soon after the attack. The immediate mortality rate in “mild” cases must be extremely low. Certainly, it is much less than the average in all myocardial infarctions. 6. (6) It is absolutely necessary to take into account the complete clinical picture, including all available laboratory data, in order to diagnose and properly classify cases of acute myocardial infarction. Although the electrocardiogram is usually of great assistance in the diagnosis of myocardial infarction, the physician should be familiar with its limitations. 7. (7) A method of management of “mild” cases is described in which gradually increasing activity is permitted after two weeks of rest and observation. 8. (8) Twenty-two cases have been successfully treated in this manner. Seven cases successfully treated with less than the usual long-term period of rest have been followed for over a year. No untoward effects were observed in any of these patients. Definite psychologic and financial benefits were apparent in all. One of these patients remained ambulatory after his first infarction but survived 29 years. 9. (9) Clinical evidence is presented which indicates that the danger of cardiac rupture or aneurysm formation in cases of mild myocardial infarction is minimal. This conclusion is supported by the finding that it is virtually impossible to rupture small infarcted areas in dogs two weeks after coronary ligation. 10. (10) In view of the very low mortality and paucity of complications in “mild” cases, it seems neither necessary nor desirable to subject such patients to the same rigorous and prolonged treatment required for more severe cases. Furthermore, early activation of these patients results in distinct physical, psychologic and financial benefits.

1. Perfusates of totally ischemic kidneys of cats contain a pressor substance which is not present in the perfusates of normal kidneys, ischemic hind limbs, or ischemic gravid uteri. 2. The pressor material in ischemic renal perfusates originates directly in the kidney as a result of complete ischemia. 3. The pressor principle contained in ischemic renal perfusates is the cause of the hypertension which follows the reestablishment of circulation in completely ischemic kidneys, since perfusates of unreleased completely ischemic kidneys contain more pressor material than perfusates of released ischemic kidneys of the same animal. 4. The pressor principle in ischemic renal perfusates is presumed to be renin for the following reasons, (a) Both substances are destroyed by boiling, (b) Both substances induce tachyphylaxis. (c) The configuration of both pressor curves is identical, (d) The pressor action of both is not reversed by 933F, proving they are not epinephrine-like substances. (e) When incubated with plasma, both form a heat-stable pressor substance. (f) The pressor effect of both is uninfluenced by a previous injection of cocaine, (g) Unreleased, completely ischemic kidneys yield more pressor material on extraction than do released ischemic kidneys of the same animal. 5. The perfusates of blood-free ischemic kidneys contain more renin than those of blood-filled ischemic kidneys. 6. A method is described by which the power of various substances to inhibit or enhance the production of renin in the ischemic kidney may be tested. 7. A small amount of the heat-stable pressor substance, presumably angiotonin or hypertensin, is formed by the reaction of the pressor material (renin) and plasma in the vessels of the kidney during the period of complete ischemia.

The four auricular arrhythmias, premature systoles, paroxysmal tachycardia, flutter, and fibrillation, have been investigated in over 200 dogs by three methods: (1) high speed cinematography, (2) cathode-ray oscillography, and (3) multiple-channel electrocardiography. The hitherto unexplored body of the left auricle has been surgically exposed and thoroughly studied. Results indicate that all four arrhythmias are of unitary origin and may occur from one ectopic focus. The resulting arrhythmia depends largely upon the rate of discharge from that focus. There is no circus movement. Corroborative observations have been made on the arrhythmias in man. This conception of the auricular arrhythmias simplifies the understanding of their mechanism.

These experiments demonstrate that liver extract, which has significant antiburn shock activity, either when administered parenterally, as in previous work,1 or orally, as in the present study, is without comparable activity in the shock states which follow hind-leg ischemia or bacterial infection. It has been demonstrated that the mechanism of tourniquet shock in rats is complicated by several factors which are difficult to control. Before a final conclusion regarding the ineffectiveness of liver extract in this type of shock could be drawn, it would appear necessary that complicating factors be controlled. The negative results obtained with liver extract after acute exsanguination permit no conclusions to be drawn regarding liver activity in hemorrhagic shock. The fact that liver is effective in burn shock, but not in tourniquet or bacterial shock, is further evidence for the concept that there are different mechanisms responsible for various types of shock, although all may give rise to a similar terminal picture. It further indicates that therapeutic measures must be evaluated individually for each type of shock, and that results obtained with one type of shock cannot be justifiably transferred to other types of shock.

1. 1. Surgical procedures for the treatment of arteriosclerotic heart disease has made the recording of direct epicardial electrocardiograms possible in 15 patients with severe classic angina pectoris. Numerous “islands” of S-T segment depression widely scattered over all epicardial surfaces of both ventricles have been demonstrated. Areas other than these “islands” showed isoelectric S-T segments. “Islands” with epicardial S-T depression were not found in control patients. 2. 2. The “islands” with S-T segment depression could not be distinguished by virtue of pallor or cyanosis from the areas with isoelectric S-T segments. 3. 3. The occurrence of S-T segment depression in standard leads in classic angina is explained by the diffuse distribution of these “islands” of S-T segment depression. Standard leads face the “islands” of depression. 4. 4. The absence of reciprocal S-T segment elevation in other standard leads in classic angina is also explained. Reciprocal S-T elevation in standard leads is not manifest since the primary areas of S-T depression are located all over the ventricles. The occurrence of primary S-T segment elevation in the variant form of angina is noted, together with its restriction to a large discrete area supplied by a large coronary artery. In the variant form of angina the S-T segment depression is reciprocal in nature, in contrast to classic angina pectoris, in which reciprocal S-T segment changes are not noted in standard leads. 5. 5. Diffuse “islands” of epicardial S-T segment depression were produced experimentally in dogs by bleeding to markedly hypotensive levels. These “islands” of S-T segment depression in dogs could not be distinguished visually from areas with isoelectric S-T segments. Similar findings were noted in human beings with angina pectoris. 6. 6. Ligation of a large branch of the anterior descending coronary artery in dogs produced a large discrete area in which only epicardial S-T segment elevation was recorded. This area with S-T elevation was distinctly cyanotic, in contrast to the previously described “islands” with S-T depression which were not visually distinguishable. These findings were similar to those in patients with the variant form of angina pectoris. 7. 7. The similarity of local hypotension at the distal end of partially constricted coronary arteries, to generalized hypotension in the presence of normal coronary arteries is noted. 8. 8. The frequent persistence of classic angina following a myocardial infarction is explained by the diffuse location of the “islands” with S-T depression. Following infarction, many such “islands” remain. The disappearance of the variant form of angina following a myocardial infarction also is explained as being due to the localization of the changes to the single area which has been infarcted. 9. 9. The occurrence of S-T elevation in the variant form of angina makes prediction of the site of future infarction possible. The occurrence of S-T depression in classic angina does not permit prediction of the site of future infarction. 10. 10. The appearance of epicardial cyanosis in areas with S-T segment elevation on temporary ligation of a coronary artery suggests that coronary artery hypertonus may precipitate the variant form of angina with its S-T segment elevation. The absence of epicardial cyanosis in patients with classic angina, and in dogs with hypotension, suggests that coronary artery hypertonus is not the usual cause of classic angina. 11. 11. Ventricular arrhythmias are noted frequently in the clinical and simulated variant form of angina. They occur after the pain has been present awhile and has risen to a certain intensity. Arrhythmias are rare in the simulated form of classic angina, except for terminal ventricular fibrillation. Sudden deaths in classic angina probably occur as a result of ventricular fibrillation developing suddenly. 12. 12. Several clinical conditions are presented in which S-T segment depression is found in the absence of changes limited to the subendocardium. A number of experiments are presented indicating that the subendocardium does not contribute in significant degree to S-T segment deviations. These experiments indicate that S-T segment depressions are due to disturbances in the outer myocardial layers. 13. 13. The marked difference between S-T changes in classic angina pectoris (with S-T depression) and those in the variant form of angina or early myocardial infarction (with S-T elevation) suggests different chemical changes within the myocardium.7

1. 1. By means of a specially designed plunge electrode, intraventricular leads were recorded from multiple sites throughout the walls, papillary muscle, septum and cavities of thirty-two dogs during normal sinus rhythm. A series of experiments was performed which established (a) that the presence of the plunge electrode in the myocardium did not alter the normal course of depolarization, and (b) that the depolarization complexes registered by the plunge electrode represented essentially local potentials. 2. 2. Pure QS or rS waves were recorded throughout at least the innermost two-thirds of the intramural myocardium in both ventricles as well as from all levels of the left papillary muscle. Intraseptal leads also exhibited essentially negative deflections, although considerable positivity was noted in the center and right side of the septum. Only the epicardial surface and a thin subjacent layer of the walls yielded predominantly positive depolarization complexes. In general, negative potentials were found to predominate in roughly 80 per cent of the musculature during ventricular depolarization while about 20 per cent of the myocardium was predominantly positive. This observation indicates that the ventricular wall does not depolarize in the same manner as the auricles. 3. 3. Pure QS waves consistently were obtained throughout the left ventricular cavity as well as from all portions of the right ventricular cavity except in the immediate vicinity of the septum. Cavity leads recorded near the right septal surface occasionally displayed a small R wave derived from the initial positivity of the right septal surface. 4. 4. The velocity of the depolarization wave was measured in twenty animals by timing the onset of the downstrokes in intramural leads from multiple depths of the left ventricular wall. As determined by this method, the rate of depolarization appears to be considerably more rapid in the innermost two-thirds of the wall than in the superficial layers. 5. 5. Currents of injury, manifested by RS-T segment elevation, always occurred for a brief period following the introduction of the plunge electrode into the myocardium. The RS-T segment deviation was markedly less in subendocardial leads than in subepicardial leads, indicating that subepicardial muscle characteristically is capable of producing more intense injury currents than are the deeper layers of the myocardium. 6. 6. The observed weakness of subendocardial injury currents in experimental animals suggests that the downward RS-T segment deviation, which is seen clinically in angina pectoris, is not attributable to subendocardial anoxia as is generally believed. On the basis of the same experimental observation, a new theory concerning the cause of RS-T segment elevation following coronary occlusion is proposed which appears to reconcile apparent discrepancies among the electrocardiographic, anatomic, and pathologic findings.

The clinical significance of the T wave in representing the electrical recovery process of the ventricular myocardium is well known. This electrical phenomenon, however, has been the subject of much less basic research than other parts of the electrocardiogram. With the development, in recent years, of more reliable recording techniques and the introduction of an incubator in which animal experiments can be performed in a more physiologic medium, this study of the repolarization process of the heart muscle seemed justified. Abundant controversy and confusion have developed over the direction of repolarization through the ventricular wall on the basis of polarity of the T wave. T polarity was studied by means of minute plunge electrodes recording simultaneously at selected depths in the ventricular walls. Moreover, the time course of the electrical recovery process was examined by comparing analogous points of the T wave in simultaneous records from the myocardial surface and the under-lying subendocardium and from different surface points, and these results compared with the polarity of the T waves. Experiments were designed also to study (a) the effect of local thermal changes upon adjacent and remote regions of the heart, (b) the effect of primary T-wave changes upon secondary ones by superimposing thermal changes upon left bundle branch block, and (c) the effect upon the T wave of ischemia due to chronic obstruction of coronary arteries.

(1) The effects of low or high potassium on the canine heart were investigated. Excessively low or high concentrations of potassium solutions were used in the experiments. The ionic concentrations, except that of potassium, were approximately the same as those in serum of normal animals.(2) Surface and intracellular electrographic changes caused by low or high potassium were described in detail.(3) Relationship between surface and intracellular electrographic changes in the repolarization and resting phases was studied by calculating the correlation coefficients and obtaining the regression equation. It was thus observed that the changes of the ST segment, T wave and TQ level produced by low or high potassium were proportional to the corresponding changes in the intracellular electrograms.(4) A reciprocal change was observed in the surface electrogram recorded from the region supplied with normal blood when another region was supplied with low or high potassium solution.(5) It is proposed that the changes of the ST segment and the T wave are the same in their origins.

The electrocardiogram of through-and-through infarction was studied in sixteen dogs with chronic lesions produced by coronary artery ligation. Failure to elicit injury currents at epicardial and intramural levels established the absence of viable muscle within the infarcted regions. Histologic examination confirmed that the regions were completely dead. Direct leads from the epicardium and from various intramural levels of each region yielded pure QS waves identical or almost identical with the cavity QS complex. This observation indicated that the negative cavity potential was transmitted unaltered through the infarct, causing the coronary QS wave.

Severe ischemia results in serious damage to myocardial cells and their membranes. As a consequence, K+ is lost from these cells and intracellular Na+ concentration probably rises. These changes produce a decrease in the transmembrane ionic gradient for these substances and probably hypopolarization of the cell membranes. This is manifested in the intracellular electrogram by a decrease in negativity of the membrane resting potential of the individual subepicardial ischemic cells. In direct electrograms from the epicardium over these cells the T-Q segment becomes depressed. This T-Q depression is indicated in the clinical electrocardiogram as S-T elevation. Perfusion of nonischemic myocardium with solutions of high K+ or low Na+ concentration produces intracellular and surface electrographic changes similar to those of severe ischemia. This supports the theory that metabolic changes such as those just described are at least part of the fundamental cause of the electrocardiographic changes of severe ischemia. In all probability, other chemical and metabolic factors also play a role in their production. Mild ischemia produces an increased uptake of K+ and probably glucose by the myocardial cells. As a result, the transmembrane ionic gradient for K+ increases and a state of hyperpolarization may occur. This causes an increase in membrane resting potential of the individual cells, manifested in the overlying surface electrogram by elevation of the T-Q segment. In the clinical electrocardiogram this appears as S-T depression. Perfusion of nonischemic myocardium with solutions of low K+ or high Na+ ion concentration produces intracellular and surface electrocardiographic changes similar to those of mild ischemia. This again provides support for the belief that such metabolic changes may be in part responsible for the electrocardiographic phenomena of mild ischemia. The increase in amplitude of the R wave often observed early in severe ischemia appears to be the result of delayed conduction in the ischemic muscle. The tall R wave is also widened because of this delay. The S wave is buried in the wide R wave and thus becomes smaller or entirely invisible. The increase in intracellular K+ and glucose in mild ischemia may represent a homeostatic mechanism by which the cells prepare themselves for injury by severe ischemia. The fact that the electrographic and electrocardiographic phenomena of the two kinds of ischemia are almost opposite in nature then becomes understandable as a manifestation of such a mechanism.

Report has previously been made1 that following the administration to dogs of such typical broncho-dilating drugs as epinephrin and atropine, there is a definite increase in intrapleural pressure, i. e., intrapleural pressure becomes more positive than is normally the case. This was interpreted as being due to lessened suction on expansion of the chest because of lessened resistance to the movement of air in and out of the lungs as a result of broncho-dilatation. It naturally became of interest to determine by direct observation whether or not the corollary is also true, viz., that broncho-constriction is followed by the development of more negative intrapleural pressure than is normally present.We employed the same dogs as had been used in our former experiments, and we had sufficient observations on normal intrapleural pressures in these animals to enable us to judge whether or not changes following drug administration were beyond normal diurnal variation. The technique used was the same as that previou...

From these observations it appears (1) that the heart is affected in the majority of patients with emphysema; (2) that the lesion, cardiac hypertrophy, with dilatation of the right ventricle when advanced, may produce symptoms, but probably has no clinical reflection in its earlier stages; (3) that the cause of the left ventricular hypertrophy remains, as yet, undetermined; (4) that there is experimental evidence which indicates that the right ventricular dilatation and hypertrophy occur chiefly in the earlier stage of emphysema, when the lungs are in the process of distention, rather than later as generally believed.

Despite the absence of the coronary Q wave, there appear to be instances when myocardial infarction can be diagnosed in the presence of left bundle branch block. The experimental evidence showed that with a transmural infarction or patchy infarction with extensive surface damage there occurs a marked reduction in the size of the R wave recorded in the direct lead from that region. In some instances, the reduction in the R wave may be reflected in the corresponding precordial lead. Changes in the magnitude of the R wave in the left precordial leads in left bundle branch block will frequently be detected only if control tracings are available for comparison or if multiple precordial leads are taken. Acute myocardial injury results in elevation of the S-T segment despite the presence of left bundle branch block. Thus, the diagnosis of acute myocardial infarction can be made from the finding of significant S-T segment elevation following the large, broad, positive complex of left bundle branch block. Other changes in the coronary circulation may also be reflected by alterations in the RS-T segment despite the presence of left bundle branch block. In our experience, coronary insufficiency as well as a positive two-step exercise test has resulted in changes in the S-T segment. It would appear that the popular opinion that coronary artery disease cannot be diagnosed in the presence of left bundle branch block should be modified. It is true that there is absence of the coronary Q wave in myocardial infarction, but the previously discussed changes should aid in making more conclusive the diagnosis of coronary artery disease in the presence of left bundle branch block.

By means of small intramural electrodes, potentials at multiple depths within the ventricular wall were recorded in myocardial infarction and in normal hearts. In 41 animals with coronary artery occlusion, electrocardiographic and histologic correlations indicated that coronary QS waves may represent negative potentials transmitted from viable intramural muscle as well as from the cavity. Coronary QR waves were obtained over transmural infarcts containing a mixture of viable and dead tissue, but not over purely subendocardial lesions. In the normal ventricle, positive depolarization potentials greatly predominated over negative potentials. Clinical applications are discussed.

Surface and intracellular electrograms and ventricular pressures were used to study the effects of epinephrine and propranolol on electrophysiological properties in the in situ heart of 21 anesthetized dogs. Five sec. after the infusion of epinephrine, the ST segment became slightly depressed. About 10 to 20sec. after epinephrine, the ST segment became elevated and the negative T wave became more inverted. Initially, the upward convexity of phase III of the membrane action potential deepened slightly. Phase II of the membrane action potential gradually decreased in amplitude and became prolonged in duration. Phase III of the membrane action potential increased slightly. The membrane resting potential remained almost unchanged. Intracellular electrographic changes due to epinephrine were of abnormal configuration. That epinephrine may cause anginal pain is well known. Propranolol inhibits epinephrine's effects on the electrophysiologic properties of the heart. It is thought that propranolol helps to relieve the pain of angina pectoris by decreasing cardiac work and by increasing coronary blood flow.

The experimental data here reported indicate that ST deviation is related largely to a change in the balance between intra- and extracellular electrolytes. This change in intra- and extracellular electrolyte balance occurs in ischemic heart disease as well as in a wide variety of noncardiac conditions.

Eight cases of revived human heart in which a reasonably normal type of electrocardiographic curve was obtained have been studied with regard to both the localization of extrasystoles and bundle-branch block. With the heart in normal position it is found that the extrasystoles were similar to those described by Barker, Macleod and Alexander. The right and left bundles were cut in five instances, and the results indicate with the heart in normal position that a lesion of the right bundle is characterized by a deflection that is downward in Lead I and upward in Lead III. When the left bundle was cut with the heart in normal position or with left axis deviation, the electrocardiographic curve was characterized by an upward deflection of the complex in Lead I and a downward deflection in Lead III. Changes in position of the heart greatly modify the character of the curves of both extrasystoles and bundle-branch block. Shifting of the human heart to the left in one instance gave a right axis deviation (old terminology); shifting of it to the right gave a left axis deviation. Rotation of the heart also causes variation in the electrical axis.

Recent studies of the mechanisms involved in the production of experimental renal hypertension show that several humoral agents may be involved. Following the hypothesis that phenolic amines may be involved in renal hypertension, Schroeder and Adams1 found tyrosinase preparations from mushrooms to be effective in lowering the blood pressures of hypertensive animals. Their studies were extended to the effects of tyrosinase preparations on arterial hypertension in man and reported results in 17 patients, with significant falls in blood pressures in 13 of these following daily administration of unspecified amounts of their tyrosinase preparations. Some phenolic substance was considered to be altered by the injected enzyme to account for the lowered blood pressures observed.The present experiments were carried out with mushroom tyro-sinase preparations made by modifications of the purification procedures of Keilin and Mann.3 The valuation of the enzymic activity was made upon a catechol-hydroquinone substrate...