Ischemic-like ST-segment depression seen during exercise in apparently healthy subjects has previously been noted, but the cause of this change is unknown. The aim of this study was to investigate the pathophysiology of this electrocardiographic change. Ten healthy subjects who developed an electrocardiographic "ischemic" pattern of ST change during treadmill exercise testing were studied. All subjects underwent both thallium-201 myocardial perfusion imaging and radionuclide angiocardiography at rest and during exercise at a time when abnormal ST changes appeared, and demonstrated a normal homogeneous pattern of thallium-201 distribution on both rest and exercise images. Overall, left ventricular ejection fraction rose from 0.60±0.06 (mean±SD) at rest to 0.65±0.07 with exercise. None of the subjects had regional wall motion abnormalities at rest or during exercise.
These results are different from the findings observed in patients with coronary heart disease and angina pectoris in whom regional abnormalities in both perfusion and left ventricular performance have been noted during exercise. Therefore it would seem that myocardial ischemia is not likely to be a tenable explanation for the electrocardiographic "ischemic" changes in these apparently healthy subjects.

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The effects of treadmill exercise (up to 85% of the predicted maximum heart rate) on platelet functions and coagulating activities were studied in 26 normal men. Blood sampling for the measurements were performed from the antecubital vein at rest, at 3, 6, 9, and 12min during exercise, immediately postexercise, and at 6 and 30min after exercise. Measurements for blood analysis included the following: platelet sensitivity and percent aggregation to ADP, platelet counts, plasma thromboxane B₂ and 6-keto-prostaglandira F_1α levels, plasma epinephrine and norepinephrine levels, plasma fibrinogen level, activity of plasma antithrombin III, and of plasma factors VIII, IX, XI, and XII.
No significant changes were induced by dynamic leg exercise in platelet sensitivities and the maximum and 3-min percent aggregation. The platelet counts increased during exercise in plateletrich plasma without a significant change in that in whole blood. During exercise, plasma thromboxane B₂ levels showed a tendency to increase, while plasma 6-keto-prostaglandin F_1α levels to decrease. Plasma epinephrine levels showed a tendency to increase and norepinephrine levels increased during exercise. Among coagulating factors, factor VIII activities and fibrinogen levels increased without altering activities of factors IX, XI, and XII. Antithrombin III activities also increased during exercise. In spite of significant changes in several coagulating factors, prothrombin time and partial thromboplastin time were not influenced by exercise.
In conclusion, dynamic leg exercise of a moderate to high intensity produced a significantly elevated plasma level of factor VIII, fibrinogen, antithrombin III, and catecholamines without affecting the hemostatic balance in normal subjects.

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The distribution of action potential durations (APD) in the left ventricle were investigated and compared to the spatial orientation of the maximum T vector (MaxTv). Eight dogs with similar vectorcardiographic spatial orientations of MaxTv were used. Action potentials were recorded from 42 to 64 sites on each isolated endocardial and epicardial specimen with glass microelectrodes. Preparations included the entire left ventricular free wall. The APD₅₀ and APD₉₀ had similar distributions, but the APD₉₀ distribution was less uniform in all 8 dogs. On the endocardium, APDs were longest between the roots of the papillary muscles, and progressively shorter toward the upper edge (base) where the shortest APDs were found. On the epicardium, APDs were longest in the lower lateral region, and gradually shortened, approximately concentrically, toward the anterior and posterior bases. APDs were longer in the endocardium than in the corresponding epicardium. Maximum APD endocardial-epicardial differences were found in the lower lateral region of the ventricular free wall. Results agree with reports of ventricular recovery properties in vivo, and partly account for the spatial orientation of the MaxTv. This study adds new details, and delineates the longest and shortest distributions of APDs.

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We have investigated the effects of catecholamines (dopamine, norepinephrine, epinephrine and isoproterenol) and tyramine on sinoatrial conduction time (SACT), sinus cycle length (SCL) and developed tension (DT) in isolated atrial muscle, using an isolated and blood-perfused dog atrial preparation, perfused with heparinized blood from the carotid artery of the anesthetized donor dog. Each substance was continuously administered intraarterially into the cannulated sinus node artery. They had dose-dependent positive chronotropic and inotropic effects. Each produced not only a shortening but a prolongation of SACT. In experiments in which only a shortening occurred, the order of the potency for inducing the shortening of the SACT was isoproterenol>norepinephrine=epinephrine>dopamine>tyramine. The ratio of doses required to produce roughly a 15-25% shortening of the SACT was 1: 10: 10: 100: 300, respectively. The isoproterenol-induced shortening of the SACT was inhibited by treatment with propranolol. Tyramine-induced shortening was inhibited by imipramine. From these results, it is suggested that sympathomimetic amines induce a short-ening of SACT through adrenergic beta-receptors and also readily induce a pacemaker shift in the SA nodal area.

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The protective effects of Young's solution (YNG solution), a cardioplegic solution, on the myocardial function and metabolism were assessed in isolated atrial preparations and isolated perfused heart preparations of the guinea pig. In atrial preparations, the time to arrest of the contraction became shorter as the concentrations of the K⁺, Mg⁺⁺, and K⁺-Mg⁺⁺ solutions increased, while the time to resumption of the contraction was lengthened. There was no difference in the time to arrest between K⁺ and K⁺-Mg⁺⁺ solutions, but the time to resumption was reduced with K⁺-Mg⁺⁺ solution to about half the value with K⁺ solution. YNG solution represented an optimum solution for obtaining a quick cardiac arrest and quick resumption of contraction. In the isolated perfused heart, the time to arrest was similar for all the cardioplegic solutions used and the heart stopped in diastole. However, the time to arrest was longer with cold Krebs-Henseleit's solution (cold cardioplegia). The time to resumption of the contraction was the shortest with YNG solution, which yielded the highest mitochondria) respiratory control ratio (RCR) and ADP/O ratio. There was a negative correlation between the time to resumption of contraction and mitochondrial RCR or ADP/O ratio (r=-0.50 and -0.58, respectively).

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Experiments were carried out in the blood-perfused canine papillary muscle preparation to evaluate the protective effect of a cardioplegic solution, Young's solution (YNG solution), on the myocardial function. Both in spontaneously contracting preparations and in electrically paced (2Hz) preparations, the time to the cardiac arrest and the time to the maximum blood flow were found to be significantly shorter when the cardiac arrest was induced with cardioplegic solutions than when it was induced with the cold modified Krebs-Ringer's solution (cold cardioplegia). The maximum blood flow of the paced preparation tended to be greater with cardioplegic solutions. The time to resumption of regular contractions was significantly shorter with YNG solution as compared with cold cardioplegia. The developed tension and the blood flow at the time of resumption of the regular contractions tended to approach the control value more quickly with YNG solution, as compared with other cardioplegic solutions and cold cardioplegia. It is concluded that YNG solution represents an optimal cardioplegic solution.

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In cats with normal intracerebral pressure (ICP), administration of sodium nitroprusside (40μg/Kg/min) through the common carotid leads to an increase of ICP, which is attributed to vasodilatation. When ICP is raised gradually to 40mmHg by intracisternal infusion of artificial CSF prior to the application of SNP, increments of ICP due to SNP become smaller. This reduced vasodilatatory response can be attributed to either a decrease in cerebral perfusion pressure or a direct influence of intra-arterially administered SNP on the autoregulatory capacity of cerebral vessels.

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Samples of myocardium with varying degrees of ischemia were obtained from subendo- and subepicardium of nonischemic, ischemic border and center zones of canine left ventricles to assess the sequence of rapid alterations of several parameters of energy metabolism induced by myocardial ischemia. Ischemia was induced by occluding the left anterior descending coronary artery. The contents of creatine phosphate (CP) and ATP decreased significantly. There was a significant accumulation of lactate. The redox potential (Eh) and phosphorylation potential (Γ) also decreased sharply, but only a slight decrease in energy charge (E.C.) was noted. A close correlation was found between ATP and total adenine nucleotide (r=0.99). There were various degrees of linear correlation between other parameters, except for ATP (and total adenine nucleotide) and Pi, and CP and Γ, which were uncorrelated. The sequence of rapid alterations in the parameters of energy metabolism induced by ischemia was: (1) Γ and CP, (2) Pi, ATP and Eh, and finally (3) lactate and E.C. A significant increase of the heart rate and a decline of the mean blood pressure and left ventricular pressure (LVP) were also observed in association with a slight change in the maximum rate of rise of the left ventricular pressure (dP/dt_max).

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We studied the involvement of renal sympathetic nervous system activity in the antihypertensive and natriuretic effects of potassium supplement in DOCA-salt treated rats. Systolic blood pressure of DOCA-salt rats rose substantially, reaching 181±3mmHg after 4 weeks of DOCA-salt administration. In contrast, the supplement of 1% KCl solution attenuated the development of the hypertension until the fourth week (120±1mmHg). After the 4-week treatments, renal norepinephrine turnover rate was calculated from the decline in specific activity after the injection of dl-³H-norepinephrine. It was markedly accelerated in DOCA-salt rats as compared to control rats. In contrast, 1% KCl supplement significantly restored to normal the increased renal norepinephrine turnover rate in DOCA-salt rats. Taken together, evidence presented suggests that the normalization of the increased renal sympathetic tone may be involved in the natriuretic and antihypertensive effects of potassium supplement in DOCA-salt hypertensive rats.

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The uterine contents and ovaries of pregnant spontaneously hypertensive rats (SHR) were compared to those of control Wistar-Kyoto rats (WKY). Although there were no strain differences in the number of released oocytes as indicated by corpora lutea, there were fewer viable fetuses in the SHR litters compared to WKY. Since there was no difference in post-implantation intrauterine loss, the lower SHR fetal number was most likely due to fewer successful implantations in the SHR. Maternal blood pressures declined significantly in both strains on day 18 of gestation.

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The spasmolytic action of nicorandil on coronary circulation was investigated in 3 Japanese monkeys (Macaca fuscata), 1 rhesus monkey (Macaca mulatta), and 1 anubis baboon (Papio anubis) anesthetized with pentobarbital. The arterial bed of the left anterior descending coronary artery (LAD) was perfused with autologous arterial blood at a constant pressure close to systolic arterial blood pressure. Single injections of nicorandil (10-300μg) into the LAD produced a dose-dependent increase in blood flow without affecting either systemic arterial blood pressure or heart rate. With continuous infusion of acetylcholine into the LAD, the LAD flow decreased to nearly half the basal level, indicating sustained coronary arterial constriction. Under these conditions intra-LAD nicorandil increased the LAD flow virtually to the same extent as before acetylcholine-infusion. These effects of nicorandil resemble those of the Ca⁺⁺-antagonists, diltiazem and nifedipine, but differ from those of nitroglycerin, which is less effective during sustained coronary arterial constriction. The results imply that nicorandil may be as effective as Ca⁺⁺-antagonists in the treatment of vasospastic angina.

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The case of a patient with severe left main trunk disease is presented, in which spasm of the right coronary artery resulted in intraoperative myocardial ischemia and perioperative myocardial infarction. It is suggested that coronary spasm may be a cause of perioperative myocardial infarction, and has to be considered in case of unknown etiology.

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Body surface maps during one cycle of atrial flutter were recorded in 2 cases. The sequences of movements of the maximum and the minimum were compared to those of the sinus P waves. The maps of normal sinus P waves usually show that a maximum first appears at the anterior chest near the sternum and moves to the left side of the thorax in the later half of the P wave. The maps of atrial flutter in Case 1 showed that a maximum first appeared on the upper right back and then moved to the right side of the anterior chest. The maps of Case 2 showed that a maximum first appeared on the upper right back and then moved down the right side of the posterior thorax. There were no movements of the maxima in either case from the right side of the chest to the left as seen in the sinus P waves.

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