Effects of cardiac size on surface potential magnitude were investigated by induction of acute changes in ventricular dimensions by rapid atrial pacing in 17 cases with ischemic heart disease (IHD) and in 15 cases without IHD. Left ventricular end-diastolic dimensions (LVDd), estimated by echocardiography, decreased along with certain changes in surface potential magnitude during atrial pacing in each case. A positive correlation between LVDd and the amplitudes of RV₅, RX, and the maximum spatial QRS magnitude was observed in most of the cases and might be explained by changes in distance between the heart and the chest electrode and/or the Brody effect. However, an inverse correlation was observed in 4 of 17 cases with IHD, and could not be explained by these factors. Other factors, such as changes in the ventricular activation sequence, should be considered as the mechanism.

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A single-dipole model and a two-dipole model have been examined to approximate the electrical activity of heart; positions as well as vector components of these dipoles were estimated from the body surface potential distribution that was measured with 64 electrodes arranged on the chest. The "residue" has been defined as a measure for how much potential component is left that cannot be attributed to the equivalent dipoles. A locus of the vector end of an equivalent dipole in the single-dipole model is very much like ordinary vectorcardiogram (VCG). The residue has a peak in the last half of QRS; this means that the single-dipole approximation is not valid there. Then another dipole is introduced, which is the two-diple approximation. The residue has been greatly reduced and the peak disappears; the resultant two dipoles move around in the right and left parts of the heart with nearly opposite directions. The moving-two-dipole model for normal subjects describes the cardiac activity in QRS much better than with the moving-single-dipole model.

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This study compares the role of M-mode and two-dimensional echocardiography in the evaluation of the nonstenotic, congenitally bicuspid aortic valve. Ten asymptomatic healthy subjects (age 20-35 years) with a systolic ejection click and short systolic murmur were evaluated. M-mode echocardiograms were entirely normal. The aortic root, diastolic closure line, eccentricity index of the aortic valve, and left ventricular size and function were normal in every subject. The two-dimensional parasternal long axis view of the aortic root was also normal in all patients with bicuspid aortic valves; there were no abnormalities of systolic excursion of the aortic cusps and doming of the aortic valve was absent. Images obtained in the two-dimensional parasternal short axis view of the aortic root at the level of the aortic valve revealed only two cusps, anterior and posterior, in all patients. The classic closure pattern of the normal tricuspid aortic valve forming a "Y" was absent in every subject. Instead, a horizontal closure line along the "X" axis was demonstrated in all patients; changing the angulation of the transducer in various positions did not alter this pattern. All subjects had increased reflectance of echoes along the line of diastolic closure, probably resulting from redundancy of the aortic cusp tissue. We conclude that because of the inability of the M-mode echocardiographic technique to accurately diagnose this condition in the study group, two-dimensional echocardiography should be the technique of choice in the evaluation of patients with a suspected bicuspid aortic valve. Recognition of this condition is important in view of its susceptibility to subacute bacterial endocarditis, aortic stenosis, and regurgitation.

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In order to investigate the change of the aortic pressure-diameter relationship during exercise, M-mode echograms and/or two-dimensional echograms of the aortic root and of the abdominal aorta were taken before and during supine ergometer exercise in 14 healthy men. The difference of the angle of the ultrasonic beam to the aorta between before and during exercise was too small to influence the measured values.
The exercise, which elevated heart rate to 100beats/min, caused a shift of the pressure-diameter relationship curve of the aortic root to a lower diameter (on an average, end-systolic diameter: from 3.1 to 2.9cm, p<0.001; end-diastolic: from 2.9 to 2.7cm, p<0.001). This was also seen in the abdominal aorta. Stroke volume showed no change during exercise. Total peripheral vascular resistance decreased. Central aortic volume decreased.
In conclusion, exercise induces active constriction of aorta with dilatation of arterioles. This might be beneficial to push the blood into the peripheral tissues.

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Pathologic data on 120 autopsied cases of infective endocarditis are presented. They constitute 1.8% of total 6, 700 and 6.3% of 1, 900 cardiac autopsies over 16 years. Ninety % of patients were below the age of 40 years, 42.5% had no pre-existing heart disease, 33.3% had previous valvular disease, mainly rheumatic, and 24.2% had congenital heart disease. Mitral and aortic valves were each the sites in one third cases, mitral slightly more than aortic. Twenty-six point six % of the cases had lesions on the right side of the heart, 16.6% exclusively so. Cardiac complications were infrequent while systemic infarcts were found in over 80% cases. A route of infection was detected only in 24.1% of the cases, puerperal sepsis being the commonest. Staphylococci were the responsible bacteria in 18 out of 28 cases in which microbiologic data were available. There were only 2 cases with infective lesions on prosthetic valves, both fungal.
The pattern of infective endocarditis in this and other reports from India and Africa differs from that in the West, in many respects including younger age of our patients, significant rheumatic background disease, absence of narcotic addicts and of "degenerative heart disease" and lower incidence of cardiac complications.

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The present study was concerned with changes in APTT and coagulation-fibrinolytic inhibitors in 2 groups of patients receiving either UK with heparin or UK with heparin and dextran sulfate (DS).
APTT just after UK treatment showed a significant prolongation in patients receiving combination treatment with DS, but contrarily a shortening in patients receiving those without DS. This result indicated the usefulness of DS combination in UK treatment.
There was a marked difference between the responses of α₂-PI and antiplasmin to the treatment, presumably as a result of immune complex formation of the α₂-PI with plasmin. However, no marked difference in α₂-PI and AT-III existed both just after and at 24 hours after UK treatment in patients receiving UK (240, 000 units) with both heparin and DS and those receiving UK (480, 000 units) with heparin. Those results suggest that the dosage of UK can be reduced by combination of DS.
Successful UK treatment in clinical cases resulted in a decrease of α₂-PI and an increase of fibrinogenolytic or fibrinolytic degradation products. For these reasons, effective UK treatment appears to require combination with DS and several treatment days under the condition with a decrease of α₂-PI (50%) and fibrinogenolysis with fibrinolysis, which are followed by administrations of UK.

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The therapeutic effect of L-carnitine on arrhythmias during hemodialysis was evaluated in 17 patients with chronic renal disease undergoing intermittent hemodialysis. In 11 of 17 patients (65%), ventricular or supraventricular premature beats appeared at 20 to 30min after the start of hemodialysis and continued throughout the dialysis. Plasma carnitine was at a lower level in the predialysis period (24.8±7.9n mole/ml) as compared with the normal human levels (46.1±8.6n mole/ml), and decreased markedly by the end of dialysis (8.2±5.9n mole/ml). Plasma free fatty acids rapidly increased immediately after the start of dialysis, reached the maximum levels after 20min (from 0.23±0.09 to 1.31±0.64mEq/L) and maintained higher levels even at the end of dialysis (0.76±0.29mEq/L). Administration of L-carnitine (2Gm orally), 2 hours before the start of dialysis, maintained plasma carnitine within normal levels throughout the dialysis and suppressed the increase in plasma free fatty acids. Both the incidence and the severity of premature beats during hemodialysis were significantly reduced by oral administration of L-carnitine (2Gm daily) for 4 to 8 weeks. These results suggest that L-carnitine is useful for the treatment of hemodialysis arrhythmias, presumably by restoring impaired oxidation of free fatty acids.

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A model of mild chronic volume hypertrophy in the dog has been described which consists of establishing a small arteriovenous (A-V) shunt. The model was utilized to evaluate the protection afforded by mild chronic volume hypertrophy against sudden coronary occlusion. Eight animals were studied, 4 with a single shunt (mean estimated 25% increase in cardiac output) and 4 with a double shunt (mean estimated 57% increase in cardiac output). The A-V shunt resulted in the expected volume hypertrophy by roentgenographic and cardiac weight criteria, but was small enough to produce no signs of exercise intolerance, cardiac failure, or definite electrocardiographic changes. After 6 months, the A-V fistulae were surgically closed and 2 weeks later, under normal hemodynamic conditions, the heart was challenged by sudden, permanent ligation of the left circumflex coronary artery at its origin. The time from ligation to death was measured and compared with 10 control animals without such fistulae. Death occurred in 2 to 13min in the control animals; in contrast, 5 of the 8 animals with mild chronic volume hypertrophy survived longer than any control animal, and 2 were long-term survivors. The actuarial estimate of the difference in survival was significant (p=0.007) and indicated that the fistulae reduced the hazard of coronary ligation by a factor of 6. A single small shunt afforded protection similar to a double one. Therefore, mild chronic volume hypertrophy induced by a small A-V fistula in the normal dog protects against sudden coronary occlusion. We speculate that the procedure may have a role in the multifactorial prophylactic management of coronary artery disease in asymptomatic high risk subjects, instead of an inapplicable exercise program.

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The present case is a 49-year-old female who began to feel a chest pain during exercise 2 years ago. Recently, the chest pain occurred during light exercise as well as at rest. The electrocardiogram during the attack showed remarkable ischemic ST segment depression. No abnormality was found in the coronary cineangiography. She was diagnosed as Syndrome X. However, coronary cineangiography during an attack on another day showed a severe spasm in the left main trunk. Thus, a spasm must be considered as one of the causes of "Syndrome X".

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A 60-year-old woman with multiple coronary aneurysms, complicated with acute infero-posterior myocardial infarction is presented.
The cine-coronary arteriogram disclosed a diffuse dilatation of epicardial coronary arteries associated with multiple aneurysms, fusiform ones in the right coronary and the left circumflex coronary arteries and saccular ones in the left anterior descending coronary artery. Distal run-off was poor. Ventriculography revealed a decrease in the ejection fraction (36%) and segmental abnormal wall motion at the apical and infero-posterior regions. The cause of the aneurysms appeared to be atherosclerotic. We suggested that coronary embolization was the cause of acute myocardial infarction in this case.

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The erythrocyte membrane abnormality in SHRSP was detected by the method using a TPP⁺ sensitive electrode even before the development of hypertension. Therefore, such an abnormality does not seem to be secondary to the effect of hypertension but rather due to genetic abnormality. Similar tendency to the findings in SHRSP was observed in erythrocytes from men with genetic disposition to stroke. This method is simple enough to determine the characteristics of erythrocyte membrane within a short period and may hopefully contribute to the prescience and prevention of hypertensive diseases.

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There are many epidemiological reports indicating that the profile of lipoproteins, especially increased LDL, is related to one of risk factors in atherosclerosis. On the other hand, it is known that HDL may have a protective effect on the development of atherosclerosis. These lipoproteins in humans were studied in details, but the specific component in the rat was not yet so well described because of differences in the components between the rat and humans. Since our study first showed that the specific HDL component was decreased in the rats fed an HFC diet, this alteration of the lipoprotein profile in the rat may have a pathogenic importance in the process of experimental hypercholesterolemia.

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Recently, Sasaki et al. have identified DPGM with DPGP (Eur. J. Biochem. 50, 581-593, 1975). This report and our results raised a possibility that in hypertension developmental state the enzyme activities of DPGM and DPGP in erythrocytes of SHRSP showed lower levels than those of WKY. And there is another possibility that in WKY these enzyme activities may be elevated by low partial pressure of O₂ in enzyme inducing process, which was not observed in SHRSP. In addition, it is supposed that in WKY erythrocytes DPGM activity may be stimulated by Hb and inhibited by HbO₂, whereas DPGP activity may be inhibited by Hb and stimulated by HbO₂ in erythrocytes of WKY, which was not observed in SHRSP erythrocytes.

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Isoelectric focusing method revealed that the heart and aorta, but not choroid plexus and the cultured vascular smooth muscle cells, had obvious differences in nonspecific esterase isozyme patterns.
The separation of the nonspecific esterase isozymes which were electrophoresed in the starch gel was already established as a method to detect a genetic marker of SHR (LAB INVEST 22: 206, 1970), but the separation of the isozyme pattern of the cardiovascular system was not so sufficiently clear. In contrast to the starch gel electrophoresis, the separation of the isozyme pattern by the isoelectric focusing was sufficient. Therefore, this technique can be regarded as a good method for analyzing nonspecific esterase isozymes and for detecting genetic markers of hypertensive strains.
Although the pathogenic relationship between the different isozyme pattern and hypertensive diseases is not yet known from the present study, such a clear genetico-biochemical differences is suggestive of the possible existance of genetic factor of hypertension in the heart and blood vessels of SHR and SHRSP.

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Functional and ophthalmoscopic changes of the retinal vessels were observed in 3 to 6 month old SHRSP rats. Fluorescein leakage and small cell infiltration were demonstrated to occur from the retinal vessels of a 4.5 month old rat.

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The hypotensive substance in a chlorella hot water extract was fractionated by ultrafiltration, Sepharose-2B, ultracentrifugation and density-gradient isoelectric focusing. On the basis of component analysis, the purified substance was considered to be a macromolecular glycoprotein.At high concentrations, this substance inhibited contractions, caused by ACh (8×10^-3g/ml), NE (3×10^-3g/ml) and Ca (2×10^-3g/ml), but it did not inhibited contractions cuased by K. Its hypotensive action is due to its direct effect upon the blood vessels.

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The results presented here show that the tumor incidence in T-cell depressed SHR after injection of MCA was higher than that in WKA rats with normal T-cell function. The depression of T-cell functions in SHR was almost completely restored by allogeneic thymus grafts or injection of NSP. At the same time, the generation of Killer T-cells was induced, and the activity of NK cells against K-562 cells was enhanced. The tumor incidence was suppressed and average latency periods were also prolonged in SHR grafted with WKA thymuses. The administration of NSP was effective in prolonging latency periods for the development of tumors. From these results, we suggest that the SHR is a suitable animal model for the investigation of the role of cell-mediated immunity in carcinogenesis.

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The present study seeks to define the pathogenesis of T-cell depression in SHR. Thymus weights of SHR did not differ from those of age-matched W rats and histological changes were not observed until the rats were 6 months old. However, SHR thymus cells showed lower sensitivity to anti-thy 1.1 and anti-T sera when compared to those of W rats. These results suggest that SHR thymus may be composed of increased numbers of immature or extra thymic T-cells and of decreased numbers of relatively mature intrathymic T-cells. Because SHR thymus grafts failed to promote T-cell numbers and functions in nude mice, whereas W thymus grafts sufficiently restored them, the indication is that deficiency of thymic hormone produced by thymic epithelium may occur and may lead to an abnormal state of thymocyte differentiation.

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1) Following successive selective breeding with appropriate hydralazine therapy, a colony of SHRSP which showed very rapid increases in blood pressures at an early stage of growth as well as a particularly high rate of stroke lesions was obtained. This strain was called M-SHRSP.
2) Using M-SHRSP, it is possible to obtain individual rat colonies which show blood pressures which vary from normotension to extremely severe hypertension.
3) It appears possible to produce strains of rats with various characteristics through different combinations of crossbreeding M-SHRSP, WKY, SHC and/or their offsprings.

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