It has been known for a long time that hypertension and diabetes mellitus are often complicated by each other. The aim of this paper was to disclose possible causes of such complications by investigating 1) whether or not hypertension and diabetes mellitus are entirely two independent diseases, 2) whether or not they occur together only by chance, 3) whether or not there are some causal factors which are shared by these two diseases and 4) whether or not these two diseases occur together with some probability. The genetic analyses of these two diseases were carried out on the basis of the genetic analyses on blood pressures (BP) and blood sugar levels (BS) in the present studies. It was proved that the genotypic correlation coefficients of BP and BS ranged from 0.075 to 0.573 with a mean value of 0.337 and their environmental correlation coefficients were from -0.029 to -0.337 with a mean value of -0.164. These results suggest that 1) the respective polygenic systems responsible for BP (hypertension) and BS (diabetes mellitus) have multiple effects and 2) the environmental factors responsible for BP and BS have inverse effects. The negative values of the environmental correlation coefficients between BP and BS indicate that the environmental factors which lower BP may elevate BS, and vice versa. An induction of an abnormal glucose tolerance as one of the side effects of thiazides, the most widely used anti-hypertensive diuretics, coincides with the inverse environmental correlation between BP and BS. This finding may be of great importance in the field of clinical genetics.

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In order to evaluate the left ventricular performance during exercise in patients with myocardial infarction, we performed a symptom-limited multistage exercise test using a bicycle ergometer in the supine position on 82 patients with myocardial infarction, and their hemodynamic responses to exercise were analyzed. Patients were subdivided into three groups according to the levels of pulmonary capillary wedge pressure (PCWP) and cardiac index (CI) obtained at the end-point of the exercise: Group I (20 patients) with PCWP<18 mmHg and CI&ges;5.0 L/min/m² ; Group II (32 patients) with PCWP&ges;18 mmHg and CI&ges;5.0 L/min/m² ; Group III (30 patients) with PCWP&ges;18 mmHg and CI<5.0 L/min/m² . Exercise tolerance expressed as the duration of exercise was 11.9±0.5 (SEM) min in Group I, 10.6±0.4 in Group II and 7.8±0.5 in Group III, which was closely correlated with the left ventricular function observed at the end-point of the exercise. During exercise stroke volume index (SVI) decreased slightly in Group III, while it increased significantly in Groups I and II. The extent of coronary artery lesion in Group III was more severe than in Groups I and II. In 50 patients without prior myocardial infarction, infarct size estimated by total released CPK was larger in Group III than in Group I. These findings indicate that coronary artery lesion and infarct size are important factors contributing to left ventricular performance during exercise in patients with myocardial infarction.

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Effects of intravenous atropine on postpacing impulse recovery time of the subsidiary pacemakers were studied by incremental atrial pacing in 9 patients with sinus nodal (SN) dysfunction. Patients having either or both of the following anomalies are used: 1) persistent sinus bradycardia (sinus cycle length>1000 msec), or documented episodes of sinoatrial block or arrest and/or 2) maximum corrected SN recovery time of longer than 525 msec before and after atropine. Seven patients had a history of cerebral ischemic symptoms. The mean ±SEM of the maximum A-V junctional recovery times (MJRTs) before and after atropine, measured in 5 patients, were 2, 485±825 msec and 1, 164±281 msec, respectively (p<0.01). The average percent reduction of the junctional escape times in these 5 patients was 53.2%. In all 9 patients MJRT shortened to less than 1, 610 msec after atropine. Moreover, a low atrial pacemaker also was the escape mechanism following pacing in 2 patients after atropine; the maximum atrial recovery times were 2, 500 msec and 1, 220 msec, respectively. We conclude that atropine can markedly enhance escape mechanism of the subsidiary pacemakers in patients with SN dysfunction.

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Myocardial fiber disarray in endomyocardial biopsies is considered to be a histologic feature of hypertrophic cardiomyopathy (HCM). To determine whether this disarray is specific for HCM, we examined the distribution of disarray in the subendocardial region in 11 autopsied hearts from patients with HCM and 41 autopsied control hearts. The percent area of disarray in the subendocardial region of the right ventricular side of the septum with maximum septal hypertrophy was 9±3% in HCM and 4±2% in the controls (p<0.001). The frequency of occurrence of disarray in this area was 38±10% in HCM and 20±7% in the controls (p<0.001). Disarray covering over 76% of a visual field, although extremely rare, was specific for HCM. In the right ventricular side of the septum in the lower half and in the left ventricular free wall, there was no significant difference between HCM and controls in regard to the percent area of disarray and its frequency of occurrence. In conclusion, although disarray in right ventricular endomyocardial biopsies is considered to be more frequent in HCM than in the controls, too much emphasis should not be placed on disarray in endomyocardial biopsy specimens as a diagnostic criterion for HCM.

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Hemodynamic responses to prostacyclin (PGI₂) were studied in sheep in the conscious state as well as under pentobarbital-halothane anesthesia. PGI₂ in doses of 0.02-1.0 μg/kg were administered as a bolus into the right or left atrium in the conscious sheep. PGI₂ decreased systemic arterial pressure (P_SA), systemic (SVR) and pulmonary vascular resistance (PVR) and increased cardiac output (CO) and heart rate (HR) in a dose-dependent manner. The changes of each parameter were almost similar regardless of the sites of administration. Pulmonary arterial pressure (P_PA) was increased. There was no change in left (P_LA) or right atrial pressure (P_RA). A bolus administration of 0.5 μg/kg of PGI₂ in the anesthetized sheep produced a decrease in P_SA, SVR and PVR, and increase in CO and HR. P_PA remained unchanged when administered into the right atrium and increased slightly when administered into the left atrium. P_LA and P_RA did not change. Comparing hemodynamic responses to 0.5 g/kg of PGI₂ of the conscious and anesthetized states, decrease in P_SA was smaller and increases in CO and HR were greater in the former. Decreases in SVR and PVR were similar in both states. Increase in P_PA was greater in the conscious sheep. This data confirms that PGI₂ dilates the systemic as well as the pulmonary circulation of the sheep and an inactivation of this compound in the lungs is minimal. Furthermore, it may be suggested that general anesthesia significantly alters hemodynamic responses to PGI₂ in the sheep.

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Serial electrocardiograms of acute viral myocarditis were recorded from Syrian golden hamsters inoculated with Coxsackievirus B₁ (CVB₁). Various electrocardiographic abnormalities similar to those reported in human viral myocarditis were observed. The reciprocal ST displacement and/or T wave flattening were most frequently found, and were detected in 80% of the animals. Occasionally, other abnormalities such as atrioventricular (AV) block, left bundle branch block (LBBB) pattern or extrasystoles were recorded. A histopathological examination disclosed the most prominent lesions of myocarditis in the endocardial third of the myocardium, particularly in the interventricular septum. These lesions were more widespread in the left ventricle than in the right. A close correlation between the electrocardiographic manifestations and distribution of the lesions in the myocardium was observed. Since electrocardiography is widely used in clinical medicine, its application to experimental viral myocarditis will promote the study of viral myocarditis and the analysis of myocardial fibrosis as its sequelae.

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We studied the origin of sodium ions which appeared in a higher concentration in the venous blood plasma obtained from the renal or femoral vein, than in the arterial blood plasma during acute renal venous congestion, acute venous congestion of hindlimbs and acute hemorrhagic hypotension. We measured the sodium concentration in the blood plasma as well as in hemolyzed blood obtained with sonication. In addition, sodium contents of the kidneys and skeletal muscle were determined. All experiments were performed on anesthetized mongrel dogs. Sodium contents of the kidneys and skeletal muscle of hindlimbs, in terms of milliequivalent per gram dry tissue weight, was decreased significantly 30 -40 min after exposure of the kidneys and hindlimbs to acute venous congestion, or after exposure of hindlimbs to hemorrhagic hypotension, indicating a release of sodium ion into the blood stream. The sodium ion concentration became slightly higher in the venous blood than in the arterial blood, in terms of both blood plasma and hemolyzed blood, during 15-30 min of exposure of hindlimbs to local venous congestion or hemorrhagic hypotension, again indicating a release of sodium ion into the blood stream. However, acute renal vein congestion caused the sodium ion concentration to become slightly higher in the venous blood than in the arterial blood, only in terms of blood plasma, and not in terms of hemolyzed blood, indicating that red blood cell sodium is the origin of sodium ions which appeared in the renal venous plasma during acute renal vein congestion.

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The effects of dietary sodium on the characteristics of angiotensin II (A II) receptor sites in the hypothalamus-thalamus-septum-midbrain (HTSM) region were examined in spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Twenty-four SHR and 24 WKY were divided into two groups respectively, which were maintained on high sodium diets or low sodium diets for 4 weeks, respectively. The binding capacity and affinity of the A II receptors were measured by radioreceptor assay. In WKY, the binding capacity of the A II receptors in the high sodium group was significantly lower than that in the low sodium group. On the other hand, the binding capacity of A II receptors was not significantly different between high and low sodium groups in SHR. The secretion of arginine vasopressin (AVP) increased significantly in SHR with high sodium intake. The present results suggest that in WKY the decrease of the binding capacity of the A II receptors in the HTSM region in response to a high sodium intake serves to attenuate an osmotical stimulus to AVP secretion. However, in SHR such a regulatory mechanism as adjusting the binding capacity of the A II receptors is lacking, and this seems to be responsible, at least in part, for the enhanced secretion of AVP on the sodium loading.

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Activities and subcellular distributions of acid hydrolases, cathepsin D, acid phosphatase and β-glucuronidase in myocardial subfractions were determined serially with reference to the initiation of myocardial necrosis in dog hearts with acute ischemia. The following results were obtained: 1)In the normal myocardium, respectable activities of three enzymes were obtained either in the sarcoplasmic reticulum or in the lysosome-containing fraction. 2) Thirty min after coronary ligation, an increase in the activities was observed in both lysosome and sarcoplasmic reticulum fractions of the ischemic heart muscle. After 60 to 90 min these activities were decreased rapidly in both fractions to about 70% of those of the normal myocardium with an increase in the cytosolic activity. Two to 3 hours after ligation, the reduction in the cytosolic activity was noted, indicating an escape of the enzymes from the necrotic myocardium. The subcellular distribution of these enzymes was further altered in the ischemic heart muscle for 12 to 24 hours reflecting an infiltration of the interstitial cells. These findings suggest that activation and release of acid hydrolases not only in lysosomes but also in the sarcoplasmic reticulum are one of the primary and the earliest factors for the evolution of ischemic myocardial injury which leads to necrosis.

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Aspartate aminotransferase (EC 2.6.1.1.:AST) is known to have two isoenzymes, one associated with the cytoplasm (c-AST) and the other with the mitochondria (m-AST). We studied the relationships of m-AST activity in the coronary sinus blood to left ventricular function, coronary blood flow, water content and high-energy phosphate stores of the left ventricle following hypothermic ischemic cardiac arrest. Under cardiopulmonary bypass with hypothermia of 20°C of myocardial temperature, 120 min of aortic occlusion was employed in 15 mongrel dogs. Left ventricular function (peak left ventricular pressure, left ventricular enddiastolic pressure, max dp/dt, cardiac index, left ventricular stroke work index), coronary blood flow, myocardial oxygen consumption, myocardial enzyme activity (m-AST, CK-MB), myocardial water content and high-energy phosphate stores (adenosine triphosphate, creatine phosphate) of the subendocardium of the left ventricle were measured. Data was obtained in the control state, and after 0, 30 and 60 min of reperfusion. Significant negative correlations were obtained between m-AST activity and peak left ventricular pressure (r = -0.81, p<0.001), max dp/dt (r = -0.83, p<0.001), cardiac product (r= -0.73, p<0.01), coronary blood flow (r = -0.59, p<0.05), adenosine triphosphate level (r = -0.72, p<0.01) and creatine phosphate level (r = -0.72, p<0.02) after 60 min of reperfusion. Significant positive correlations were obtained between m-AST activity and left ventricular end-diastolic pressure (r = 0.75, p<0.01) and water content (r = 0.78, p<0.0 1 ) after 60 min of reperfusion. These results led to the assumption that serum m-AST activity in the coronary venous blood is a useful index to evaluate the degree of myocardial injury.

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A case of right ventricular aneurysm due to myocardial fatty infiltration was reported. A 39-year-old man was admitted to our hospital for evaluation of several episodes of syncopal attack presumably induced by malignant arrhythmia. There were frequent observations of ventricular premature beats, which occurred occasionally in couples. Cardiac catheterization disclosed the aneurysm situated at the outflow tract of the right ventricle. Aneurysmectomy was performed and the ventricular premature beats and syncopal attacks were effectively abolished. Etiology of the aneurysm was proved to be a fatty infiltration in the myocardium. To the best of our knowledge, there has been no case report of right ventricular aneurysm due to fatty infiltration in the myocardium.

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