In 24 children with atrial septal defect of the secundum type and/or partial anomalous pulmonary venous connection, the pulmonary to systemic blood flow ratio (Qp/Qs) was estimated by echocardiography. Using M-mode echocardiography, right ventricular diameter (RVD), left ventricular diameter (LVD), total cardiac diameter (TCD) and aortic root (AOR) were measured, and the following 5 indices were obtained: RVD/LVD, RVD/TCD, RVD/AOR, RVD/BSA (body surface area) and TCD/BSA. The single linear correlation coefficients between these 5 indices and Qp/Qs, obtained by the Fick method during cardiac catheterization, were 0.88, 0.80, 0.74, 0.75 and 0.55, respectively. Thus, RVD/LVD ratio was the most sensitive echocardiographic index to assess Qp/Qs in these children. Clinically, however, the multiple linear regression equation derived from 3 indices (RVD/BSA, RVD/LVD and TCD/BSA) might be more useful (r= 0.89). Although the abnormal motion of the interventricular septum was analyzed, the quantification of this motion as an index of Qp/Qs was difficult.

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Twenty-three patients with chronic respiratory failure and 30 normal subjects were studied to assess the sympathetic nervous activity in chronic hypoxic states, especially in chronic cor pulmonale. Of the 23 patients, 13 had a right ventricular hypertrophy (RVH) pattern on the electrocardiogram. Plasma norepinephrine (NE), dopamine-β-hydroxylase (DBH), cyclic adenosine 3', 5'-monophosphate (cyclic AMP) and cyclic guanosine 3', 5'-monophosphate (cyclic GMP) concentrations were measured before and after oxygen inhalation. Plasma NE concentrations were 0.57 ± 0.07 ng/ml in patients with chronic respiratory failure and 0.22 ± 0.02 ng/ml in controls (p<0.001). Moreover, plasma NE concentrations were higher in patients with RVH than without (p<0.05), and these concentrations decreased significantly (p<0.05) in the former patients after oxygen inhalation. Plasma cyclic AMP concentrations were 31.2 ± 2.6 pmol/ml in cases of chronic respiratory failure and 17.4 ± 0.7 pmol/ml in controls (p<0.001) with no difference in plasma cyclic GMP and DBH concentrations. These results suggest that a significant proportion of patients with chronic respiratory failure, especially with cor pulmonale, were in hyper-adrenergic states partially due to hypoxia.

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Mean concentration of plasma norepinephrine of 66 normal subjects was 0.23 ± 0.02 ng/ml, but that of 81 hypertensives was 0.25 ± 0.02 ng/ml. There was no significant difference of plasma norepinephrine concentration between the normotensives and the hypertensives. However, a significant correlation was demonstrated between the concentration of norepinephrine and age in the normotensives (r = 0.51, p<0.001). Nonetheless, this correlation was not found in the group with essential hypertension. Age matching revealed a significant higher concentration of norepinephrine in the twenties and the thirties and no significant difference in the forties and the fifties. There was also significant negative correlations between the concentration of norepinephrine and both the percent changes in mean blood pressure (r = -0.31, p<0.01) and the percent changes in diastolic pressure (r = -0.32, p<0.005) after twenty minutes in the recumbent position in the clinic. Mean concentration of plasma cyclic AMP and cyclic GMP of 70 normal subjects were 17.7 ± 0.4 pmol/ml and 4.3 ± 0.02 pmol/ml respectively. There was a significant correlation between the concentration of plasma cyclic GMP and age (r = 0.30, p<0.001), and no correlation between the concentration of cyclic AMP and age in normal subjects. Mean concentration of plasma cyclic AMP of 68 hypertensives was 25.0 ± 0.8 pmol/ml and significantly higher than normal subjects (p<0.001 ). But, that of cyclic GMP of the same patients was 4.4 ± 0.2 pmol/ml and there was no significant difference between the normotensives and the hypertensives. Thus, it was suggested that sympathetic nervous activity was not elevated in older patients with essential hypertension but was elevated in younger patients and that the second messenger system of cyclic AMP was augmented in all patients with essential hypertension.

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The relationship between myocardial infarct size and serum levels of cardiac myosin light chain II (LC II; 20000 daltons) was studied in 24 dogs with left anterior descending coronary artery occlusion. LC II in the serum was measured by the radioimmunoassay which we have recently developed. In our assay, 0.1-5.0 ng of LC II were effectively measurable. Serum LC II levels rose rapidly and stayed elevated long after coronary occlusion. Infarct size was determined by gross inspection. In 24 dogs, infarct size ranged from 0.3 to 41.7 per cent of left ventricular weight. LC II release was calculated by the formula of Shell and associates. Regression analysis showed good correlation between infarct size and LC II release (r = 0.78). Infarct size also correlated with maximal LC II level (r = 0.77), and LC II level 24 hours after coronary occlusion (r = 0.69). Detection of circulating LC II is a useful method since it can be applied to the diagnosis of acute myocardial infarction at the early as well as late stage and infarct size can be assessed by analysis of serum LC II levels.

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A study was conducted on the effects of perhexiline on myocardial phosphorylase activity, myocardial catecholamine content and heart rate. Phosphorylase a activity and heart rate were investigated as an indicator of sympathetic nerve tone in order to clarify the characteristic of perhexiline with regard to the effects on myocardial metabolism in hyperthyroid rats and catecholamine deficient rats. Myocardial catecholamine and phosphorylase a activity were measured by von Euler's method and Cori's method respectively. Conclusion of this study are summarized as follows: 1) Perhexiline reduces the heart rate, and its effect is not always dependent upon the changes in myocardial norepinephrine content. 2) Perhexiline reduces myocardial phosphorylase a activity. It cannot be always said that the reduction is dependent upon the changes in myocardial norepinephrine. 3) Though slightly different from propranolol and dichloroisoproterenol, perhexiline possesses cardiac effects resembling β-blockers.

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Acute effects of captopril (SQ 14 225) on blood pressure were investigated in pentobarbital anesthetized dogs. Intravenous captopril (0.1 -3 mg/kg) caused reduction of blood pressure dose-independently, while dose-dependent attenuation of exogenous angiotensin I-induced pressor response and potentiation of bradykinin-induced reduction of blood pressure were observed with the same doses of this agent. This acute decrease in blood pressure was partially inhibited by a pretreatment with any one of aprotinin, Sar¹-Ile⁸-angiotensin II and indomethacin. More significant inhibition of the blood pressure decrease was observed after the combined pretreatment with Sar¹-Ile⁸-angiotensin II and indomethacin or that with all the three drugs, though no complete abolition of the blood pressure decrease was achieved. These results suggest that captopril may decrease blood pressure in anesthetized dogs through other mechanism(s) in addition to angiotensin converting enzyme inhibition, including the prostaglandin release probably from the kidney.

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Male SHR of young prehypertensive (5-6 weeks) and mature hypertensive (24-28 weeks) ages and age and sex matched control normotensive Wistar rats (NWR) were studied for aortic smooth muscle contractility in response to rabbit aorta contracting substance (RCS), serotonin, norepinephrine and potassium. Production of prostacyclin (PGI₂) in SHR and NWR aortae of these two age groups was also compared. The contractility of young SHR in response to the agonists was all depressed as compared with the matched NWR. With age advances to 24-28 weeks, aortic responsiveness of NWR to all agonists were reduced and the contractility became the same for SHR and NWR except for the response to RCS which was now greater in SHR than in NWR. The PGI₂-like substance released from young SHR aortae was the same as that from the matched NWR. The PGI₂-like substance in mature aged rat aortae was much higher than that in young rat aortae and the activity in mature SHR was 1.8 times higher than that of the age matched NWR. The increased production of PGI₂ -like substance in aorta walls of the mature aged SHR may be a compensatory mechanism to reduce the elevated blood pressure .

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In order to evaluate the protective effects of L-carnitine on ischemic myocardium, its effects on tissue levels of acyl carnitine, acyl coenzyme A (CoA) and high energy phosphate were studied in ischemic dog hearts. Myocardial ischemia was induced by the ligation of left anterior descending coronary artery for 15 minutes. L-carnitine ( 100 mg/kg) was administered intravenously prior to coronary ligation. In ischemic myocardium, tissue levels of free carnitine decreased from 1043 ± 358 to 623 ± 180 n mol/g (p<0.001). On the other hand, long chain acyl carnitine increased from 214 ± 54 to 498 ± 149 n mol/g (p<0.001) and long chain acyl CoA increased from 15.7 ± 4.8 to 23.2 ± 5.4 n mol/g (p<0.01 ). Pretreatment of L-carnitine increased tissue levels of free carnitine to 863 ± 318 n mol/g (p<0.005) and decreased long chain acyl carnitine and long chain acyl CoA to 368 ±128 n mol/g (p<0.02) and 19.2 ± 6.5 n mol/g (p<0.1) respectively. Tissue levels of adenosine triphosphate (ATP) that was reduced by myocardial ischemia from 5.43± 0.67 to 2.80 ± 0.58 μ mol/g (p<0.001) was increased to 3.28 ± 0.63 μ mol/g (p< 0.02) by L-carnitine. Positive correlation was observed between ATP and free carnitine (p<0.01). On the other hand, negative correlation was observed not only between ATP and the ratio of long chain acyl CoA to free carnitine but also between ATP and the ratio of long chain acyl carnitine to free carnitine (p<0.01 respectively). These results suggest that the accumulation of long chain acyl carnitine may play an important role on cellular damage in ischemic myocardium and that administration of exogenous L-carnitine is beneficial for the protection of ischemic myocardium, probably because it reduces the accumulation of long chain acyl carnitine as well as long chain acyl CoA.

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In a series of studies on experimental coxsackie B-3 virus myocarditis, ultrastructural changes of the myocardium in mice were observed for 18 months. On the 5th day a number of necrotic myocardial cells were connected with apparently intact cells at intercalated discs in multiple myocardial lesions. In the necrotic cells, myofibrils underwent lysis, and mitochondria contained very electron-dense spicular or granular inclusions and moderately electron-dense amorphous ones. X-ray analytical electron microscopy proved that the former type of inclusions contained calcium. Macrophages phagocytosed cell debris and many calcified mitochondria which were aggregated into large masses in the cytoplasm. As the macrophages were disorganized, calcified masses remained naked in the interstitial space and were identificable by light microscopy. On the 9th day a crystalloid structure of virus was identified in degenerated myocardial cells. On the 21st day acute inflammatory reaction was rare in the myocardium. In the 3rd month some myocardial cells degenerated near fibrotic or calcified foci. In the 12th and 18th months calcified foci remained, and interstitial fibrosis was extensive in some animals; some myocardial cells showed various degenerative changes including myofibrillar disorientation and lysis, numerous spherical microparticles adjacent to the sarcolemma, amorphous mitochondrial inclusions, and thickening of the basement membrane. Adjacent to fibrotic or calcified foci, some myocardial cells were hypertrophied or atrophied. The hypertrophied cells occasionally possessed multiple intercalated discs and extensive side-to-side junctions. Except for the calcified foci, most myocardial changes in the late chronic phase resembled those seen in myocardial biopsies obtained from patients with various heart diseases including cardiomyopathies and were assumed to be non specific in nature.

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Following intraperitoneal inoculation with coxsackie B3 virus all weanling Syrian golden hamsters (60 animals) developed severe myocarditis. In the acute phase, light and electron microscopy revealed massive cellular infiltration and myocytolysis in the myocardium which were most prominent on the 5th day and least obvious in 3 weeks. In the necrotic myocytes, mitochondria contained moderately electron dense inclusions different from the calcified granules seen in the myocardium of mice with coxsackie B3 virus myocarditis. Macrophages ingested and digested necrotic cell debris, leaving moderate fibrosis but no calcification in the myocardium. Viruses were isolated from the myocardium on the 3rd to 9th day, and virus particles were seen in a necrotic cardiocyte on the 9th day. In the chronic phase, most animals developed no cardiomegaly; light microscopy revealed minimal myocardial fibrosis; electron microscopy showed various degenerative changes in some cardiocytes. A few animals (two animals) developed significant cardiomegaly with moderate to marked myocardial fibrosis in the 6th and 14th month. In one heart there was marked biventricular dilatation. In these animals with cardiomegaly, ultrastructural changes of the myocardial cells were similar to those described in congestive cardiomyopathy in man. Golden hamsters appear to be a unique model for a study of the possible relationship between viral myocarditis and idiopathic cardiomyopathy in man.

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A special balloon catheter for creation of an adequate interatrial opening by expansile force was devised. This balloon catheter was used on 9 adult dogs and 5 sucking pigs for nonoperative creation or enlargement of an interatrial opening. The balloon catheter was introduced via femoral vein into the left atrium by transseptal left heart catheter technique in adult dogs using special guide wire, and across the existing foramen ovale in the sucking pigs. Then the atrial septum was torn by expansile force of the balloon which was fixed through the atrial septum during expansion by means of the specially transformed balloon figures. Necropsy findings revealed that all animals had interatrial openings larger than fossa ovalis with tearing the floor of fossa ovalis completely and cleaving the limbus fossa ovalis and sinus inferior venosus.

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