Physical works and cardiovascular disease--effect of exercise on the heart and current state of exercise therapy in Japan.
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Biomedical subjects
Publications and source records attributed to M Murayama.
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A method is described for the determination of trace selenium (impurities in medicinal organic compounds) by ion chromatography (IC) after oxygen flask combustion. All selenium compounds formed by oxygen flask combustion are converted to selenate ion by heating with nitric acid and potassium permanganate. The selenate ion is then determined by IC, using a simple recycle system to eliminate interfering ions. The detection limit of selenium is 0.4 nmol in 50 mg of sample. The recoveries of selenium added to seven drugs are ca. 95-103% with relative standard deviations of 1-6%.
The incidence and forms of ventricular premature complexes (VPCs) in apparently healthy subjects were studied to determine long-term reproducibility of day to day variation on Holter electrocardiogram. The study included 152 men and 68 women ranging in age from 20 to 78 years who were having routine check-ups that revealed no cardiovascular abnormalities. In addition to routine measurements, Holter electrocardiography was recorded during daily life, and the total number of VPCs occurring during 24 hours was visually calculated on replayed electrocardiographic tracings. Forms of VPCs and incidence of VPCs in 10-year age groups of the subjects were also recorded. No VPCs were observed in 56% of the subjects; 93% showed less than 50 VPCs and the other 7% of the 220 subjects had greater than or equal to 50 VPCs. Forty-one of the 220 subjects returned for routine follow-up 1 year later. Repeated Holter electrocardiograms at this time showed high reproducibility of less than 50 VPCs. A small number of multiform VPCs were reproducible but paired VPCs were not. Physiologic definition of VPCs in healthy subjects appears to be clinically significant.
Using 4-methylumbelliferyl-N-acetylneuraminic acid (4MU-NeuAc) as substrate, we measured sialidase activity in the salivary glands and other organs of the rat. The pH optima of salivary gland sialidase were between 4.0 and 4.5, which were similar to those of the enzyme in the brain, liver and kidney. Among the salivary glands, the submandibular one showed the highest sialidase activity followed by the parotid and the sublingual glands. However, sialidase activity in these glands was lower when compared with the activity in the brain, liver and kidney. From the subcellular distribution study, salivary gland sialidase was found to be mainly localized in the lysosomes. The pH optima of the lysosomal sialidase of the salivary glands were between 4.0 and 4.5; and Km values for 4MU-NeuAc approximately 0.09 mmol/l. In the submandibular and parotid glands, a soluble sialidase with a different pH optimum (5.5) and Km value (0.25 mmol/l) was also detected.
It has been proposed that a major target organelles damaged by the ischemic process, probably by the oxygen free radicals generated, is the portion of the excitation-contraction coupling system that regulates Ca2+ delivery (the sarcoplasmic reticulum and sarcolemma) to the contractile proteins. We tested this hypothesis by studying the effect of in vitro generation of oxygen free radicals from xanthine-xanthine oxidase system or dihydroxyfumarate (DHF)/Fe3+-ADP system on Ca2+ flux behavior of canine cardiac sarcoplasmic reticulum (SR); sarcolemmal (Na+, K+)-ATPase and Na+-Ca2+ exchange activities; and myofibrillar (Ca2+, Mg2+)-ATPase activity. Generation of oxygen free radicals by xanthine oxidase acting on xanthine as a substrate increased the passive Ca2+ efflux and decreased intravesicular Ca2+ with no effect on active Ca2+ influx (Ca2+-ATPase) of SR vesicles. Similar exposure of sarcolemmal vesicles to xanthine plus xanthine oxidase stimulated Na+-Ca2+ exchange activity. When sarcolemmal vesicles were incubated with DHF plus Fe3+-ADP, (Na+, K+)-ATPase activity was decreased. It is postulated that the SR Ca2+ efflux pathways but not catalytic activity of the Ca2+ pump and sarcolemmal (Na+, K+)-ATPase involving Na+-Ca2+ exchange activity are altered by oxygen free radicals, and such changes may partly account for the occurrence of intracellular Ca2+ overload during the course of myocardial ischemia. Interestingly, oxygen free radicals from xanthine-xanthine oxidase system had no effect on myofibrillar pCa-ATPase curve. From this set of observations we would hypothesize that the SR and sarcolemma may be the principal target organelles of oxygen free radicals attack in the ischemic injury and not the contractile proteins per se.
Prevalence of silent myocardial ischemia in exercise test was retrospectively reviewed from 749 tests performed for 513 patients with definite evidence of ischemic heart disease. The clinical significance was studied and absence of transient ischemia, occurrence of transient ischemia with and without pain were observed in 48%, 30% and 22% of the tests, respectively. Anginal pain was frequently observed in exercise tests for patients with severe coronary artery disease and low exercise tolerance. A large number of tests showing ischemic response were discontinued due to symptoms other than anginal pain and hence silent myocardial ischemia could be thought to be a result of ischemic state which does not reach the angina threshold. Silent myocardial ischemia was frequently observed during usual daily life. However, a definite correlation between severity of transient ischemia and presence or absence of chest pain in the same individuals was not obtained from the study. A day to day variation in the angina threshold might be responsible. In general, silent myocardial ischemia was not rare. However, the consistent condition was very unusual. In angina of effort (EA) and old myocardial infarction (OMI), 3.7% and 12.3% were silent, respectively. A higher incidence was obtained in OMI than in EA. This is important for the management of these patients. The mechanism of silent myocardial ischemia and the cause of the different incidence of this state between EA and OMI were not defined and remained to be further studied.
A case of arteriovenous fistula between the internal mammary artery and the pulmonary artery was presented. In a recent review of the literature only 19 cases of this abnormality were described. In most instances, patients had continuous precordial murmur that might be confused with a patent ductus arteriosus. Definitive diagnosis was enabled by selective angiography.
The analgesic effect and the acute toxicity of a medical drug "kako-bushi-matsu" (S-01), which was produced through several processing of raw aconite roots, were examined in comparison with those of ibuprofen, indomethacin and aspirin. S-01 (p.o.) inhibited the acetic acid- and phenylquinone-induced writhing dose-dependently. From the ED50 values, indomethacin showed more potent inhibitory action on the phenylquinone-induced writhing than on the acetic acid-induced writhing. Ibuprofen and aspirin showed the same tendency as indomethacin. The potency of the writhing inhibition by S-01 was almost to the same degree in both writhing methods. In the tail pressure method, S-01 raised the pain threshold ratio to almost the same degree as ibuprofen did. In Randall-Selitto's method, the analgesic effect of S-01 on inflamed foot was less than that of ibuprofen. In the normal foot, S-01 raised the pain threshold ratio dose-dependently, but ibuprofen did not influence the pain threshold ratio. On adjuvant-induced arthritic pain, S-01 and ibuprofen had an analgesic action, and this action of S-01 was less than that of ibuprofen. The oral LD50 value of S-01 was more than 10,000 mg/kg in mice and rats of both sexes. The above evidence indicates that S-01 has analgesic action and suggests that the mode of the analgesic action of S-01 may differ from those of ibuprofen, indomethacin and aspirin, which inhibit prostaglandin biosynthesis.
To elucidate the clinical significance of the exercise-induced negative U-wave (NU) in patients with anterior myocardial infarction, we compared the angiographic and scintigraphic findings in 15 patients with and 20 patients without NU, and obtained the following results: 1) On coronary angiography, all patients in the NU (+) group showed over 90% stenosis or total occlusion of the left anterior descending coronary artery (LAD). In the latter cases moderate to abundant collaterals were visualized on the anterior wall. In contrast, such a tendency was not observed in the NU (-) group. 2) Segments composed of viable myocardium (estimated by preservation of contraction at rest and T1-201 redistribution after exercise) numbered 30 of 45 segments (67%) in the NU (+) group, and 13 of 60 segments (22%) in the NU (-) group. Segments composed of lost myocardium (estimated by loss of contraction at rest and persistent defect in T1-201 uptake) numbered 7 of 45 segments (16%) in the NU (+) group, and 38 of 60 segments (63%) in the NU (-) group. 3) Exercise-induced NU was frequently observed on R-wave preserved leads with ST depression, but was also observed over abnormal Q waves, ST elevation and in isolation in some instances. 4) In 3 patients, preexisting exercise-induced NU was no longer observed and a transient stress-induced T1-201 defect disappeared after successful LAD revascularization. In conclusion, exercise-induced NU on precordial leads in patients with anterior myocardial infarction may be a sign suggesting the presence of jeopardized, but still salvageable, myocardium in the infarcted area.
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In this study, we elucidated some characteristics of soluble sialidases in the rat salivary glands, brain, liver and kidney. 1) Soluble sialidases in the submandibular and parotid glands were inactivated by about 75 and 60%, respectively, and the enzymes in the brain, liver and kidney were also inactivated by 16-48%, when preincubated at 40 degrees C for 1h. When preincubated at 60 degrees C, the enzymes in all tissues were completely inactivated within 10 min. 2) Ca2+ ion in low concentrations tended to activate soluble sialidases in both the submandibular and parotid glands, but had no apparent effect on the enzymes in the brain, liver and kidney. The enzyme in the submandibular gland tended to be activated also by low concentrations of Mg2+. Both Cu2+ and Hg2+ ions caused a marked inhibition on the soluble sialidases in all tissues. 3) The molecular weight of soluble sialidases in the submandibular and parotid glands was determined to be about 68,000 and 46,000, respectively, by means of Sephadex G-200 gel filtration. The molecular weight of the enzymes in the brain and liver was almost similar to that of the enzyme in the parotid gland. In the kidney, soluble sialidase was separated into two enzymes, one having high (more than 500,000) and the other having low (about 46,000) molecular weight. 4) By isoelectric focusing analysis, three isozymes were detected in the submandibular gland and brain sialidases and two isozymes detected in the enzymes of other tissues. The isoelectric point of the major isozymes in the submandibular and parotid glands was 6.4 and 6.9 respectively. In the brain, liver and kidney sialidases, the isozymes with isoelectric point in the range of 4.4 to 6.7 were detected.
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In this study, the role of psychological make-up was assessed as a risk factor in the etiology of vasospasm in variant angina (VA) using the Cornell Medical Index (CMI). Study subjects consisted of 15 patients with VA; 32 with effort angina or old myocardial infarction having no vasospasm (EA + OMI); and 34 healthy men. For a neurosis discriminative diagram, the areas I and II were judged as normal and the areas III and IV were judged compatible with a neurotic disorder. Correlation of serum lipid levels with psychological factors was attempted. 1. Among the VA patients, 46.7% belonged to the areas III and IV, as compared to 18% of the patients with EA + OMI, and 2.6% of the healthy subjects. 2. Seventy-three percent of the VA group showed anxiety states indicating a correlation with a psychological disorder. 3. A majority of the VA patients had a variety of psychological symptoms unrelated to myocardial ischemia. 4. Total cholesterol, triglycerides, LDL cholesterol, serum uric acid and the atherogenic index were all lower in the VA group than in the EA + OMI group. 5. In the EA + OMI group, triglycerides, serum uric acid and the atherogenic index were higher in the psychological group than in the non-psychological group. However, total cholesterol, LDL cholesterol and HDL cholesterol were lower in the former than in the latter group. It was concluded that an anxiety state constitutes a contributing background for developing VA and it was speculated that such an anxiety state may lead to an exaggerated secretion of stress hormones, resulting in vasospasm of the coronary arteries.
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A review of five cases of surgically proven bronchogenic cysts was undertaken. One case was mediastinal bronchogenic cyst and other four cases were pulmonary bronchogenic cysts. Pulmonary bronchogenic cysts varied in roentgenologic features. They presented as cyst with air-fluid level, air-filled cyst, sharply delineated spherical, oval or lobulated mass shadow. Pulmonary bronchogenic cysts with homogeneous water-density shadow were not necessarily easy to be differentiated from malignant pulmonary neoplasm.
We report here that the rate of fibrin polymerization is accelerated by decompression: the rate is essentially doubled by reducing the pressure by one-half (380 torr, 14.7 PSI or 1/2 ATM) and increased by 3.6 times with respect to the control at 25 torr (0.48 PSI or 1/30th ATM). We also report here that the rate of fibrin polymerization is decelerated by compression; at 5.2 X 10(5) torr (10,000 PSI or 680 ATM) polymerization is inhibited and/or reversed.
The influence of age on 125I-epidermal growth factor (EGF) binding to rat brain plasma membranes was investigated. The specific binding of EGF to membranes decreased gradually with age in both male and female rats. There was no significant difference in the specific binding between males and females. Scatchard analysis of the binding data showed that the decrease in EGF binding with age was due to a decrease in the number of EGF receptors.
Rates of human red blood cell hemolysis were measured as a function of temperature. Three distinct temperature intervals for hemolysis were noted: a) At temperatures equal to or less than 37 degrees C no hemolysis was observed for the duration of the incubation (30 hr). b) For temperatures exceeding 45 degrees C hemolysis rates are rapid and are accompanied by gross changes in cellular morphology. The activation energy for hemolysis is 80 kcal/mole; this value is characteristic of protein denaturation and enzyme inactivation suggesting that these processes contribute to hemolysis at these high temperatures. c) Between 38 and 45 degrees C the energy of activation is 29 kcal/mole, indicating that a fundamentally different process than protein inactivation is responsible for hemolysis at these relatively low temperatures. A mechanism based on the concept of the critical bilayer assembly temperature of cell membranes (N.L. Gershfeld, Biophys. J. 50:457-461, 1986) accounts for hemolysis at these relatively mild temperatures: The unilamellar state of the membrane is stable at 37 degrees C, but is transformed to a multibilayer when the temperature is raised; hemolysis results because formation of the multibilayer requires exposing lipid-free areas of the erythrocyte surface. An analysis of the activation energy for hemolysis is presented that is consistent with the proposed unilamellar-multibilayer transformation.