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R Takeda

Publications and source records attributed to R Takeda.

At least 343 records · Page 19Linked to original sources
PubMed1986

[Left ventriculography and serial ECG changes in hypertrophic cardiomyopathy with special reference to the negative T wave].

To clarify the correlation between the configuration of the left ventriculogram and serial ECG changes, 16 patients with hypertrophic cardiomyopathy (HCM) associated with asymmetrical septal hypertrophy were examined. In the right oblique view at end-diastole, the configurations were classified by form as round (R, n = 7), round with inferior concavity (R-i, n = 2), spade (S, n = 4) and spade with inferior concavity (S-i, n = 3). These patients were divided into two groups according to serial T wave changes; nine with marked changes (A group) and seven without (B group). Furthermore, group A was separated into two subgroups; seven with increasing negativity or appearance of the negative T wave (A-1 group) and two with decreasing negativity or disappearance of the negative T wave (A-2 group). The results were as follows: Five (71%) of the seven cases with the S and S-i form belonged to the A group. Their apical walls showed marked hypertrophy and their ECGs showed deep negative T waves. The other two cases (29%) belonged to the B group, and did not show marked apical hypertrophy. Four (44%) of the nine cases with the R and R-i form belonged to the A group. They showed mild apical hypertrophy, and initially did not show deep negative T waves. A deep negative T wave appeared in three during observation. The initial depth of the maximum negativity of T wave correlated significantly with apical wall thickness, SV1 + RV5, and the total depth of the negative T wave in precordial leads. During the observation, the A-1 group showed a marked increase of SV1 + RV5. The A-2 group showed a decrease of SV1 + RV5. In conclusion, HCM with deep negative T waves has a tendency to present wide changes in the T wave during serial ECG observation and to show apical hypertrophy on left ventriculography. Cases of increasing negativity of the T wave showed marked increase in voltage of SV1 + RV5. However, cases of decreasing negativity of the T wave showed decreasing SV1 + RV5. These ECG changes, especially the negative T wave changes are reputed to be related to apical wall thickness.

Cardiomyopathy, Hypertrophic↗
PubMed1986

[Two cases of thrombosis of an aneurysm in the acute stage].

Thrombus formation within aneurysm is common and has generally been proved to be a slowly progressive phenomenon. We report two cases of acute completely thrombosis of aneurysms. The initial angiogram failed to reveal aneurysm and other etiology of subarachnoid hemorrhage. CT revealed diffuse cisternal blood and acute hydrocephalus. We decided to operate on these patients in the acute stage because of the generally-known strict correlation between the amount of cisternal high density on CT and the subsequent development of vasospasm and ischemic event. Case 1. A 68 year-old female was admitted on Day 1 with neurological deterioration of Grade 3 (H & K). Complete angiographic study was done, including the basal view and stereotechnique, but failed to reveal aneurysm. On Day 2 we operated on this patient and discovered a thrombosed aneurysm of the anterior communicating artery (3 X 7 mm in size). Case 2. A 51 year-old male suffering from subarachnoid hemorrhage was transferred to our hospital on Day 0. Emergency angiography gave no information, but the pattern of cisternal clots on CT was suggested the existence of an aneurysm of the right internal carotid artery. The next day we performed angiography once more, at that time 2 X 5 mm internal carotid bifurcated aneurysm was revealed. Shortly thereafter we operated and found the intra-aneurysmal clot. Through consideration of these we have reached the following conclusions. When CT findings in a patient with subarachnoid hemorrhage show the diffuse cisternal clots due to rupture of aneurysm, we should consider immediate surgery even if the angiogram is negative in order to lessen the risk of delayed vasospasm.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1985

Dual effects of acetaldehyde on electrical activity in the isolated frog spinal cord.

Acetaldehyde (1.4 X 10(-7)-1.4 X 10(-5) M) produced a transient depolarization followed by a distinct hyperpolarization of the ventral and dorsal roots as recorded by sucrose-gap in the isolated spinal cord. This effect occurred more frequently at lower concentrations than at higher concentrations of acetaldehyde, and the depolarization increased with doses increasing. The ventral root reflex potentials evoked by the dorsal root stimulation had decreased amplitudes during depolarization and increased during hyperpolarization. In the presence of Mg2+ or tetrodotoxin, acetaldehyde produced only hyperpolarization. Acetaldehyde slightly prolonged glutamate-induced depolarization of both roots. These results suggest that acetaldehyde acts not only on the spinal motoneuron resulting in membrane hyperpolarization but also on the presynaptic sites, which causes postsynaptic membrane depolarization probably through an increased release and decreased uptake or inactivation of the excitatory transmitter.

Acetaldehyde↗
PubMed1985

[The effect of ketoconazole and some other inhibitors of steroidogenesis on P-450 11 beta-catalyzed reactions].

Ketoconazole (Nizoral), an orally active antimycotic agent with a broad spectrum, has been reported to interfere with steroidogenesis both in patient and in vivo rat studies. It has also been shown that the same drug inhibits some P-450--catalyzed reactions in adrenal cortex mitochondria. In the present work, we studied the inhibitory effect of Ketoconazole, along with some other known inhibitors of steroidogenesis, on the reconstituted steroid monooxygenase system, which consists of adrenodoxin, its reductase and P-450 11 beta as the protein components being purified from bovine adrenal cortex mitochondria. The results indicated that; Ketoconazole completely inhibited hydroxylation of deoxycorticosterone at the 11 beta-position to form corticosterone and at the 18-position to form 18-hydroxydeoxycorticosterone. The Ki value for Ketoconazole, calculated either from the 11 beta-hydroxylase reaction or the 18-hydroxylase reaction, was 0.56 microM, which was comparable to the value obtained for metyrapone in the same system. Ketoconazole also inhibited 18-hydroxylation of corticosterone to form 18-hydroxycorticosterone, with 50% inhibitory concentration of less than 0.03 microgram/ml. The corresponding value for this inhibitor in the deoxycorticosterone 18-hydroxylase reaction was found to be 0.3 microgram/ml. The contrast between these values for the two substrates is striking. Thus, in a series of reaction steps, the inhibitory effect of corticosterone to 18-hydroxycorticosterone was more potent than deoxycorticosterone to 18-hydroxycorticosterone reaction. Both trilostane and o, p'-DDD over the wide concentration range failed to inhibit any of the reconstituted P-450 11 beta system similar to those applied to the Ketoconazole study.(ABSTRACT TRUNCATED AT 250 WORDS)

18-Hydroxycorticosterone↗
PubMed1985

Left ventricular endomyocardial biopsy findings in patients with essential hypertension and hypertrophic cardiomyopathy with special reference to the incidence of bizarre myocardial hypertrophy with disorganization and biopsy score.

To investigate whether bizarre myocardial hypertrophy with disorganization (BMHD) is characteristic of hypertrophic cardiomyopathy (HCM), the histopathology of the biopsied left ventricular myocardium in 18 patients with essential hypertension (HT) and 14 patients with HCM was studied. A "biopsy score" was devised for a more quantitative evaluation of the BMHD and a comparative study on the biopsy score of the left ventricular biopsied specimen was also performed. The patients with HT were judged to be in stages I or II of the WHO criteria and had a history of hypertension of more than 5 years. The BMHD was defined as myocardial cells showing hypertrophy, disorganization, and bizarre nuclei. "Disorganization" of myocardial cells was distinguished both by the terminology and histopathological characteristics from "disarrangement" of myocardial cells. The biopsy score employed four factors and was determined according to the following formula: Biopsy score = hypertrophy of myocardial cells + (disorganization of myocardial cells) x 2 + bizarre nuclei + whorling of muscle bundles. Both the hypertrophy and the disorganization of myocardial cells were regarded as essential conditions indicating the presence of BMHD. The BMHD was found in 2 of 18 patients with HT (11%) and in 10 of 14 patients with HCM (71%) in the left ventricular biopsied specimens (P less than 0.005). However, "disarrangement" of myocardial cells was found in 13 of 18 HT patients (72%) and in 10 of 14 HCM patients (71%) in the left ventricular biopsied specimens, showing no difference between the two groups. The biopsy score in HCM patients was larger than that found in HT patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Quantitative approach to the histopathology of the biopsied right ventricular myocardium in patients with diabetes mellitus.

For the purpose of studying the clinicopathology of the biopsied myocardium in patients with diabetes mellitus, the diameter of right ventricular myocardial cells and diffuse perimysial fibrosis of biopsied myocardium were measured quantitatively. Seven healthy controls and nine diabetic patients without hypertension or coronary arterial disease were subjected to this study. The degree of diabetic complications was mild to moderate. The diameter of myocardial cells was measured and the degree of diffuse perimysial fibrosis was assessed by the point-counting method using a square grid, in which the distance between the points was 10 micron. Over 2000 points which lay on the longitudinally cut myocardial cells and on the interstitial fibrosis stained by the Mallory-Azan method were measured. Percentage fibrosis was calculated according to the formula: percentage fibrosis = (points lying on the interstitial fibrosis)/[(points lying on the myocardial cell) + (points lying on the interstitial fibrosis)] X 100. The results were as follows. The mean diameter of right ventricular myocardial cells in patients with diabetes mellitus was significantly larger than that of controls (P less than 0.01). The percentage fibrosis of diabetic patients was significantly higher than that of controls (P less than 0.01). There was no significant correlation between the histopathological measurements and clinical features. It is concluded that hypertrophy of myocardial cells and interstitial fibrosis of the myocardium exist even in mild diabetes mellitus.

Adult↗
PubMed1985

Deficiency of serum cholesteryl-ester transfer activity in patients with familial hyperalphalipoproteinaemia.

Lipoprotein patterns and cholesteryl ester transfer activity (CETA) were examined in 2 patients with familial hyperalphalipoproteinaemia (FHALP). The proband was a healthy 58-year-old Japanese male who had an HDL cholesterol of 7.83 mmol/l (301 mg/dl). His sister's HDL cholesterol was 4.52 mmol/l (174 mg/dl), which suggested that both were homozygous carriers of FHALP. In both subjects HDL showed a high cholesterol/apo A-I ratio and appeared to be a larger-sized particle than normal HDL on agarose gel chromatography. Two of the proband's children showed higher HDL cholesterol levels (1.74 mmol/l, 2.16 mmol/l) than normal, but another 2 children showed normal levels (1.48 mmol/l, 1.40 mmol/l). However, the ratios of HDL cholesterol to total cholesterol and to apo A-I in all children were higher than normal. These data suggest, but do not prove, that all his children were heterozygotes. Apo B levels in all of the family members studied were lower than normal (47-80 mg/dl). Deceased members of the same family had not died from cardiovascular disease. Cholesteryl-ester transfer activity was studied in both patients. When serum or lipoprotein deficient serum (d greater than 1.21) and [3H]cholesteryl ester labelled HDL3 were incubated in the presence of an LCAT inhibitor, there was no evidence of cholesteryl ester transfer from HDL to VLDL and/or LDL, unlike normal subjects. The deficiency of CETA in these patients with FHALP presumably accounted for the increase in particle size and cholesterol enrichment of HDL.

Adult↗
PubMed1985

Normalization of low-density lipoprotein levels and disappearance of xanthomas during pregnancy in a woman with heterozygous familial hypercholesterolemia.

Serum lipids and lipoproteins were studied prior to conception, during pregnancy, and after delivery in a woman heterozygous for familial hypercholesterolemia. Prior to conception, serum and low-density lipoprotein (LDL) cholesterol levels were 613 and 528 mg/dL, respectively. At 37-week gestation, serum and LDL cholesterols decreased to the normal levels, 226 and 90 mg/dL, respectively. At two-week postpartum serum and LDL cholesterols returned to the preconception levels, 547 and 427 mg/dL, respectively. At delivery her cutaneous xanthomas almost disappeared. The patient was challenged by ethinyl estradiol of 120 micrograms/d for two months, as a result serum cholesterol decreased from 565 to 385 mg/dL, and LDL cholesterol fell from 460 to 208 mg/dL. During her second pregnancy, serum and LDL cholesterol decreased again significantly. Thus, this case, which showed dramatic reductions of serum and LDL cholesterol levels, may be considered a new variant of heterozygous familial hypercholesterolemia, and the reductions were probably brought about by the action of estrogens, which are known to increase LDL degradation through LDL receptors.

Adult↗
PubMed1985

Single-blind study of epoprostenol and 6-keto-prostaglandin E1 in man: effects of platelet aggregation and plasma renin.

The effects of epoprostenol (PGI2, 2-8 ng kg-1 min-1) and 6-keto-prostaglandin E1 (6-keto-PGE1, 7.5-30 ng kg-1 min-1) on ADP-induced platelet aggregation, blood pressure (BP), heart rate and plasma renin activity (PRA) were studied in six healthy male volunteers. During graded intravenous administration of PGI2, platelet aggregation was inhibited at a minimum dose of 4 ng kg-1 min-1. The dose required to produce the same degree of platelet inhibition was approximately 15 ng kg-1 min-1 for 6-keto-PGE1. Diastolic BP was significantly reduced and PRA was increased by PGI2 at a dose greater than 8 ng kg-1 min-1. In contrast, 6-keto-PGE1 did not produce BP and PRA changes up to a dose of 30 ng kg-1 min-1. These data indicate that PGI2 has approximately four times more potent antiplatelet activity than 6-keto-PGE1 on a molar basis in man. The cardiovascular and PRA changes were less prominent for 6-keto-PGE1 than PGI2.

Adenosine Diphosphate↗
PubMed1985

Impaired metabolism of guanidinoacetic acid in uremia.

In order to investigate the guanidinoacetic acid (GAA) metabolism in uremia, we have measured serum guanidino compounds in patients with chronic renal failure (CRF) in comparison with normal subjects, and the renal content of GAA and glycine amidinotransferase (GAT) activity in the kidney of experimental CRF rabbits. Serum concentrations of guanidinosuccinic acid (GSA) and methylguanidine (MG) in the patients with CRF were higher than those in the normal subjects, as well as serum urea nitrogen (BUN) and creatinine (Cr) levels. The serum GAA levels were however, significantly lower and showed a tendency to decrease inversely with the elevation of BUN in the patients with CRF under conservative therapy. On the contrary, in the patients under maintenance hemodialysis (MHD) therapy, the serum GAA level did not decrease in spite of the elevation of BUN. Four anephric patients under MHD therapy showed a level of serum GAA similar to the other MHD patients. In the CRF rabbits, the renal GAA content was significantly lower than in the sham-operated rabbits and showed an inverse correlation with BUN. Renal GAT activity was also significantly lower in the CRF rabbits, showing a positive correlation with serum GAA concentration and an inverse correlation with BUN. These results indicate that renal GAT activity decreases as the BUN level rises in the course of renal damage, resulting in lower concentration of serum GAA in the uremic state; in a more advanced stage of renal failure, the inability of the kidney to synthesize GAA may be compensated by other organ(s). Some dialyzable substances which might inhibit renal GAT activity may also be present.

Adult↗