Intramural coronary angiitis of periarteritis nodosa proved by endomyocardial biopsy.
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Biomedical subjects
Publications and source records attributed to R Takeda.
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In order to elucidate whether pituitary peptides other than ACTH which are derived from the proopiomelanocortin (POMC) are involved for aldosterone secretion in primary aldosteronism, we administered ovine corticotropin releasing factor (CRF), beta-endorphin and naloxone to seven patients with aldosterone producing adenoma. One hundred micrograms of CRF produced an augmented aldosterone response in patients with aldosteronism, while 500 micrograms of beta-endorphin infusion failed to cause any significant changes in neither normal subjects nor patients. An opioid antagonist, naloxone (10 mg, iv) produced no noticeable change in plasma aldosterone in normal subjects, while it caused a slight increase in patients with primary aldosteronism. Plasma cortisol increased to a similar degree in response to CRF and naloxone in normal subjects and patients. In three patients with isolated ACTH deficiency, neither aldosterone nor cortisol responded to these stimuli. The present results indicate that POMC-derived pituitary peptides other than ACTH are unlikely to participate in the aldosterone secretion in normal subjects or in patients with primary aldosteronism.
In order to investigate the influence of delivery mode on biological inactive renin levels in fetal circulation, plasma inactive renin (PIR), plasma renin activity (PRA) and plasma total renin (PTR) were measured in umbilical venous blood samples of 21 infants delivered vaginally after spontaneous labor and of 9 infants delivered by elective cesarean section after the onset of labor. Biological renin activities were measured by bioassay. The PIR levels in infants delivered vaginally were significantly lower than those in infants delivered by cesarean section, while the PRA levels were the opposite. However, the PTR levels were not significantly different between the two groups. These results suggest that the plasma levels of biological inactive renin in infants delivered vaginally may decrease, probably due to its conversion to active renin in the second stage of labor.
Gene mutations at the low density lipoprotein (LDL) receptor locus were screened in 210 alleles of Japanese patients with familial hypercholesterolaemia (FH). In the present study, two types of novel mutation were identified by genomic Southern blotting using human LDL receptor cDNA probes. An approximately 12 kb deletion including exons 2 and 3 (and possibly 4) was identified in a patient (M.I.). The patient with this mutant gene will be referred to as 'FH-Kanazawa'. Two patients born in Okayama Prefecture in Japan had another unique 13 kb partial deletion, from exons 7 to 14, in their LDL receptor genes (FH-Okayama). This mutant allele is the first reported case in which the central portion of the LDL receptor gene, the epidermal growth factor (EGF) precursor homology region, is eliminated.
1. The effects of porcine endothelin-1 (10(-12)-5 x 10(-10) mol/kg) on arterial blood pressure (BP) and the renal, mesenteric and carotid blood flow (BF), and the effects of endothelin-1 antibody were studied in rabbits. 2. Endothelin-1 caused a sustained increase in BP. The renal, mesenteric and carotid BF were decreased dose-dependently by endothelin-1. The approximate half-maximal effective values (ED50) were 5.5 x 10(-11), 8.6 x 10(-11) and 2.0 x 10(-10) mol/kg for renal, mesenteric and carotid BF respectively. Compared with carotid BF, the renal and mesenteric BF responses were significantly more sensitive to endothelin-1. 3. Combined administration of endothelin-1 and its antibody showed a significant inhibition of the BP and renal BF responses. However, endothelin-1 antibody alone did not change either BP, renal BF, mesenteric BF or carotid BF in vivo. 4. The present results demonstrate that endothelin is a potent vasoconstrictor in vivo. However, circulating endothelin may not contribute to the control of BF and BP. The role of endothelin as a local modulator of the vascular tone remains to be investigated.
The effects of ethanol on two types of bulbar expiratory neurones, post-inspiratory (early expiratory) and expiratory (late expiratory) neurones, were studied in decerebrated, paralyzed and artificially ventilated cats. Intravenous injection of ethanol (300 mg/kg) depressed the efferent activity in the phrenic and recurrent laryngeal nerves which displayed the augmenting discharge during inspiration and the decrementing discharge during the early stage of expiration (stage I expiration). It reduced the duration of expiration, with a preferential effect on stage I expiration. Out of 22 medullary respiratory neurones consisting of 14 post-inspiratory and 8 expiratory neurones, 12 neurones were depolarized by ethanol and 10 neurones were hyperpolarized. In both cases, the respiratory fluctuations of membrane potential diminished and synaptic noises decreased. Input resistances of these neurones remained unchanged. Ethanol depressed the spike activity during stage I expiration of the post-inspiratory neurones. In expiratory neurones, a suppression of firing was greater in stage I expiration than in later stages of expiration. The present results demonstrate that ethanol reduces the expiratory period mainly through the depression of the post-inspiratory neuronal activity in the bulbar respiratory control mechanism.
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1. Bulbar respiratory neurons of unanesthetized, decerebrate cats were impaled with the center pipette of a compound, coaxial microelectrode. This electrode allowed intracellular recording of membrane potential (MP) through the central pipette and extracellular iontophoresis of glycine or gamma-aminobutyric acid (GABA) from micropipettes encircling the center pipette with their tips recessed 20-40 microns from the tip of the center pipette. 2. Seventy-seven studies were carried out on 32 inspiratory and 28 postinspiratory neurons with the use of brief pulses (0.3-0.5 s) or long pulses (3-10 s) spanning one or more respiratory cycles. In both neuronal types, GABA and glycine decreased spike frequency, synaptic "noise," respiratory fluctuations of MP, and "input" resistance in a dose-related fashion. 3. In most cases, the membrane was hyperpolarized by the amino acid. The reverse response (depolarization) was observed when the membrane had been hyperpolarized by current clamp. This reversal from hyperpolarization to depolarization occurred at a MP of -81 +/- 2.3 mV (mean +/- SE, n = 7) for glycine and -81 +/- 1.6 (n = 6) for GABA. 4. After intracellular iontophoresis of chloride ions, application of GABA and glycine depolarized the membrane. 5. During relatively long (3-10 s) periods of iontophoresis of glycine or GABA, the effects on MP and input resistance waned. In some cases (23%), the amino acid depolarized the membrane at the most hyperpolarizated portion of the MP trajectory. This was never observed with brief iontophoretic pulses. Such effects of long duration iontophoresis may reflect changes in membrane properties secondary to the primary action of the amino acid on the membrane of the impaled neuron or indirect synaptic actions via changes in discharge of neighboring neurons. 6. Extracellular iontophoresis of a GABA uptake inhibitor, nipecotic acid, potentiated the effects of GABA. 7. Extracellular application of tetrodotoxin appeared to act pre- and postsynaptically to reduce respiratory fluctuations in membrane potential and to increase input resistance without altering the effects of iontophoresed glycine and GABA, suggesting that the amino acids act on postsynaptic membrane receptors not linked to fast sodium channels.(ABSTRACT TRUNCATED AT 400 WORDS)
Advances in echocardiography have made possible simple, noninvasive evaluation of the heart. We report the echocardiographic findings in a case of intrapericardial bronchogenic cyst. The patient, a 36-year-old woman, was hospitalized because of pericarditis. Echocardiography revealed a large unilocular cystic structure extending from behind the left atrium to the base of the left ventricle. Although the lesion was diagnosed as an intrapericardial bronchogenic cyst histopathologically, echocardiography was also of use in arriving at the correct diagnosis.
Since several aldosterone metabolites are known to be active, we have assessed the mineralocorticoid biological and renal receptor binding activities of the aldosterone metabolites, 21-deoxyaldosterone (21-deoxy-Aldo), 21-deoxytetrahydroaldosterone (21-deoxy-THAldo), and 3 alpha, 5 beta-tetrahydroaldosterone (THAldo). We synthesized these steroids by bioreduction of aldosterone with intestinal bacteria. Mineralocorticoid agonist activity of 21-deoxy-Aldo, 21-deoxy-THAldo and THAldo, determined by bioassay using adrenalectomized rats, was 1-5%, less than 0.01%, and 0.1-0.5% that of aldosterone, respectively. 21-Deoxy-Aldo showed no antagonist activity. The relative affinity in competing with [3H]aldosterone for binding to mineralocorticoid receptors in adrenalectomized rat kidney cytosols was 94%, less than 0.01%, and less than 0.01% that of aldosterone. The relative binding affinity for rat renal glucocorticoid receptors was 23%, less than 0.01%, and less than 0.01% that of dexamethasone, and for corticosteroid-binding globulin 17%, less than 0.01%, and less than 0.01% that of cortisol. These results show that the naturally occurring steroid, 21-deoxy-Aldo, possesses mineralocorticoid agonist activity which is equivalent to that of 11-deoxycorticosterone, and has substantial affinity for rat renal mineralocorticoid and glucocorticoid receptors. The results also implicate the pathophysiological role of 21-deoxy-Aldo as a potential mineralocorticoid in 21-hydroxylase deficiency, where urinary excretion of this steroid is invariably elevated.
In polyadenylate directed polylysine synthesis, homologously cell-free extracts containing ribosomes and S-100 (105,000 x g supernatant) from staphylococcal cells have less than one-half (one-tenth, when the extracts were stored at -80 degrees C within a few weeks) of the activity of the extracts from Escherichia coli Q13. The present study is concerned with further improving the activity of staphylococcal ribosomes. The polylysine-synthesizing ability by staphylococcal ribosomes increased up to about two times as much as that by E. coli Q13 ribosomes, when S-100 from E. coli Q13 was mixed with staphylococcal ribosomes which had been washed with a high salt HEPES buffer containing 10 mM HEPES, 1 mM EGTA, 16 mM magnesium acetate, 1.0 M ammonium chloride and 0.1 mM dithiothreitol (pH7.6). Polylysine synthesis by the heterologous extracts has an advantage over polyuridylate-directed polyphenylalanine synthesis in the analysis of ribosome sensitivity for macrolide antibiotics, especially erythromycin.
Angiotensin II (ANG II) generation in the mesenteric arteries was studied in four groups of rats: deoxycorticosterone (DOCA)/salt treated, glucocorticoid treated, nephrectomized and control rats. Basal plasma renin activity (PRA) was undetectable in the nephrectomized group and suppressed in the DOCA/salt treated rats, but was increased in the rats treated with glucocorticoid. The Basal plasma ANG II concentration changed comparably with PRA in all four groups of rats. In the control rats, ANG II was released from the mesenteric arteries at a rate of 43.0 +/- 12.0 pg/h, and it was not decreased by nephrectomy. In DOCA/salt rats and glucocorticoid rats, ANG II release significantly decreased to 12.8 +/- 7.1 and 6.9 +/- 1.5 pg/h, respectively. Captopril treatment significantly reduced ANG II release from the mesenteric arteries in both controls and nephrectomized rats, but did not influence ANG II output in DOCA/salt rats or in glucocorticoid treated rats. In nephrectomized rats, captopril lowered blood pressure in association with a significant reduction in the mesenteric ANG II formation. These results indicate that the renal and vascular renin-angiotensin system (RAS) may be independently regulated, and in nephrectomized animals the vascular RAS contributes in part to the maintenance of blood pressure. The present results also suggest that volume expansion per se and/or pharmacological intervention by DOCA and glucocorticoid could modulate vascular ANG II generation.
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The relation of left ventricular diastolic function and the histopathological findings of the myocardium in patients with diabetes mellitus were observed using echocardiography and endomyocardial biopsy. The subjects consisted of six diabetic patients (mean age 49.3 years) and eight normal control subjects (mean age 44.8 years). Coronary angiography had no significant stenotic lesions in their coronary arteries. Their diabetic complications were mild to moderate in severity. Echoes from the left ventricular margin of the septum and from the posterior left ventricular wall were traced on a digitizing board; then the isovolumic relaxation period, rapid filling period, slow filling period and atrial contraction period were determined to calculate fractional shortening (FS), isovolumic relaxation time (IRT), and three filling volumes (RFV, SFV and ACV). The quotients of the left ventricular filling volume and stroke volume were also determined. Right ventricular endomyocardial biopsies were performed to determine the diameters of myocytes, the percentage of fibrosis and the eccentricity e, as a parameter of the degree of myocardial dysarrangement. The results were as follows: IRT was significantly longer and RFV/SV was significantly greater in patients with diabetes mellitus than those among the controls. Also the diameters of myocytes and the percentage of fibrosis were significantly greater, while the eccentricity e was less compared to that of the controls. There were no significant correlations, among IRT, RFV/SV, the diameters of myocytes, and eccentricity e, but the percentage of fibrosis significantly correlated with IRT and RFV/SV (r = 0.62, r = -0.63). IRT and RFV/SV were mainly responsible for the percentage of fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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In this study, we investigated correlations of left ventricular hypertrophy and its histopathology with diastolic dysfunction in patients with hypertrophic cardiomyopathy. Nine control subjects and 14 hypertrophic cardiomyopathy (HCM) patients with asymmetrical septal hypertrophy were evaluated. M-mode echocardiography was used to assess fractional shortening (FS), isovolumic relaxation time (IRT), and the left ventricular filling volume index during rapid and slow filling periods and atrial contraction period (RFVI, SFVI and ACVI). End-diastolic thickness of the interventricular septum and posterior wall was determined using biventriculography. Right ventricular endomyocardial biopsies were performed to calculate the diameters of myocytes, the percentage of fibrosis and the eccentricity e which indicates the degree of myocardial disarrangement including disorganization. The FS was normal in the two groups. The IRT of the HCM group was significantly greater and the RFVI significantly less than those of the controls. The left ventricular wall thickness, the diameters of myocytes and the percentage of fibrosis in the HCM group were significantly greater; and the eccentricity e was significantly less, suggesting that myocardial disarrangement was significantly more severe than that in the controls. Significant positive correlations were observed between the IRT and the wall thickness (r = 0.647), between the diameter of myocytes (r = 0.681) and the percentage of fibrosis (r = 0.628), and there was a significantly negative correlation between the IRT and the eccentricity e (r = -0.759). There was a significantly negative correlation between the RFVI and the wall thickness (r = -0.663); and a significantly positive correlation between the RFVI and the eccentricity e (r = 0.579). Multiple regression analyses showed that the diameter of myocytes, the percentage of fibrosis and the eccentricity e all correlated significantly with the IRT (R = 0.821) and the RFVI (R =0.604). The standard regression coefficients of the diameter of myocytes, the percentage of fibrosis and the eccentricity e were 0.253, 0.278 and -0.431 in respect to IRT, and those of the percentage of fibrosis and the eccentricity e were -0.204 and 0.469 in respect to RFVI, respectively. These results indicated that diastolic dysfunction in hypertrophic cardiomyopathy is related not only to the degree of left ventricular hypertrophy, but also to the degree of myocardial hypertrophy, increased interstitial fibrosis, and especially to myocardial disarrangement including disorganization.
The present study was performed to clinically clarify the pathogenesis of hypertensive cardiac hypertrophy (HT) and hypertrophic cardiomyopathy (HCM). Exercise thallium-201 (Tl-201) myocardial scintigraphy using a bicycle ergometer was performed for controls, HT and HCM. The scintigrams were evaluated by the circumferential profile analysis. Furthermore, the changes in Tl-201 dynamics in exercise Tl-201 scintigraphy with verapamil injections were examined in these three groups. Analysis of exercise Tl-201 scintigraphy without verapamil injections showed that the initial uptake did not differ among the three groups, but the washout rate three hours after the Tl-201 injections (WR3) did differ among the three groups. Although the WR3 of HT did not differ from that of the controls, the WR3 of HCM was lower than that of the controls. The WR3 with and without verapamil were compared. Although the WR with verapamil injections equalled that without verapamil injections in the controls and HT, the WR3 with verapamil injections decreased more than did that without verapamil injections in HCM. As an index of great and rapid changes in circulation, the washout rate one hour after the Tl-201 injection (WR1) was calculated. The WR1 without verapamil did not differ among the three groups and did not differ from that with verapamil injections in each group. These results suggest that Tl-201 dynamics of HT differ from those of HCM and lowering of the WR3 in HCM may not be caused by disturbance in the microcirculation, but rather by disturbance of Tl-clearance through the cell membrane and its cytoplasm.
We report a case of 33 years old woman who developed hemolytic anemia after blood transfusion. In this case no abnormalities were observed by the cross-match test performed before blood transfusion. She was undergone the surgical resection of liposarcoma of her right arm in June, 1984 and 8 units of the concentrated red blood cells were transfused during the operation. During the following 2 months 13 units of the concentrated red blood cells were transfused. Immediately after blood transfusion, she developed icterus and oliguria and was diagnosed acute renal failure associated with hemolytic anemia. At this time we examined the antigen type of her red blood cells and of three donors' red blood cells which had been given to her. As the result, either C (Rh-hr), Pi (P), Lea (Lewis), Fyb (Duffy) antigens were found in some of donors' RBC, but no such antigens were detected in her RBC. The half life span of RBC measured using 51Cr labeled RBC was 6.2-14.5 hours, in respect of the antigen-positive RBC, where as it was 49.4 hours in the RBC without the antigens. It is more likely that the blood transfusion was the cause of hemolytic episode in this case, because the half life span of the donors' RBC was extremely shortened, compared with that of her own blood which was 16 days.