[Coexistence of dual AV nodal pathways in patients with anomalous bypass tracts].
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Biomedical subjects
Publications and source records attributed to S Takata.
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For the treatment of familial hypercholesterolemia, Liposorber LA-40 was clinically applied. The Liposorber is a commercially developed affinity adsorbent for plasma perfusion which selectivity adsorbs low density lipoproteins and very low density lipoproteins and is specially designed for plasmapheretic treatment of hypercholesterolemia. The Liposorber column, containing activated cellulose beads having an affinity for lipoprotein containing apolipoprotein-B, has an excellent adsorption capacity, excellent selectivity, minimum albumin loss. This new apheresis system was applied to 2 clinical cases. After seven months of trial perfusion every 2 weeks, patient condition was good, with a level of total cholesterol under 300 mg/dl. No replacement fluids were given during or after treatment. In this paper, clinical results of these patients were shown and the mechanism of adsorption of this specific adsorbent was discussed.
Binding, internalization, and degradation of 125I-labeled-rat atrial natriuretic peptide (rANP) were studied in cultured rat aortic vascular smooth muscle cells (VSMC). At 37 degrees C, 125I-labeled-rANP rapidly bound to VSMCs, but the cell-bound radioactivity rapidly decreased upon subsequent incubation, while the binding was slow at 4 degrees C, reaching to an apparent equilibrium after 6 hrs. The cell-bound 125I-labeled-rANP at 37 degrees C is rapidly dissociated from VSMC (t 1/2: approximately 40 min) with the appearance of degradaded product(s) of radioligand in the medium, whereas the degradation was minimal at 4 degrees C. This degradative process was blocked by inhibitors of metabolic energy production (azide, dinitrophenol), inhibitors of lysosomal cathepsins (leupeptin, pepstatin), and lysosomotropic agents (NH4Cl, chloroquine, lidocaine, methylamine, dansylcadaverine), but not by inhibitors of serine or thiol proteases. 125I-labeled-rANP initially bound to the cell-surface was rapidly internalized, and delivered to lysosomal structures, which was confirmed by autoradiographic studies. These data indicate that rANP, after binding to the cell-surface receptors, is rapidly internalized into the cells through receptor-mediated endocytosis, and subsequently degradaded by lysosomal hydrolases.
Specific binding sites for vasoactive intestinal peptide (VIP), a potent vasodilatory polypeptide, and its effect on formation of intracellular cyclic AMP levels were studied in cultured vascular smooth muscle cells (VSMC) from rat aorta. Specific binding of 125I-labeled-VIP to cultured VSMCs was time- and temperature-dependent. Scatchard analysis of binding studies suggested the presence of two classes of high and low affinity binding sites for VIP; the apparent Kd and the number of maximal binding capacity were approximately 8 X 10(-9) M and 60,000 sites/cell (high-affinity sites) and approximately 4 X 10(-8) M and 140,000 sites/cell (low-affinity sites), respectively. Unlabeled VIP competitively inhibited the binding of 125I-labeled-VIP to its binding sites, whereas neither peptides structurally related to VIP, nor other vasoactive substances affected the binding. VIP stimulated formation of intracellular cyclic AMP in cultured VSMCs in a dose-dependent manner; the stimulatory effect of VIP on cyclic AMP formation was not blocked by propranolol and was additive with isoproterenol. The present study first demonstrates the presence of specific receptors for VIP in VSMCs functionally coupled to adenylate cyclase system. It is suggested that VIP exerts its vasodilatory effect through its specific receptors distinct from beta-adrenergic receptors.
Specific binding sites for atrial natriuretic peptide (ANP) were studied in cultured mesenchymal nonmyocardial cells (NMC) from rat heart. Binding study using 125I-labeled synthetic rat (r) ANP revealed the presence of a single class of high-affinity binding sites for rANP in cultured NMCs derived from both atria and ventricles; the apparent dissociation constant (Kd) was approximately 0.2 - 0.3 nM and the number of maximal binding sites was approximately 190,000 - 300,000 sites/cell. rANP significantly stimulated intracellular cGMP formation of cardiac NMCs in a dose-dependent manner (1.6 X 10(-8) M - 3.2 X 10(-7) M). rANP had no effect on synthesis of prostaglandin I2 by cultured cardiac NMCs. The physiological significance of ANP action on cardiac tissue remains to be determined.
The effects of oral nifedipine on limb hemodynamics were studied in 7 normal subjects, 8 patients with congestive heart failure and 2 patients who underwent sympathectomy of unilateral limb. Forearm venous capacitance remained unchanged both in normal subjects and in patients with congestive heart failure. In normal subjects, systemic vascular resistance decreased without change in forearm vascular resistance. On the other hand, both systemic and forearm vascular resistance decreased simultaneously in patients with congestive heart failure. In 2 patients with normal left ventricular function undergoing sympathectomy, limb vascular resistance decreased in the denervated side and increased in the contralateral innervated side. These findings indicate that the effects of nifedipine on forearm vascular resistance are dependent upon the circulatory state of the patient at the time the drug is administered, while venous dynamics were not changed by nifedipine, and that the difference in the density of sympathetic innervation results in a reordering of territorial blood flow by modifying the vasodilatation due to the calcium antagonistic action of nifedipine.
Peripheral circulatory effects of insulin were studied in the diabetic patients with and without autonomic neuropathy. Forearm blood flow, calf venous volume and calf venous distensibility were measured by strain gauge plethysmography. In the diabetic patients with autonomic neuropathy, mean blood pressure fell from 96 +/- 5 to 88 +/- 5 mmHg after an intravenous injection of 4 U of monocomponent insulin (p less than 0.001). Forearm vascular resistance decreased from 53.99 +/- 8.29 to 45.88 +/- 7.76 mmHg X ml-1 X 100ml-1 X min-1 after insulin (p less than 0.01). Insulin increased calf venous volume from 1.20 +/- 0.19 to 2.23 +/- 0.44 ml/100ml (p less than 0.05) and calf venous distensibility from 0.039 +/- 0.004 to 0.082 +/- 0.016 ml/mmHg (p less than 0.05). In contrast, in the diabetic patients without autonomic neuropathy, there were no significant changes in the mean blood pressure, forearm vascular resistance, calf venous volume and calf venous distensibility. Symptoms of hypoglycaemia did not occur in any patient. These results suggest that insulin has a vasodilator action on both resistance and capacitance vessels, which may be one of the main factors in insulin-induced hypotension.
Six skeletal congeners of polychlorinated quaterphenyls (PCQs), namely polychlorinated o-quaterphenyl (2,2'-PCQ), 2,3'-diphenylbiphenyl (2,3'-PCQ), 2,4'-diphenylbiphenyl (2,4'-PCQ), m-quaterphenyl (3,3'-PCQ), 3,4'-diphenylbiphenyl (3,4'-PCQ) and p-quaterphenyl (4,4'-PCQ), were orally administered to Wistar rats at a dose of 10 mg/rat. On the 5th day after administration of PCQs, the rats were examined for accumulation of PCQ congeners, hepatic enzyme activities and organ weight changes. Accumulation of 3,3'-PCQ, 3,4'-PCQ and 4,4'-PCQ were 1.5-3.2% of dose in the liver, while those of 2,2'-PCQ, 2,3'-PCQ and 2,4'-PCQ were only 0.1 to 0.2%. The amount of 4,4'-PCQ accumulated in the mesenteric adipose tissue, 20 micrograms/rat, was much higher than those of other PCQ congeners. Large amounts of the PCQ congeners administered were excreted in the feces on the first day, accounting for 96 to 98% of dose for 2,2'-PCQ and 4,4'-PCQ, and 55 to 75% for the other PCQ congeners, and the daily excretions of PCQs after the second day were very small, less than 10% of the dose. Benzo [a] pyrene 3-hydroxylase activity was significantly depressed by the treatment with 3,3'-PCQ, 3,4'-PCQ and 4,4'-PCQ, contrasting to the toxic congeners of polychlorinated biphenyls and dibenzofurans which enhanced markedly this enzyme activity. DT-Diaphorase activity was also depressed by the treatment with 2,3'-PCQ, 2,4'-PCQ and 3,4'-PCQ. Significant atrophy of the thymus was observed by the treatment with 4,4'-PCQ.
Baroreflex control of heart rate, pressor responses to alpha agonist (phenylephrine) and isometric exercise before and during salt loading were compared between 13 normotensive subjects with hypertensive relatives (group A) and 9 normotensive subjects with no family history of hypertension (group B). Baroreflex slope was significantly lower in group A than in group B (9.6 +/- 1.6 vs 17.6 +/- 1.9 msec/mmHg; p less than 0.01), although blood pressure, heart rate and aortic distensibility were not different between two groups. Pressor responses to phenylephrine and isometric exercise were identical for both groups. During salt loading, pressor responses to phenylephrine and isometric exercise were significantly greater in group A than in group B. Baroreflex slope was not affected by salt loading in the two groups. These results suggest that baroreflex control of heart rate is impaired in normotensive young subjects with hypertensive relatives and this defect may be inherited rather than the result of elevated arterial pressure and decreased aortic distensibility. Pressor responses to alpha agonist and isometric exercise during high-sodium diet were augmented in subjects with a family history of hypertension.
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This study was performed to determine whether baroreflex control of heart rate is impaired in young normotensive subjects with hypertensive relatives. Blood pressure, baroreflex function, pressor response to phenylephrine, aortic distensibility (pulse pressure/stroke volume) and minimal forearm vascular resistance (minFVR) were assessed in 13 normotensive subjects with hypertensive relatives (group A) and 11 normotensive subjects with no family history of hypertension (group B). Baroreflex sensitivity was significantly lower in group A than in group B (9.4 +/- 1.7 versus 17.5 +/- 1.7 ms/mmHg, P less than 0.01), although blood pressure, aortic distensibility and minFVR were not different between two groups. Pressor response to phenylephrine was identical for both groups. These results suggest that baroreflex control of heart rate is impaired in normotensive young subjects with hypertensive relatives and this defect may be inherited rather than the result of elevated blood pressure and decrease aortic distensibility.
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The clinical records of 68 patients with primary carcinoma of the gallbladder (39 cases) and the extrahepatic biliary tracts (29 cases) were comparatively reviewed. The survivals with carcinoma of the gallbladder were limited to five patients operated upon because of cholelithiasis and/or cholecystitis. The majority of the cases preoperatively diagnosed as cancer of the gallbladder were not able to undergo radical cholecystectomy. Of seven patients with radically resected tumors among 29 cases with carcinoma of the extrahepatic biliary tracts, only two patients survived and other five died with locally recurrent tumors. This experience reemphasizes the inadequacy of the present diagnosing approaches to the diseases. Therefore, for discovery of the early cases with primary carcinoma of the gallbladder and the extrahepatic biliary tracts, it may be far more important to make more aggressive measures by using newly developed diagnosing tools.
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1. We have monitored intra-arterial pressure continuously throughout the day and analysed every beat by computer. 2. Baroreflex sensitivity (ms/mmHg) was measured four times a day (07.00, 12.00, 17.00 and 20.00 hours) in seven patients and three times a day (07.00, 12.00 and 17.00 hours) in 23 patients. The diurnal variation of baroreflex sensitivity in individual patients was 0--5.3 ms/mmHg and was not consistent. Mean baroreflex sensitivity was reduced in hypertensive patients compared with normotensive subjects. 3. A negative correlation was seen between baroreflex sensitivity and the variability of systemic blood pressure. 4. Baroreflex sensitivity was well correlated with the variability of heart rate.
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