PubMed Health⌕ Search

Biomedical subjects

K Atarashi

Publications and source records attributed to K Atarashi.

At least 37 records · Page 2Linked to original sources
PubMed1996

Ouabainlike compound in hypertension associated with ectopic corticotropin syndrome.

Molecular mechanisms related to sodium retention have been implicated in the pathogenesis of hypertension. It is unclear how sodium retention leads to a rise in blood pressure, but ouabainlike compound may act as a final common pathway in sodium-induced hypertension. In ectopic corticotropin syndrome, hypertension has been attributed to cortisol inactivation overload, giving rise to mineralocorticoid-type hypertension. We sequentially measured plasma and urinary levels of ouabainlike compound over 2 months to evaluate its role in the hypertensive mechanisms in a 64-year-old man with this syndrome caused by lung cancer. His data included hypokalemia and increased cortisol concentrations, corticotropin levels, and urinary 17-hydroxycorticosteroid excretion. Plasma renin activity was suppressed. Plasma and urinary levels of ouabainlike compound were markedly increased concomitantly with high blood pressure. The maximum plasma level was 40-fold the normal range of the subject. After chemotherapy, ouabainlike compound levels gradually decreased in parallel with the decline in blood pressure and rise in potassium concentration. A correlation was observed between plasma and urinary levels of ouabainlike compound (P < .05). Plasma and urinary levels of ouabainlike compound correlated with systolic (P < .01) and diastolic (P < .05) pressures, respectively. The peak of ouabainlike compound in plasma and urine coincided with that of authentic ouabain on high-performance liquid chromatography. Ouabainlike compound derived from urine inhibited [3H]ouabain binding to human erythrocytes. These findings suggest that ouabainlike compound with biological activity could partly account for hypertension in ectopic corticotropin syndrome.

ACTH Syndrome, Ectopic↗
PubMed1996

Recurrent histiocytic necrotizing lymphadenitis (Kikuchi's disease) in an human T lymphotropic virus type I carrier.

We describe a case of recurrent histiocytic necrotizing lymphadenitis (HNL) with aseptic meningitis. The patient was a 46-year-old male and a carrier of human T lymphotropic virus type I (HTLV-I). The patient had a past medical history of at least three relapses of HNL. In addition, his sister, who was also an HTLV-I carrier, had recurrent clinical episodes consistent with those of HNL, suggesting familial HNL occurrence. This observation suggests the possibility that HTLV-I infection is relevant to the pathogenesis of HNL.

Antibodies, Viral↗
PubMed1996

[Sevoflurane comparably decreases the threshold for thermoregulatory vasoconstriction as isoflurane].

The core temperature triggering thermoregulatory arteriovenous shunt constriction is defined as the threshold for vasoconstriction. Vasoconstriction helps prevent further core hypothermia by decreasing cutaneous heat loss and constraining metabolic heat to the core thermal compartment. A previous study showed isoflurane inhibited thermoregulatory threshold. However there is no study to confirm whether sevoflurane perturb thermoregulatory vasoconstriction or not. Consequently we tested the hypothesis that 1.0 minimum alveolar concentration (MAC) sevoflurane and 1.0 MAC isoflurane would reduce the vasoconstriction threshold comparably. With institutional review board approval, we studied 20 patients, aged 20-60 yr, undergoing open abdominal surgery. No premedication was given. Ten patients each were anesthetized with 1.0 MAC sevoflurane (2.0%) alone or 1.0 MAC isoflurane (1.2%) alone. A forearm minus fingertip, skin temperature gradient 0 degree C was considered to demonstrate significant vasoconstriction; the esophageal temperature triggering vasoconstriction identified the threshold. Morphometric characteristics were comparable in each group. The threshold for vasoconstriction was 35.1 +/- 0.4 degrees C in the patients given 1.0 MAC sevoflurane, which was comparable that in those given 1.0 MAC isoflurane: 35.3 +/- 0.7 degrees C. We thus conclude that sevoflurane impairs thermoregulation comparably with isoflurane.

Adult↗
PubMed1995

Nitrous oxide decreases the threshold for vasoconstriction less than sevoflurane or isoflurane.

The core temperature triggering thermoregulatory arteriovenous shunt constriction is designated the threshold for vasoconstriction. High thresholds are generally desirable because vasoconstriction helps prevent further core hypothermia by decreasing cutaneous heat loss and constraining metabolic heat to the core thermal compartment. Previous studies suggest that nitrous oxide (N2O) may inhibit thermoregulatory vasoconstriction less than comparable doses of volatile anesthetics. To confirm this impression, we tested the hypothesis that 0.5 minimum alveolar anesthetic concentration (MAC) N2O combined with 0.5 MAC sevoflurane or isoflurane would reduce the vasoconstriction threshold less than 1.0 MAC sevoflurane or isoflurane. With institutional review board approval, we studied 40 patients, aged 20-60 yr, undergoing open abdominal surgery. No premedication was given. Ten patients each were anesthetized with: 1) N2O (50%) and 0.5 MAC sevoflurane (1%); 2) sevoflurane alone (2%); 3) N2O (60%) and 0.5 MAC isoflurane (0.6%); and, 4) isoflurane alone (1.2%). A forearm minus fingertip, skin temperature gradient > or = 0 degree C was considered significant vasoconstriction; the esophageal temperature triggering vasoconstriction identified the threshold. Morphometric characteristics were comparable in each group. The threshold for vasoconstriction was 35.8 +/- 0.3 degrees C in the patients given 50% N2O combined with 0.5 MAC sevoflurane, which was significantly greater than that in those given 1.0 MAC sevoflurane: 35.1 +/- 0.4 degrees C. Similarly, the threshold for vasoconstriction was 35.9 +/- 0.3 degrees C in the patients given 60% N2O combined with 0.5 MAC isoflurane, which was significantly greater than that in those given 1.0 MAC isoflurane: 35.0 +/- 0.5 degrees C. We thus conclude that N2O impairs thermoregulation less than sevoflurane or isoflurane.

Adult↗
PubMed1995

[A case of thymic carcinoma successfully controlled by combined chemotherapy and irradiation].

There is no well established therapeutic protocol for advanced thymic carcinoma, although chemotherapy and irradiation can apparently be used to control the malignancy. Here we report a case of advanced thymic carcinoma successfully controlled by combination of treatment with systemic chemotherapy and irradiation. A 79-year-old man was admitted to the Hiratsuka Kyosai Hospital with complaints of productive cough and dyspnea. Chest roentgenogram and computerized tomography on admission revealed a tumorous lesion in the anterior mediastinum and on accumulation of left pleural and pericardial effusion fluid. The tumor was diagnosed as a thymic squamous cell carcinoma, after percutaneous needle biopsy. Because of extension to the left pleura and cardiac sac, the tumor was considered to be unresectable and systemic chemotherapy (CDDP + VDS + MMC) was begun. After drainage of the pericardial effusion fluid, intrapericardial injection of MMC was also done. The anterior mediastinum was irradiated. The patient has been doing well, with regression of the thymic tumor for 48 months after irradiation. This case provides important information that can be used to establish an effective therapeutic regimen for advanced thymic carcinoma.

Aged↗
PubMed1994

Adamantinoma of the rib metastasizing to the liver.

Adamantinoma is a rare bone tumor, most of which originates in the long bone. Here, we present a case of adamantinoma of the rib with liver metastasis. The patient, a 69-year-old man, complained of dull chest pain for over 6 months. Chest X-ray and CT film revealed osteolytic mass of the right 7th rib. Under the clinical diagnosis of hepatic tumor with rib metastasis, resection of the rib and partial hepatectomy were performed. Pathologically, the bone tumor was diagnosed as primary adamantinoma and the liver tumor was its metastasis. The patient has been well without adjuvant chemotherapy for 5 years after the operation.

Aged↗
PubMed1994

[Comparison between diltiazem and nicardipine used during anesthesia for coronary revascularization].

The effects of diltiazem (0.1 mg.kg-1 + 3 micrograms.kg-1.min-1) and nicardipine (0.01 mg.kg-1 + 2 micrograms.kg-1.min-1) on circulatory parameters were compared in 30 patients with ischemic heart disease, who underwent coronary revascularization. These drugs were administered intravenously via a Swan-Ganz catheter after induction of fentanyl anesthesia. The group injected with diltiazem showed significant decreases in heart rate, mean arterial pressure, cardiac output, left ventricular stroke work and rate-pressure product. The group injected with nicardipine showed significant decreases in mean arterial pressure, systemic vascular resistance, rate-pressure product and pressure-rate quotient. There were significant differences between the two groups in cardiac output, stroke volume, systemic vascular resistance and left ventricular stroke work. The results suggest that diltiazem protects the ischemic heart by slight cardiac suppression and that nicardipine reduces afterload by marked vascular dilatation during anesthesia for coronary revascularization. Both Ca-channel blockers were demonstrated to be useful.

Aged↗
PubMed1992

A biphasic effect of noradrenaline on renin release from rat juxtaglomerular cells in vitro is mediated by alpha 1- and beta-adrenoceptors.

The direct effect of noradrenaline on renin release from juxtaglomerular (JG) cells in vitro were investigated in a dynamic superfusion system of dispersed rat renal cortical cells. At low concentrations (1-100 nmol/l), noradrenaline stimulated renin release in a dose-dependent manner, while at higher concentrations (0.1-1 mmol/l) it inhibited renin release. The stimulatory effect of 0.1 mumol noradrenaline/l was completely blocked by a beta-adrenoceptor antagonist, propranolol (0.1 mumol/l). When applied at concentrations of 1 mumol/l or 10 mumol/l, noradrenaline had no consistent effect on renin release, although 10 mumol noradrenaline/l had an inhibitory effect in the presence of propranolol (0.1 mumol/l). The inhibitory effect of noradrenaline (0.1 mmol/l) was converted to a stimulatory effect by the addition of an alpha 1-adrenoceptor antagonist (bunazosin, 1 mumol/l), but was not altered by the addition of an alpha 2-adrenoceptor antagonist (yohimbine, 1 mumol/l). These results indicate that low concentrations of noradrenaline directly stimulate renin release from JG cells by the activation of beta-adrenoceptors, while high concentrations of noradrenaline inhibit renin release by the activation of alpha 1-adrenoceptors. Accordingly, a dynamic balance may exist between beta-adrenergic stimulation and alpha 1-adrenergic depression of renin release.

Adrenergic alpha-Antagonists↗
PubMed1992

Effects of manidipine and delapril on glucose and lipid metabolism in hypertensive patients with non-insulin-dependent diabetes mellitus.

Effects of manidipine, a new calcium antagonist, and delapril, an angiotensin converting enzyme inhibitor, on glucose and lipid metabolism were investigated in mild to moderate hypertensive patients with non-insulin-dependent diabetes mellitus (NIDDM). The patients were treated with either manidipine 10 mg/day (n = 12, mean age 63 +/- 2 years) or delapril 30 mg/day (n = 8, 62 +/- 3 years) for 12 weeks. Glucose and insulin (IRI) responses to 75 g oral glucose load, glycosylated hemoglobin A1c (Hb A1c), serum levels of total cholesterol (TC), high-density lipoprotein (HDL) cholesterol, triglyceride and apolipoproteins, and 24 h urinary excretion of C-peptide were measured before and at the end of treatment. Both manidipine and delapril showed adequate hypotensive effects. Neither manidipine nor delapril affected blood glucose and IRI responses to glucose load. Manidipine showed no effect on lipids whereas delapril increased HDL cholesterol (47 +/- 5 mg/dL to 61 +/- 7, p < 0.05), although total cholesterol and triglyceride were not altered. The ratio of TC-HDL cholesterol/HDL cholesterol was decreased by delapril (3.44 +/- 0.30 to 2.61 +/- 0.45, p < 0.05). There were no significant changes in apolipoproteins. Both manidipine and delapril have adequate antihypertensive actions without unfavorable effects on glucose and lipid metabolism in hypertensive patients with NIDDM. Delapril seems to have a beneficial effect on lipid metabolism.

Aged↗
PubMed1991

Plasma renin activity and norepinephrine as predictors for antihypertensive effects of nifedipine and captopril.

To examine predictors for the efficacy of antihypertensive agents, we investigated the effects of nifedipine and captopril on blood pressure (BP) and humoral factors in patients with essential hypertension. Eleven essential hypertensive patients (mean age: 54) were treated with long acting nifedipine at 20 to 40 mg/day for 8 weeks and 25 essential hypertensives (mean age: 51) were treated with captopril at 37.5 to 75 mg/day. Blood pressure was measured every 2 weeks. Plasma renin activity (PRA), and plasma concentrations of aldosterone, epinephrine and norepinephrine were determined before and at the end of treatment. Both nifedipine and captopril decreased BP (nifedipine: mean BP 119 +/- 3 to 101 +/- 2 mm Hg, captopril: 124 +/- 2 to 100 +/- 2, P less than .01 for each), whereas neither of them affected heart rate. The 8-week treatment of nifedipine showed no significant effect on humoral factors. Captopril increased PRA by 63% (P less than .05) and decreased plasma epinephrine by 42% (P less than .01) and norepinephrine by 35% (P less than .01). The change in mean BP was positively correlated with pretreatment PRA (r = 0.68, P less than .01) in nifedipine-treated patients and inversely with pretreatment norepinephrine (r = -0.53, P less than .01) in captopril treatment. The results suggest that both nifedipine and captopril were effective antihypertensive agents and that the long term treatment of nifedipine is more effective in essential hypertensives with lower PRA, while captopril is more effective in those with higher plasma norepinephrine concentration.

Aged↗
PubMed1991

[Clinical study on the priming principle of muscle relaxants: comparison of pancuronium with vecuronium].

The priming principle of non-depolarizing muscle relaxants was treated in this study. The subjects were 48 patients. We administered divided doses (p) and single dose (s) using pancuronium (P) and vecuronium (V), and compared the 4 groups (Pp, Ps, Vp, Vs). Pp and Vp groups received intravenous injection of 0.02 mg.kg-1 first, and 0.08 mg.kg-1 after 5 minutes. Ps and Vs groups received intravenous injection of 0.1 mg.kg-1. Relaxograph was used for monitoring muscle relaxation. First-twitch (T1) and train-of-four ratio (TR) were recorded, and the time intervals required to decrease T1 to 25% (T1-25) and 5% (T1-5) were determined. T1-25 (sec) was 126.2, 153.1, 82.7, and 132.7 in Pp, Ps, Vp, and Vs group, respectively; and T1-5 (sec) was 192.8, 229.8, 112.7, and 165.2 in Pp, Ps, Vp, and Vs group, respectively. As these values suggest, there were no significant differences between Pp and Ps group, while significant differences were noted between Vp and Vs group. The following conclusions were obtained. Clinical usefulness of the priming principle was not shown with pancuronium, but was noted with vecuronium. However, the action of vecuronium appeared rapidly after single dose, and some patients complained of dyspnea during priming. Consequently, the priming principle was not considered to be clinically beneficial.

Adult↗
PubMed1990

Role of adenosine A1 and A2 receptors in the regulation of aldosterone production in rat adrenal glands.

To investigate the roles of adenosine A1 and A2 receptors in the regulation of aldosterone production, we examined the effects of adenosine and adenosine agonists (N6-cyclohexyl adenosine; selective adenosine A1 receptor agonist and 5'-N-ethylcarboxamine adenosine; selective adenosine A2 receptor agonist) on aldosterone and cyclic AMP production in rat adrenal capsular cells. Neither adenosine nor 5'-N-ethylcarboxamine adenosine caused significant effects on basal aldosterone or cyclic AMP production. Also, adenosine (10(-3) M) showed no consistent effects on aldosterone and cyclic AMP production induced by ACTH. On the other hand, N6-cyclohexyl adenosine exhibited a significant inhibition of basal aldosterone and cyclic AMP production at doses of 10(-4) M and 10(-3) M; furthermore, 10(-3) M N6-cyclohexyl adenosine inhibited aldosterone and cyclic AMP production stimulated by ACTH. These results suggest that adenosine A1 receptors are coupled to and inhibit adenylate cyclase and may be involved in the inhibition of aldosterone production.

Adenosine↗
PubMed1990

Immunohistochemical study of vascular lesions in severe hypertension induced by DOCA and salt administration to spontaneously hypertensive rats.

In order to evaluate whether immunoglobulin deposition in vessels plays some role in the development of vascular lesions in severe hypertension, an immunohistochemical study was performed in spontaneously hypertensive rats (SHRs), to which deoxycorticosterone acetate (DOCA) and salt were administered. DOCA and salt rapidly induced severe hypertensive vascular lesions, including necrotizing arteriolitis and productive endarteritis. In these rats, considerable deposits of IgG and IgM were found in the small arteries and arterioles of the kidneys. These deposits were accompanied by complement (C3), and could be eluted by acid incubation. They were localized in periodic acid-Schiff-positive insudative lesions, which were thought to be an early phase of the hypertensive vascular lesions. These results suggest that the immunoglobulins might be bound to an unknown antigen in the vascular lesions and that some immunological mechanism mediated by the immunoglobulins is involved in the development of vascular lesions in severe hypertension.

Animals↗
PubMed1990

The extrarenal effects of atrial natriuretic peptide on body fluid distribution.

To study the effects of atrial natriuretic peptide (ANP) on body fluid volume regulation, we estimated the changes in intra- and extravascular fluid volume by measuring hematocrit (Hct), plasma protein concentration and water balance, and the changes in intra- and extracellular fluid volume by the electrical impedance method during intravenous infusion of ANP. We did two studies, as follows: ANP was infused into 18 patients with essential hypertension, 29 with renal parenchymal hypertension and 15 normotensives at 0.025 microgram/kg/min for 40 min. Both hypertensive groups showed greater natriuretic responses to ANP than normotensives. ANP infusion into essential hypertensive patients increased the urinary excretion of water by 125%, Na by 205%, Hct by 4.2% and plasma total protein (TP) by 5.2% (each P less than .001). In 9 patients (1 with renal hypertension and 8 normotensives) who did not show a natriuretic response (-2.1%), the infusion of ANP also significantly increased Hct (3.8%) and plasma TP (3.1%, each P less than .01). The electrical impedance method was applied to 12 subjects to simultaneously detect the intracellular (Ri) and extracellular resistivities (Re), of which reciprocals reflect the fluid volume in the extra- and intracellular spaces, respectively. ANP infusion increased Re in all subjects (3.96 +/- 0.16 [SE] v 4.03 +/- 0.16 omega.m, P less than .05), but decreased Ri in 7. Changes in urinary Na excretion correlated positively with those in both Re (r = 0.62, P less than .05) and Ri (r = 0.75, P less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Effects of magnesium on changes in blood pressure and plasma aldosterone induced by angiotensin II.

This study examined the effects of magnesium on changes in blood pressure and plasma aldosterone concentration (PAC) elicited by angiotensin II in rats. The infusion of angiotensin II (0.1 nmol/kg/min) for 30 min increased mean arterial pressure (MAP) and PAC. Simultaneous infusion of magnesium sulphate (5 mumols/kg/min) attenuated the MAP elevation (157.0 +/- 5.2 (SE) v 141.6 +/- 3.5 mm Hg, P less than .01) and the increase in PAC (447 +/- 70 v 233 +/- 50 pg/mL, P less than .01) brought about by angiotensin II. These effects of magnesium were abolished when endogenous angiotensin II was suppressed by the administration of captopril, an angiotensin converting enzyme inhibitor. The results suggest that magensium may attenuate the biological actions of angiotensin II.

Aldosterone↗
PubMed1989

Magnesium ion: a possible physiological regulator of aldosterone production.

We examined the direct effect of magnesium ion on aldosterone production by adrenal cells using collagenase-dispersed zona-glomerulosa cells in rats. The effects of magnesium on aldosterone production stimulated by angiotensin II or ACTH were also investigated. Both magnesium sulphate (MgSO4) and magnesium chloride (MgCl2) (0 to 2 mM) decreased aldosterone production in a dose-dependent manner. In comparison with magnesium-free medium, 2 mM MgSO4 inhibited aldosterone production by 73% and MgCl2 by 65%. In addition, MgSO4 showed an inhibitory effect on aldosterone production stimulated by angiotensin II (10pM to 10nM), whereas it had no significant effect on aldosterone production due to ACTH stimulation (10pM to 10nM). These data suggest that magnesium has an inhibitory action on aldosterone production in vitro and may be a physiological regulator of aldosterone production.

Adrenocorticotropic Hormone↗