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Biomedical subjects

H Tomonari

Publications and source records attributed to H Tomonari.

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

Effect of cilazapril on hyperdipsia in hemodialyzed patients.

To investigate whether angiotensin-converting enzyme inhibitor (ACE-I) potentially alleviates hyperdipsia, the effect of cilazapril on dialysis-associated excessive thirst was studied by evaluating various dipsogenic parameters in patients undergoing chronic hemodialysis (HD) who manifest an excessive interdialysis body weight gain of more than 5%, and show simultaneous severe-to-moderate hyperdipsia. An initial single dose of 1 mg of cilazapril given at the end of the HD session produced a marked improvement in the interdialysis thirst scores and a simultaneous reduction in plasma angiotensin II (AII) concentration due to the inhibition of ACE activity. The interdialysis body weight gain in the cilazapril treatment period was significantly smaller than that in the nontreatment period. None of the other parameters including blood pressure, plasma osmolarity, and serum Na and K concentration were different in the treatment vs. the nontreatment period. The present data help to explain the potential pharmacological action of AII in the physiology of thirst and suggest that cilazapril may effectively alleviate dialysis-associated hyperdipsia at least on some occasions. The mechanism by which ACE-I exerts an antidipsogenic action may, in part, be accounted for by the reduction in plasma concentration of AII, as a result of the ACE inhibition.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

[Endothelial cell dysfunction in patients with impaired renal function].

In order to investigate endothelial cell dysfunction in patients with impaired renal function, we measured circulating endothelin (ET-1) and thrombomodulin (Tm) concentrations used as markers for endothelial cell injury in patients with renal failure. 1) ET-1 and Tm were significantly higher in patients with renal failure and pre-dialysis patients than in normal subjects. Tm in CRF patients was significantly greater than that in ARF patients. In contrast, ET-1 was significantly greater in ARF than in CRF. 2) A positive correlation was found between serum creatinine concentration (Cr) and Tm in pre-dialysis patients. However, no correlation was found between Cr and ET-1. 3) A positive correlation was found between Tm and the duration of dialysis in HD patients, but not in CAPD patients. 4) With the improvement of renal function after regular HD treatment, a substantial reduction was found in ARF patients in both Tm and ET-1, but not in CRF patients. The present study suggests the presence of endothelial cell dysfunction in patients with impaired renal function. The progression of endothelial cell damage may differ between patients on HD and those on CAPD. In addition, it is suggested that endothelial cell dysfunction reverses in ARF patients with improved renal function.

Acute Kidney Injury↗
PubMed1996

[Sarcoidosis representing multiple splenic nodules in a patient with IgA nephropathy].

We have encountered a 49-year-old female with persistent proteinuria and hematuria. Blood pressure, renal function, physical findings and chest X-p showed no abnormality, but blood tests disclosed mild thrombocytopenia, elevated serum ACE activity, serum lysozyme activity and serum IgA concentration. Abdominal echography and CT revealed multiple nodules in her spleen. In order to make a definite diagnosis and exclude the possibilities of malignant lymphoma or metastatic malignant tumor, splenectomy, and open renal biopsy were performed at the same time. On histological examinations, light microscopic appearance of the spleen was characterized by non-caseating granulomas compatible with sarcoidosis. Renal biopsy specimen showed diffuse proliferative glomerulonephritis with positive staining of IgA predominantly located in the mesangial area, compatible with IgA nephropathy. The present case may provide suggestive evidence for a link between sarcoidosis and IgA nephropathy in the pathogenesis. IgA nephropathy complicated by sarcoidosis is rare, and thus is of particular interest because common immunological abnormalities might be considered in the disease process of both diseases. We feel that despite a low index of suspicion, physicians must be alert to the possibility of IgA nephritis associated with sarcoidosis. The literature is reviewed regarding the relationship between IgA nephropathy and sarcoidosis.

Female↗
PubMed1995

Rhabdomyolysis associated with bacteremia due to Streptococcus viridans.

A 25-year-old man was admitted with complaints of fever and macrohematuria. Laboratory tests showed a substantial increase in serum creatine phosphokinase and creatinine in association with myoglobinuria and proteinuria. Blood culture grew Streptococcus salivarius and Streptococcus oralis. Findings of renal biopsy were compatible with IgA nephropathy. The glomeruli had a mild mesangial proliferation without crescentic lesions. Changes of the interstitium and tubules were not evident. The clinical course and laboratory results strongly suggested a possible link between Streptococcus salivarius/oralis infection, and rhabdomyolysis. Rhabdomyolysis is rarely seen as a complication of bacterial infection, and the present case emphasizes the importance of suspecting bacteremia due to Streptococcus salivarius/oralis in the presence of rhabdomyolysis.

Acute Kidney Injury↗
PubMed1995

[Effect of cyclosporin monotherapy on proteinuria in a patient with membranoproliferative glomerulonephritis].

A-34-year-old man with a 16-year history of proteinuria was successfully treated with cyclosporin A (CsA). He was diagnosed as having membranoproliferative glomerulonephritis (MPGN) by renal needle biopsy and was treated with dipyridamole. In July 1992, he was readmitted for the treatment of anasarka. Although conventional predonisolone was administered for 5 months after one cycle of methyl-predonisolone pulse therapy, his nephrotic state did not improve. Immediately after the cessation of this treatment, he was given CsA 3 mg/kg/day. A marked reduction in proteinuria and edema occurred during the use of CsA for 6 months, with a reduction in the fractional excretion of protein. The nephrotic condition of this patient was subsequently stable without massive proteinuria despite the discontinuation of CsA at least for several months. These findings suggest that CsA monotherapy may be useful in patients with MPGN and steroid-resistant nephrotic syndrome.

Adult↗
PubMed1994

Differential regulation of cation transport of vascular smooth muscle cells in a high glucose concentration milieu.

To gain new insights into the pathogenesis of diabetic angiopathy, the influence of high glucose concentration on cation transport of vascular smooth muscle cell (VSMC) membrane was investigated by measuring Na, K and Ca transport in serially passaged cultured VSMC. (1) Na-K pump activity, described as ouabain sensitive 86Rb uptake, and Na-K cotransport, described as bumetanide sensitive 86Rb washout of VSMC, grown in high glucose concentration medium (460 mg/dl), was lower than that grown in normal glucose concentration medium (100 mg/dl). A smaller 5-N,N-hexamethylene amiloride (HMA) sensitive 22Na uptake (Na-H antiport) in high glucose concentration medium. accounted for this difference. (2) 45Ca uptake was also smaller in VSMC cultured in high glucose concentration medium. However, the washout rate constant for 45Ca was comparable between high and normal glucose cultured VSMC. (3) Both intracellular concentration of Na and cytosolic free Ca concentration concentration ([Ca]i) of high glucose cultured VSMC were greater than normal glucose cultured VSMC. (4) Intracellular water volume based on the equilibrium distribution of 3-O-methyl-[14C]glucose was not different between normal and high glucose cultured VSMC. It is concluded that VSMC grown in high glucose concentration milieu manifests a decreased Na-K, and Ca transport in conjunction with an increase in intracellular concentration of Na and [Ca]i. These results suggest that high glucose, per se, may alter membrane permeability to cations, possibly leading to changes in VSMC contractility and/or proliferation. This abnormality seen in the diabetic state may closely link to the pathogenesis of diabetic angiopathy, thus as a result risking hypertension and vascular disease.

Amiloride↗
PubMed1994

Ethanol injection sclerotherapy for Baker's cyst, thyroglossal duct cyst, and branchial cleft cyst.

Six patients with Baker's cysts, 3 with branchial cleft cysts, and 2 with thyroglossal duct cysts were treated with percutaneous aspiration and absolute ethanol sclerotherapy using a 7-French pigtail catheter. Cystography was performed before ethanol injection to confirm that there was no extravasation and that it was a monocystic lesion. One recurrence of a Baker's cyst was revealed in follow-up examinations, which ranged from 11 months to 36 months (mean, 25 months). The major complication of hypoesthesia of the popliteal region was observed in 1 patient treated for Baker's cyst. The results of this series suggest that ethanol sclerotherapy is the treatment of choice for Baker's cyst, branchial cleft cyst, and thyroglossal duct cyst.

Adolescent↗
PubMed1994

Intermittent outpatient based ECUM. A case report.

Extracorporeal Ultrafiltration Method (ECUM) could be used in patients with refractory congestive heart failure (CHF). We have encountered a 56-year-old woman with refractory congestive heart failure (CHF) (NYHA II-III) due to coronary artery disease, complicated by moderately advanced diabetic nephropathy (Cr = 2.4 mg/dl). Due to the non-responsiveness to medical treatments, she has begun receiving the intermittent ECUM once or twice a week on an outpatient basis. ECUM effectively reduced cardiac preload and temporarily relieved her intractable respiratory distress. Based on our present clinical experience, we propose that one could consider an outpatient based intermittent ECUM as one of the useful therapeutic modalities to ameliorate refractory CHF.

Female↗
PubMed1993

A combination surgical method for preaxial polydactyly of the foot.

A combination procedure was performed on the medial two toes in a 6-month-old child with preaxial polydactyly of the left foot. The first toe had the appearance of a cosmetically intact great toe, but the second toe had better function. A method to combine the advantages of these two toes was therefore applied, with favorable results seen at 1.5 years after surgery.

Follow-Up Studies↗
PubMed1993

Lowered insulin-sensitive Ca2+ transport in cultured glomerular mesangial cells from spontaneously hypertensive rats.

Insulin-resistant state has been postulated in the pathogenesis of hypertension. To investigate the role of insulin in Ca2+ regulation of the glomerular mesangial cell (MC) in hypertension, the effect of insulin on Ca2+ transport and intracellular-free calcium concentration ([Ca2+]i) was measured in serially passaged cultured MC obtained from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Insulin produced a substantial increase in 45Ca uptake as well as [Ca2+]i in quiescent cultured MC from both strains. These stimulatory effects of insulin were completely inhibited by diltiazem, and partially inhibited by H-7, TMB-8 and 5-N,N (hexamethylene) amiloride (HMA), but were not inhibited by W-7 or trifluoroperazine. Although basal ([Ca2+]i) values were not different, insulin-sensitive 45Ca uptake of SHR MC was significantly less than that of WKY MC. Insulin-sensitive increase in ([Ca2+]i) of SHR MC was also less than that of WKY MC. We concluded that insulin increased 45Ca uptake, leading to an increase in ([Ca2+]i), presumably through the voltage-dependent Ca2+ channel, intracellular Ca2+ release and/or proteinkinase C-mediated mechanisms in cultured MC. Blunted response of insulin-sensitive Ca2+ uptake and ([Ca2+]i) in SHR MC suggested differential regulation of Ca2+ transport in response to insulin in the kidney with primary hypertension.

Animals↗
PubMed1993

[Effect of human recombinant erythropoietin (Epo) on cellular Ca2+, Na+, and K+ regulation of vascular smooth muscle cells grown in vitro--a new insight into the pathogenesis of Epo induced hypertension].

To gain an insight into the effect of erythropoietin (Epo) upon cation transporters and cytosolic free Ca2+ concentration ([Ca2+]i) of vascular smooth muscle cells (VSMC), we studied whether 1) Epo, per se, alters Ca2+ Na+, K+ fluxes and [Ca2+]i of VSMC, and 2) Epo may modify the effect of endothelin (ET-1). Using serially passaged quiescent cultured VSMC, the following results were obtained. 1) Epo had no direct effect on steady state Na(+)-K+ transporters (Na(+)-K+ pump, Na(+)-K+ cotransport and Na(+)-H+ antiport). 2) ET-1 alone substantially stimulated Na(+)-K+ pump, Na(+)-H+ antiport and 45Ca uptake, although these effects were not potentiated in the presence of Epo. 3) Epo alone substantially stimulated 45Ca uptake, leading to an increase in [Ca2+]i, which effect was not seen in Ca2+ deficient medium, and was partially inhibited with diltiazem but not with TMB-8. 4) Even in the presence of Epo, ET-1 and angiotensin II (A II) had substantial stimulatory effect on [Ca2+]i of cultured VSMC. The present data indicate that Epo, per se, elicits an increase in [Ca2+]i of VSMC through the stimulation of inward Ca2+ flux without affecting Na(+)-K+ transporters. In contrast, Epo did not potentiate ET-1's stimulatory effect on the transporters. Although the effect of Epo was subtle compared to ET-1 and A II, it may alter an overall characteristic of vascular smooth muscle cell contractility, possibly leading to blood pressure elevation in patients on maintenance dialysis.

Animals↗
PubMed1992

Endothelin-induced calcium responses in human vascular smooth muscle cells.

The effects of endothelin-1 (ET) on the cytosolic free Ca (Cai) and cytosolic pH (pHi) were examined in primary cultures of human umbilical artery (HUA) vascular smooth muscle cells (VSMCs), respectively, loaded with fura-2 and 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. In 1 mM Ca, ET produced a dose-dependent, biphasic increase in the signal with a maximal effect at 400 nM ET. At this concentration, ET produced a Cai transient (mean +/- SE; a rise from basal Cai of 86 +/- 16 to 216 +/- 33 nM) that lasted for approximately 50-60 s. The Cai transient was followed by a slow but sustained increase in Cai. Both ET-induced Cai transient and posttransient Cai were attenuated in Ca deficient medium or by verapamil and nicardipine. In contrast to ET, thrombin elicited only a monophasic Cai response in HUA VSMCs. This response was also partially sensitive to Ca removal or verapamil. KCl (45 mM) depolarization did not elicit a Cai response. However, the presence of voltage sensitive Ca channels in HUA VSMCs was demonstrated by enhanced Mn uptake in cells depolarized with KCl. Both ET and thrombin treatment did not alter pHi. HUA VSMCs demonstrated a single class of ET receptors (approximately 13,000 sites/cell) with an equilibrium dissociation constant of 0.34 nM. Nicardipine did not alter ET binding. These observations suggest a dual effect of ET on the Cai profile in HUA VSMCs that is mediated by Ca mobilization and Ca entry through Ca channels. The Ca entry could include influx through receptor-operated Ca channels, voltage-sensitive Ca channels, or both, but without a direct interaction between ET and these channels.

Calcium↗
PubMed1992

Increased Na-K transport in glomerular mesangial cell membrane from spontaneously hypertensive rats.

To investigate the differences in the Na-K transport of the mesangial cell (MC) membrane in hypertension versus normotension, the activity of the Na-K pump and the passive cation permeability were measured in serially passaged cultured MC obtained from both spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. When Na-K pump was active, Na-K pump activity, described as ouabain-sensitive 86Rb uptake, was significantly greater in the cultured MC from SHR than WKY rats. The outward Na-K cotransport, described as the washout rate constant of bumetanide-sensitive 86Rb washout, was also greater in SHR MC than in WKY rat MC. When Na-K pump was inhibited by 1 mM ouabain, overall intracellular Na uptake was significantly greater in SHR MC. A greater 5-(N,N-hexamethylene)amiloride-sensitive Na uptake in SHR MC accounted for this difference. There was no difference in the intracellular concentration of Na and K in the cultured MC from the 2 strains when Na-K pump was active. It is concluded that there is an increased activity of Na-K pump in the cultured MC from SHR, and that this abnormality may be innate to SHR cells. It is also suggested that an increase in Na-K cotransport and Na-H antiport may explain this difference, and that these abnormalities observed in the SHR kidney may be involved in the pathogenesis of hypertension in this model.

Animals↗
PubMed1991

Differential effects of antihypertensive agents on proliferation of vascular smooth muscle cells from spontaneously hypertensive rats.

We have previously shown that Ca-antagonists and alpha-blockers substantially inhibit the cellular proliferation of cultured rat vascular smooth muscle cells (VSMC). This study explored whether these inhibitory effects on cellular proliferation differ between cultured VSMC from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). SHR VSMC proliferated much faster than WKY VSMC in 10% FCS. Cellular proliferation, determined by both cell number count and 3H-thymidine incorporation, was significantly blunted in the presence of either nifedipine (Nif) or bunazosin (Bun). The magnitude of these inhibitory effects was more pronounced for SHR cells than WKY cells (% reduction of 3H-thymidine uptake with Nif: 62.1 +/- 7.8% for SHR vs 75.3 +/- 10.2% for WKY, n = 6, p less than 0.05, and with Bun: 70.2 +/- 7.8% for SHR vs 82.1 +/- 9.9% for WKY, n = 6, p less than 0.05). In contrast, the intracellular water volume was unaffected by these antihypertensive agents based on equilibrium distribution of 3-O-methyl-D-glucose14C. It is concluded that SHR VSMC grow much faster than WKY VSMC and that this abnormality is innate to the SHR cells. It is also concluded that both Ca-antagonists and alpha-blockers exerted a substantial inhibitory effect on cellular proliferation of the cultured VSMC of either SHR or WKY. Furthermore, the greater inhibition of proliferation in the SHR VSMC suggests that Ca mediated- and/or alpha-receptor mediated processes of cellular proliferation of SHR could differ from that of WKY and that these abnormalities may contribute to the hyperproliferative changes of VSMC in this model.

Adrenergic alpha-Antagonists↗