Search PubMed⌕ Search

Biomedical subjects

M Minami

Publications and source records attributed to M Minami.

At least 271 records · Page 15Linked to original sources
PubMed1997

Relation of 24-h ambulatory blood pressure with plasma potassium in essential hypertension.

The established associations between blood pressure (BP) and electrolytes are mostly based on either dietary intake or urinary excretion data. We measured office BP, ambulatory BP (ABP) using the automated oscillometric ABPM-630 device, and plasma electrolytes in 82 essential hypertensive patients to examine the relation between BP and plasma electrolytes. Significant negative correlations were observed between plasma potassium concentration and 24-h systolic BP (r = -0.336) and diastolic BP (r = -0.298) in our patients. Plasma potassium concentration inversely correlated also with both daytime and nighttime systolic and diastolic BPs. There was no relation between office BP and plasma potassium concentration. These findings indicate that in essential hypertensives plasma potassium concentration is inversely related to ABP including daytime and nighttime BPs and suggest that potassium may be a factor determining the whole day BP in essential hypertension.

Adult↗
PubMed1997

Chemoprevention of DMBA-induced mammary carcinogenesis in rats by low-dose EPA and DHA.

We investigated the effects of low-dose eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on the incidence and growth of 7,12-dimethylbenz(a)anthracene (DMBA)-induced mammary carcinoma in rats fed a high-fat (HF) diet. We also examined the effects of these treatments on the fatty acid composition of tumour and serum. Tumour incidence was significantly decreased by the administration of low-dose EPA and DHA, whereas their inhibitory effects on tumour growth did not reach significance. Serum arachidonic acid (AA) level was decreased by the administration of low-dose EPA and tended to be decreased by the administration of low-dose DHA, whereas tumour AA levels were not changed. The administration of low-dose EPA and DHA may be useful for inhibiting the incidence of breast cancer.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1997

Use of percutaneous cardiopulmonary support system with rotary blood pump in graft replacement of the descending thoracic and thoracoabdominal aorta.

Graft replacement of the descending thoracic or thoracoabdominal aorta was successfully performed in 3 patients using percutaneous cardiopulmonary bypass. Femoral inflow and outflow cannulas were inserted percutaneously after induction of anesthesia with the patient in supine position, and low flow normothermic bypass was established before thoracotomy. Next the patient was placed in a right lateral position to create an operating field. With this body position and even an almost prone position, which was sometimes necessary for easy dissection of adhesion of lung to the aneurysmal wall, the bypass flow was easily maintained adequately. The bypass circuit was coated with heparin, and the activated clotting time (ACT) was controlled to be between 150 and 200 s during the entire operating period. Percutaneous insertion of the cannulas avoided local bleeding in the groin, and the low ACT made control of hemorrhage in the operating field easy. For descending aortic surgery, heparin-coated percutaneous cardiopulmonary bypass proved to be a useful adjunctive measure.

Adult↗
PubMed1997

Dopamine as a novel antimigration and antiproliferative factor of vascular smooth muscle cells through dopamine D1-like receptors.

Vascular smooth muscle cell (VSMC) migration and proliferation are believed to play key roles in atherosclerosis. To elucidate the role of vascular dopamine D1-like receptors in atherosclerosis, the effects of dopamine and specific D1-like agonists SKF 38,393 and YM 435 on platelet-derived growth factor (PDGF) BB-mediated VSMC migration and proliferation were studied. We observed that cells stimulated by PDGF-BB (5 ng/mL), showed increased migration and proliferation. These effects were prevented by coincubation with dopamine, SKF 38,393, or YM 435 (1 to 10 mumol/L), and this prevention was reversed by Sch 23,390 (1 to 10 mumol/l), a specific D1-like antagonist. These actions are mimicked by forskolin (1 to 10 mumol/L), a direct activator of adenylate cyclase and 8-bromo-cAMP at 0.1 to 1 mmol/L and are blocked by a specific protein kinase A inhibitor, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline-sulfonamide (H 89), but not blocked by its negative control, N-[2-(N-formyl)-p-chlorociannamylamino)ethyl]-5-isoquinoline sulfonamide (H 85). PDGF-BB (5 ng/mL)-mediated activation of phospholipase D, protein kinase C, and mitogen activated protein kinase activity were significantly suppressed by coincubation with dopamine. These results suggest that vascular D1-like receptor agonists inhibit migration and proliferation of VSMC, possibly through protein kinase A activation and suppression of activated phospholipase D, protein kinase C, and mitogen-activated protein kinase activity.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1997

Dopamine D1-like receptor stimulation inhibits hypertrophy induced by platelet-derived growth factor in cultured rat renal vascular smooth muscle cells.

Vascular smooth muscle cell (VSMC) hypertrophy is believed to play some roles in atherosclerosis. To elucidate the role of vascular D1-like receptors in VSMC hypertrophy, the effects of dopamine and specific D1-like receptor agonists SKF 38393 and YM 435 on platelet-derived growth factor (PDGF) BB-mediated VSMC hypertrophy was studied. We observed that cells stimulated by PDGF-BB 5 ng/mL showed increased VSMC hypertrophy. These effects were prevented by coincubation with dopamine, SKF 38393, and YM 435 1-10 mumol/L, and this prevention was reversed by Sch 23390 1 to 10 mumol/L, a specific D1-like receptor antagonist. These actions are mimicked by forskolin 1 to 10 mumol/L, a direct activator of adenylate cyclase and 8-bromo-cAMP 0.1 to 1 mmol/L, and are blocked by a specific protein kinase A (PKA) inhibitor N-[2-(P-bromcoinnamylamino)ethyl]-5-isoquinoline-sulfonamide (H89) but not blocked by its negative control. PDGF-BB (5 ng/mL)-mediated mitogen-activated protein kinase (MAPK) activity was significantly suppressed by coincubation with D1-like receptor agonists, which were reversed by PKA inhibitor H 89. These results suggest that vascular D1-like receptor agonists inhibit hypertrophy of VSMC, possibly through PKA activation and suppression of activated MAPK activity.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1997

Adrenomedullin is a potent inhibitor of angiotensin II-induced migration of human coronary artery smooth muscle cells.

The migration of coronary artery medial smooth muscle cells (SMCs) into the intima is proposed to be an important process of intimal thickening in coronary atherosclerotic lesions. In the current study, we examined the possible interaction of adrenomedullin, a novel vasorelaxant peptide, and angiotensin II (Ang II) on human coronary artery SMC migration using Boyden's chamber method. Ang II stimulated SMC migration in a concentration-dependent manner between 10(6) and 10(8) mol/L. This stimulation was clearly blocked by the Ang II type 1 receptor antagonist losartan but not by the type 2 receptor antagonist PD 123319. The migration stimulatory effect of Ang II was chemotactic in nature for cultured human coronary artery SMCs but was not chemokinetic. Human adrenomedullin clearly inhibited Ang II-induced migration in a concentration-dependent manner. Human adrenomedullin stimulated cAMP formation in these cells. Inhibition by adrenomedullin of Ang II-induced SMC migration was paralleled by an increase in the cellular level of cAMP. 8-Bromo-cAMP, a cAMP analogue, and forskolin, an activator of adenylate cyclase, inhibited the Ang II-induced SMC migration. These results suggest that Ang II stimulates SMC migration via type 1 receptors in human coronary artery and adrenomedullin inhibits Ang II-induced migration at least partly through a cAMP-dependent mechanism. Taken together with the finding that adrenomedullin is synthesized in and secreted from vascular endothelial cells, this peptide may play a role as a local antimigration factor in certain pathological conditions.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1997

Effect of natriuretic peptide family on the oxidized LDL-induced migration of human coronary artery smooth muscle cells.

The migration of medial smooth muscle cells (SMCs) into the intima is proposed to be an important process of intimal thickening in atherosclerotic lesions. The present study examined the possible effect of a novel endothelium-derived relaxing peptide, C-type natriuretic peptide (CNP), on oxidized low-density lipoprotein (LDL)-induced migration of cultured human coronary artery SMCs by the Boyden's chamber method. The effect of CNP was compared with that of atrial and brain natriuretic peptides (ANP and BNP, respectively). Oxidized LDL stimulates SMC migration in a concentration-dependent manner between 20 and 200 micrograms/mL. This stimulation was chemotactic in nature but was not chemokinetic. By contrast, native LDL was without significant activity. CNP-22 clearly inhibited SMC migration stimulated with 200 micrograms/mL oxidized LDL in a concentration-dependent manner between 10(-9) and 10(-6) mol/L. ANP-(1-28) and BNP-32 also inhibited oxidized LDL-induced SMC migration at concentrations of 10(-7) and 10(-6) mol/L, but these effects were weaker than the effect of CNP-22. Such inhibition by these natriuretic peptides was paralleled by an increase in the cellular level of cGMP. Oxidized LDL-induced migration was significantly inhibited by a stable analogue of cGMP, 8-bromo-cGMP, or an activator of the cytosolic guanylate cyclase, sodium nitroprusside. These natriuretic peptides did not suppress the cell adhesion either in the absence or presence of oxidized LDL. These data indicate that oxidized LDL stimulates migration of human coronary artery SMCs and that natriuretic peptides, especially CNP, inhibit this stimulated SMC migration, at least in part, through a cGMP-dependent process. Taken together with the finding that oxidized LDL is present in the intima, CNP may play a role as a local antimigration factor during the process of intimal thickening in hypercholesterolemia-induced coronary atherosclerosis.

Cell Movement↗
PubMed1997

Mechanisms of action of troglitazone in the prevention of high glucose-induced migration and proliferation of cultured coronary smooth muscle cells.

Recent findings suggest that high glucose levels may promote atherosclerosis in coronary vascular smooth muscle cells (VSMCs). To explore the intracellular mechanisms of action by which troglitazone affects this process, we examined the effect of troglitazone on the migration and growth characteristics of cultured rabbit coronary VSMCs. Treatment with chronic high glucose medium (22.2 mmol/L) for 5 days increased VSMC migration by 92%, [3H]thymidine incorporation by 135%, and cell number by 32% compared with VSMCs treated with normal glucose (5.5 mmol/L glucose + 16.6 mmol/L mannose) medium. Trolitazone at 100 nmol/L and 1 mumol/L significantly suppressed high glucose-induced VSMC migration by 34% and 42%, respectively, the proliferative effect (as measured by cell number) by 17% and 27%, and [3H]thymidine incorporation by 45% and 60% (n = 6, P < .05). The high glucose-induced impairment of insulin-mediated [3H]deoxyglucose uptake was blocked by a protein kinase C (PKC) inhibitor (calphostin C, 1 mumol/L) and was also improved by troglitazone without any change in insulin receptor number and affinity. The high glucose-induced insulin-mediated increase in cell number and in [3H]thymidine incorporation was suppressed by troglitazone. Troglitazone (1 mumol/L) also suppressed high glucose-induced phospholipase D activation, elevation of the cytosolic NADH/NAD+ ratio (as measured by the cytosolic ratio of lactate/pyruvate), and membrane-bound PKC activation. Flow cytometric DNA histogram analysis of cell cycle stage showed that high glucose-induced increase in the percentage of cells in the S phase was suppressed by 1 mumol/L troglitazone. These findings suggest that PKC may be a link between impairment of insulin-mediated glucose uptake and the increase in migration and proliferation induced by high glucose levels and that troglitazone may be clinically useful for the treatment of high glucose-induced coronary atherosclerosis.

Animals↗
PubMed1997

[Specific modulation of vascular smooth muscle cell functions by docosahexaenoic acid].

There are increasing evidences that fish oil-enriched diets attenuate the progression of several types of human and experimental renal, intestinal and cardiovascular disorders including hypertension. Docosahexaenoic acid (DHA) may be one of the active biological component. We previously reported that dietary DHA suppressed the progression of hypertension in stroke-prone spontaneously hypertensive rats (SHRSP). The purpose of this study was to clarify the in vitro effect of DHA on vascular smooth muscle cell functions such as cell growth, hypertrophy, NO release, and intracellular Ca+2 dynamics which involves in the regulatory mechanisms of vascular tone. Addition of DHA to the culture medium of aortic smooth muscle cells isolated from SHRSP and normotensive Wistar Kyoto rats (WKY) had no significant effects on the cell growth, and cell hypertrophy induced by angiotensin II as measured by flow cytometer. DHA did not have a significant effect on interleukin-1 beta (10 ng/ml)-induced nitric oxide release from smooth muscle cells of SHRSP. However, the treatment of smooth muscle cells with DHA (30 microM) for 2 days significantly suppressed the increase in the intracellular Ca2+ concentration induced by 5-hydroxytryptamine, angiotensin II, depolarizing concentration of KCl, but not by thapsigargin. This suppression seems to be due to the suppression of Ca2+ influx, as determined by Mn2+ influx experiment. These results suggest that DHA specifically suppresses receptor-mediated Ca2+ influx in smooth muscle cells. This may be one of the mechanisms by which dietary DHA prevents the development of hypertension in SHRSP.

Animals↗
PubMed1997

Herbal medicine-associated lead intoxication.

A female patient visited our hospital with abdominal pain and anemia. Examination for a gastrointestinal disease gave no diagnostic information. Laboratory studies of the parameters of heme biosynthesis revealed an enzymatic inhibition by lead. The diagnosis of lead poisoning was confirmed by detection of an elevated blood lead level. Excessive lead ingestion was thought to be caused by herbal medicines and/or by an earthen teapot.

Abdominal Pain↗
PubMed1997

Interhemispheric chronic subdural hematoma--case report.

A 74-year-old male presented with right hemiparesis greater in the lower than the upper extremity. He had no apparent head trauma. He had been treated with anticoagulants for cerebral and myocardiac infarction. Computed tomography (CT) and magnetic resonance imaging demonstrated an unusual combination of subdural hematomas in the interhemispheric space on the left, and the left temporoparietal and right frontotemporooccipital regions. The left convexity hematoma was irrigated through a single burr hole. Postoperatively, the size of the left convexity hematoma was diminished and the left interhemispheric subdural hematoma disappeared. However, his consciousness deteriorated, and a second irrigation of the recurrent left convexity hematoma was performed 7 days after the first surgery. CT obtained 3 days after the second operation showed a right interhemispheric subdural hematoma, which diminished spontaneously. The convexity hematoma on the left reaccumulated, and was treated by shunting. His neurological status did not improve, and he died from myocardial infarction 39 days later. Irrigation of convexity hematoma may be effective to treat an associated ipsilateral interhemispheric subdural hematoma.

Aged↗
PubMed1997

[The effects of judge's roles on probability judgment].

A number of studies on probability judgment have reported that people often tend to neglect the base-rate in the Cab Problem (Bar-Hillel, 1980). To explain the base-rate neglect, the present research hypothesized that subjects presented with the Cab Problem focused on the case information in the problem, because the subjects were asked to estimate probability based on that particular case. In 'two experiments, subjects' individuated or general interpretation of the Cab Problem was manipulated by instructing the subjects to play either responsible or neutral judge's role, respectively. The results suggested that in the responsible judge condition the case information had large impact on subjects' judgment, whereas in the neutral judge condition it did not. These results implied that the subject's base-rate neglect arose from taking the individuated interpretation.

Adult↗
PubMed1997

Vascular dopamine-I receptors and atherosclerosis.

Vascular smooth muscle cell (VSMC) migration and proliferation are believed to play key roles in atherosclerosis. To elucidate the role of vascular dopamine D1-like receptors in atherosclerosis, the effects of dopamine, specific D1-like agonists SKF 38,393, and YM 435 on platelet-derived growth factor (PDGF) BB-mediated VSMC migration, proliferation, and hypertrophy were studied. We observed that cells stimulated by 5 ng/ml PDGF BB showed increased migration, proliferation and hypertrophy. These effects were prevented by coincubation with dopamine, SKF 38,393, or YM 435 at 1-10 mumol/l, and this prevention was reversed by Sch 23,390 (1-10 mumol/l), a specific D1-like antagonist. These actions are mimicked by 1-10 mumol/l forskolin, a direct activator of adenylate cyclase and 8-bromocyclic AMP at 0.1-1 mmol/l. The actions are blocked by a specific protein kinase A (PKA) inhibitor N-[2-(p-bromocinnamylamino) ethyl]-5-isoquinoline-sulfonamide (H 89), but are not blocked by its negative control, N-[2-(N-formyl-p-chlorocinnamylamino) ethyl]-5-isoquinoline sulfonamide (H 85). PDGF-BB (5 ng/ml)-mediated activation of phospholipase D (PLD), protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) activity were significantly suppressed by coincubation with dopamine. These results suggest that vascular D1-like receptor agonists inhibit migration, proliferation and hypertrophy of VSMC, possibly through PKA activation and suppression of activated PLD, PKC and MAPK activity.

Animals↗
PubMed1997

Changes in plasma cardiac natriuretic peptides concentrations during 1 year treatment with angiotensin-converting enzyme inhibitor in elderly hypertensive patients with left ventricular hypertrophy.

Plasma concentrations of atrial and brain natriuretic peptides (ANP and BNP) are high in patients with hypertension and congestive heart failure. The present study examined changes in plasma ANP and BNP concentrations during 1 year of monotherapy with enalapril in elderly hypertensive patients with left ventricular (LV) hypertrophy. Eight elderly hypertensive patients with LV hypertrophy were treated with enalapril for 1 year, during which time serial changes were recorded in LV mass index, LV systolic function, and plasma concentrations of ANP and BNP. Enalapril maintained systolic and diastolic blood pressure in the normal range for over 1 year. Treatment significantly reduced posterior wall thickness at 6 months, and more so at 1 year, and tended to reduce septal wall thickness and LV mass index at 1 year. LV ejection fraction was slightly but significantly increased at 1 year. Plasma ANP and BNP, which were markedly elevated at study entry, both decreased after 1 year of enalapril. These results suggest that 1 year of treatment with enalapril caused both a modest regression of LV hypertrophy and a modest improvement in LV systolic function in our selected group of elderly hypertensive patients. The drug reduced elevated plasma ANP and BNP levels but did not alter BUN and serum creatinine levels. Enalapril appears to be useful for the treatment of elderly hypertensive patients with LV hypertrophy.

Aged↗
PubMed1997

[Successful surgical repair of composite graft detachment occurred 5 months after combined Bentall's operation and graft replacement with active aortitis syndrome].

Ninteen-year-old male with annuloaortic ectasia and resultant massive aortic valvular regurgitation, along with aortic aneurysmal dilatation extending from the root to the distal arch, underwent surgical repair at our hospital. Operative procedure comprised composite graft replacement of aortic valve-ascending aorta (Bentall's operation with Piehler's modification), combined with the aortic arch replacement with reconstruction of the neck vessels. Physical, laboratory, and histopathological findings revealed active aortitis syndrome as the etiology of this aortic disease. Five months after operation, this patient was readmitted because of his anemia and complaint of dyspnea. Two days after admission, his condition rapidly deteriorated into pulmonary edema with fall of blood pressure to 70 mmHg. Fluoroscopic examination taken after emergency intubation and mechanical ventilatory support showed malfunction of the aortic valve prosthesis. Circulatory assist was accomplished with intraaortic balloon counterpulsation and percutaneous cardiopulmonary bypass support, and emergent operation was carried out. On reentry into the anterior mediastinum, expansion of the aortic wall wrapping the graft was found. Incision into the wrapped aortic wall revealed dehiscence of the composite graft from the aortic annulus at the sites of right coronary cusp and noncoronary cusp position. Pooled blood between the graft and the wrapped aortic wall compressed the composite graft, resulting in tilting of the bi-leaflet mechanical valve prosthesis and restraint of the motion of one occluder. Retachment of the composite graft to the annulus from outside of the wrapped aortic root wall by seven felt-buttressed mattress sutures of 3-0 polypropylene was performed. Postoperative course was smooth and successive strict antiinflammatory therapy with corticosteroid has successfully controlled the aortitis and the patient has been well after a follow-up of 18 months.

Adult↗
PubMed1997

Effects of talipexole on emesis-related changes in abdominal afferent vagal activity and ileal serotonin metabolism in rats.

The involvement of abdominal afferent vagal activity and serotonergic mechanisms were examined following intravenous administration of talipexole, a dopamine D2 receptor agonist used for treatment of Parkinson's disease, in anesthetized rats. Intravenous administration of dopamine receptor agonists including D1/D2 components increased the spontaneous firing of afferent vagal neurons as did 2-methyl-5-hydroxytryptamine. Both talipexole (0.25-1.0 mg/kg) and bromocriptine (1.0-10.0 mg/kg) increased vagal nerve activity in a dose-dependent manner, and the effect of 10 mg/kg of bromocriptine was significantly greater than that noted with 1.0 mg/kg of talipexole. Increasing vagal firing induced by talipexole was prevented by pretreatment with granisetron, but not with metoclopramide or by spinal section, indicating that afferent vagal firing was mediated via stimulation of the 5-HT3 receptors on the neurons and secondarily caused by stimulation of dopamine receptors. On the other hand, bromocriptine at 5 mg/kg increased 5-HIAA concentration in the ileum, and serotonin turnover (5-HIAA/5-HT) was increased approximately 4-fold when compared to the vehicle group. Bromocriptine also increased the activities of tryptophan hydroxylase and monoamine oxidase. Talipexole at 0.5 mg/kg did not affect ileal 5-HT metabolism and the enzymatic activities. These findings suggest that dopamine receptor agonists may induce changes in abdominal afferent vagal activity and ileal 5-HT metabolism similar to those observed with emetic compounds, and that talipexole has a much smaller influence on serotonin-mediated responses than does bromocriptine with equipotent antiparkinsonian doses. One of the possible reason why talipexole showed fewer emetic side effects in patients with Parkinson's disease may be that the emetic responses triggered by D2 receptor stimulation may secondarily cause an increase of abdominal afferent vagal activity, which may be weakened by the 5-HT3 receptor antagonistic property of talipexole.

Abdomen↗
PubMed1997

[Perioperative management of uremia and fluid balance in patients with compromised renal function undergoing open heart surgery].

Five patients with renal dysfunction underwent coronary artery bypass grafting (CABG). Three patients were in cardiogenic shock with acute myocardial infarction for whom CABG was carried out on emergent basis. Immediate preoperatively these patients were in almost anuria which was derived from sustained renal dysfunction plus decreased renal perfusion due to low cardiac output. The other two patients were operated on electively, and hemodynamic instability and artificial perfusion (cardiopulmonary bypass) affected their chronic renal disease (polycystic kidney and nephrosclerosis, respectively) so unfavorably that intraoperative anuria took place. In all patients intraoperative control of fluid balance and prevention of azotemia were accomplished by intraoperative hemofiltration (HF), in which 10 litters of body fluid was filtered out through a hemofiliter incorporated into the cardiopulmonary bypass circuit, and replaced with saline solution. In emergent cases (three patients) complete anuria was sustained and continuous hemodialysis/hemofilitration (CHDF) was successively performed to control water balance and to prevent exacerbation of uremia. Although they all were in profound low cardiac output state necessitating intraaortic balloon counterpulsation (IABP) and infusion of considerable amount of catecholamines, there was no hemodynamic instability occurred throughout the period of CHDF. In four cases renal function recovered significantly along with the recover from their cardiogenic shock so that they could wean from the hemodialysis therapy. In the remaining case intermittent hemodialysis was necessary in chronic phase. There were no hospital death nor late mortality. From this experience we might conclude that the combined use of intraoperative HF and successive postoperative CHDF is an effective method for controlling fluid balance and preventing uremia in cardiac surgical patients with severe renal dysfunction along with considerable hemodynamic instability.

Aged↗