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Biomedical subjects

I Nishio

Publications and source records attributed to I Nishio.

At least 163 records · Page 9Linked to original sources
PubMed1987

The cause of death, risk factors and long-term prognosis of acute myocardial infarction.

Three hundred and eighty-six patients with acute myocardial infarction in the past 11 years between 1975 and 1985 were investigated retrospectively to clarify fatality, cause of death and long-term prognosis in relation to their risk factors and age. The average number of patients admitted in each year was 24.4 for the first 5 years and 44.0 cases per year in the last 5 years. The fatality decreased from 20.3% in the first 5 years to 15.7% in the last 5 years. A major cause of hospital death was cardiogenic shock and congestive heart failure. One hundred and thirty-six patients had coronary arteriography within 2 months after admission. They were divided into three groups; the young (less than or equal to 40 year old)-, middle (41-50 year old)-, and old (greater than or equal to 51-year old)-aged groups. Among the young-aged group, serum cholesterol levels at admission were significantly higher in patients with multi-vessel lesions than those in patients without multi-vessel lesions, while there were many heavy smokers who did not show a significant lesion of the coronary artery. These observations suggest that hypercholesterolemia may act as an important risk factor for coronary arteriosclerosis in young patients, and also that a heavy smoking may promote an initiation of myocardial infarction in young patients without severe coronary artery stenosis. The cumulative 5 and 10 year survival rate for all groups was 84% and 61%, respectively. Fifty-seven patients had reinfarctions, and thirty patients died. The survivors were younger and had a good tolerance to treadmill exercise test at discharge.

Age Factors↗
PubMed1987

Inhibitory action on alpha-human atrial natriuretic polypeptide on vascular adrenergic neurotransmission is attenuated in spontaneously hypertensive rats.

The purpose of the present study is twofold, firstly to investigate the effects of alpha-human atrial natriuretic polypeptide (alpha-hANP) on norepinephrine overflow from sympathetic nerve endings, and secondly to compare vascular responsiveness in perfused mesenteric preparations in spontaneously hypertensive rats (SHR, Okamoto and Aoki, 7-9 weeks old) and a cohort of Wistar Kyoto rats (WKY). In preliminary studies using normotensive Wistar rats, the pressor responses to electrical nerve stimulation or exogenous norepinephrine application were inhibited by alpha-hANP. Norepinephrine overflow was also suppressed by alpha-hANP, during nerve stimulation. The pressor responses and norepinephrine overflow during nerve stimulation were significantly greater in SHR than in WKY rats. The inhibitory effect of alpha-hANP on these responses was reduced in SHR. These results indicate that alpha-hANP could affect both pre- and post-synaptic sites of the resistance vessels. Further, the reduced inhibition of pressor responses and norepinephrine overflow by alpha-hANP in SHR suggests an insufficient regulation of adrenergic transmission by alpha-hANP in hypertension.

Animals↗
PubMed1987

Effects of calmodulin antagonists on norepinephrine release and vascular responsiveness in rat mesenteric vasculature.

This study was designed to investigate the role of calmodulin in adrenergic neurotransmission of resistance vessels. The effects of various calmodulin antagonists (trifluoperazine, W-7, calmidazolium, chlorpromazine, fluphenazine) on the vascular responsiveness and norepinephrine overflow from adrenergic nerve endings were examined in perfused rat mesenteric vasculature preparations. Pressor responses to electrical nerve stimulation or exogenous norepinephrine were inhibited dose-dependently by each calmodulin antagonist. Norepinephrine overflow from the sympathetic nerve endings during electrical nerve stimulation was also suppressed by calmodulin antagonists. These results indicate that calmodulin antagonists affected both pre- and post-synaptic sites of adrenergic neurotransmission, suggesting that calmodulin is involved both in neurosecretion and vascular smooth muscle contractions in peripheral resistance vessels.

Animals↗
PubMed1987

Alterations in calcium-handling of erythrocytes in spontaneously hypertensive rats. Calcium-induced changes in the osmotic fragility of erythrocytes in hypertension.

To investigate the sensitivity to calcium of erythrocytes in hypertension, changes in the osmotic fragility of erythrocytes following Ca-loading were observed. Washed erythrocytes were obtained from spontaneously hypertensive rats (SHR, Okamoto and Aoki) and age-matched normotensive Wistar Kyoto rats (WKY). Treatment of erythrocytes with Ca-ionophore A23187 and Ca in the medium caused a reduction in the osmotic fragility which correlated with the Ca-concentration. The degree of alteration in the osmotic fragility of erythrocytes was greater in SHR than in WKY. Oral administration of hydralazine to SHR significantly reduced the blood pressure. However, the alterations in the osmotic fragility of erythrocytes secondary to Ca-loading were not different between hydralazine-treated and untreated SHR. In the presence of a Ca-antagonist (verapamil or diltiazem) in the medium, the reduction of the osmotic fragility of erythrocytes caused by Ca-loading was inhibited, and the differences between SHR and WKY were abolished by Ca-antagonists. These results suggest that the greater changes in osmotic fragility of erythrocytes caused by Ca-loading in SHR could be due to a genetic abnormality of Ca-handling by the cell membranes, and that this abnormality might cause an increase in intracellular Ca, which contributes, in part, to the pathogenesis of hypertension.

Animals↗
PubMed1987

Diminished prostaglandin-mediated inhibition of norepinephrine release from the sympathetic nerve endings in spontaneously hypertensive rats.

This study was performed to investigate prostaglandin (PG)-mediated regulation of norepinephrine release from the sympathetic nerve endings in spontaneously hypertensive rats (SHR). The effects of PGE2 on the pressor responses and norepinephrine overflow during the periarterial nerve stimulation were examined in the perfused mesenteric vascular beds from SHR and age-matched Wistar Kyoto rats (WKY). In preliminary studies using normotensive Wistar rats, PGE2 inhibited the overflow of norepinephrine in response to the electrical nerve stimulation. On the contrary, when indomethacin was infused into the preparations, the norepinephrine overflow induced by the nerve stimulation was increased. In SHR, the neurogenic vasoconstriction and norepinephrine overflow during the nerve stimulation were significantly greater than in WKY. PGE2 in the medium inhibited the pressor responses and norepinephrine overflow during the nerve stimulation dose-dependently in WKY, while the inhibitory effects of PGE2 in SHR were blunted. These results suggest that PGE2 is an important hormone in regulating sympathetic vascular tone and that presynaptic inhibition of vascular adrenergic transmission by PGE2 is attenuated in SHR.

Animals↗
PubMed1987

Effects of captopril on neurosecretion and vascular responsiveness in hypertension.

The purpose of the present study was to investigate the mechanisms of hypotensive action of an angiotensin converting enzyme inhibitor (captopril) in hypertension. In perfused mesenteric vasculatures from spontaneously hypertensive rats (SHR) and normotensive Wistar kyoto rats (WKY), the effects of captopril on the vascular responsiveness and norepinephrine overflow from the adrenergic nerve endings were examined. The vasoconstrictor responses and norepinephrine overflow during the electrical nerve stimulation was significantly enhanced in SHR compared with WKY. Captopril reduced not only vasoconstrictor responses but also norepinephrine overflow during the nerve stimulation in a dose-dependent fashion. The suppressions of these responses by captopril were significantly greater in SHR than in WKY. These results demonstrate that captopril could affect the presynaptic site of the resistance vessels and cause a decrease in electrically-stimulated norepinephrine overflow from the adrenergic nerve endings. The marked reduction of the pressor responses and norepinephrine overflow to nerve stimulation by captopril in the SHR suggests that the renin-angiotensin system in the vascular beds in enhanced in this model of hypertension.

Animals↗
PubMed1987

Effects of nicardipine on blood pressure and platelet cytosolic free calcium concentration in SHR.

Intracellular free calcium concentration was measured by the fluorescent calcium indicator quin2 method in platelets of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats, and the effects of nicardipine on platelet cytosolic free calcium concentration were investigated. Cytosolic free calcium concentration was significantly increased in platelets of 4-, 11-, and 14-week-old SHR compared with age-matched WKY rats. Platelet cytosolic free calcium concentration in 14-week-old male SHR was significantly decreased 1 h after the administration of nicardipine (5 mg/kg p.o.), while that in WKY rats remained unchanged. These results suggest that transmembrane Ca2+ influx is genetically increased in SHR.

Administration, Oral↗
PubMed1987

Ca mobilization from the intracellular Ca store in spontaneously hypertensive rats.

To evaluate the size of the intracellular Ca store in spontaneously hypertensive rats (SHR), caffeine-induced contractions were investigated in mesenteric artery preparation. Twelve-week-old SHR and age-matched Wistar-Kyoto (WKY) rats were used. The isolated mesenteric artery was prepared by the method of McGregor. Caffeine (2 mg)- and norepinephrine (2 micrograms)-induced pressor responses were measured in both normal (Ca, 2 mM) and Ca-free solution (1 mM EGTA solution). In the presence of Ca, pressor responses to exogenous norepinephrine in SHR were higher than those in WKY rats. In Ca-free solution, pressor responses to norepinephrine were markedly reduced in SHR compared to WKY rats and caffeine-induced contractions in SHR were lower than those in WKY rats. These results suggest that pressor responses to norepinephrine in SHR may be more dependent on extracellular Ca than in WKY rats and the caffeine-sensitive intracellular Ca store might be less in SHR.

Animals↗
PubMed1987

[ECG-gated magnetic resonance imaging of the left ventricle: visualization of anatomical characteristics and quantification of wall thickness and ventricular volume in left ventricular hypertrophy].

Electrocardiography- and respiration-gated magnetic resonance imaging (MRI) was performed using a 0.15-Tesla resistive magnet system in 54 patients with left ventricular hypertrophy to define the site and extent of abnormal wall thickness and to estimate left ventricular function. Because the major cardiac axes are not orthogonal to the conventional transverse, sagittal or coronal planes, the long-axis and short-axis images of the left ventricle were obtained at the end-diastolic and end-systolic phases. The anatomic characteristics of concentric hypertrophy, asymmetric septal hypertrophy, and asymmetric apical hypertrophy were clearly demonstrated by MRI, even in patients with poor echocardiographic images. Quantitatively, left ventricular wall thicknesses obtained from MR images correlated well with those obtained from echocardiography (r = 0.95), and regression was y = 0.99x + 0.39, and so did the ratios of wall thickness of the interventricular septum to the left ventricular posterior wall (r = 0.91, y = 0.80x + 0.24). Left ventricular volumes calculated by the area-length method from MRI and those from left ventriculography also correlated well (r = 0.98, y = 1.13x + 24.5). In conclusion, using the gated long-axis and short-axis MR images of the left ventricle, the anatomical location and extent of hypertrophy and left ventricular volumes are noninvasively demonstrated.

Aged↗
PubMed1987

Dynamic light scattering in the intact rabbit lens. Its relation to protein concentration.

The physical-chemical properties of highly concentrated protein systems as seen in the lens are poorly understood. Using the technique of dynamic laser light scattering spectroscopy, the authors have determined changes in the dynamics of lens proteins from the intact rabbit lens as a function of position and age. The authors have identified two heterogeneous populations of mobile scatterers with relaxation times of less than 0.5 msec and greater than 1 msec. A decrease in scattered light intensity at 90 degrees, an increase in protein concentration, and aging are associated with lengthening of the relaxation times of the less mobile population of scatterers. This data provides evidence for the existence of a gel-like structure of the lens proteins.

Aging↗
PubMed1986

Light-scattering study of depolymerization kinetics of sickle hemoglobin polymers inside single erythrocytes.

The time course of intracellular depolymerization of hemoglobin S aggregates is directly observed by using microscope laser light-scattering spectroscopy in single sickle erythrocytes upon slow reoxygenation. From the correlation functions of the light intensity scattered from a single cell, we determine the average diffusion coefficient as well as the fraction of hemoglobin aggregates that have intracellular mobility. The oxygen saturation of the hemoglobin of the same cell is measured by single-cell absorption spectrophotometry. Combining the results obtained with these techniques and information on the cellular morphology, we propose a model for the depolymerization process of hemoglobin inside single erythrocytes as they transform from the fully sickled to the normal biconcave shape upon reoxygenation.

Anemia, Sickle Cell↗
PubMed1986

Enhanced calcium-sensitivity of erythrocytes in hypertension--calcium-induced changes of erythrocyte osmotic fragility in essential hypertension.

To investigate the Ca-sensitivity of the erythrocyte membrane in hypertension, the changes of the osmotic fragility of erythrocytes by Ca-loading and the effects of Ca-channel blockers or calmodulin-antagonist were observed in patients with essential hypertension. Erythrocytes were obtained from untreated patients with essential hypertension and age-matched normotensive subjects. Treatment of erythrocytes with Ca-ionophore A23187 and Ca in bathing medium caused the reduction of the osmotic fragility of erythrocytes dose-dependently on Ca-concentration. The degree in alteration of the osmotic fragility of erythrocytes was greater in essential hypertension than that in normotensive controls. In addition, Ca-induced changes of erythrocyte osmotic fragility was inversely correlated with the plasma renin activity in essential hypertension. In the presence of Ca-antagonists (verapamil, diltiazem) or calmodulin-antagonist (trifluoperazine), the reduction of the osmotic fragility of erythrocytes by Ca-loading was inhibited, and the differences of the osmotic fragility of erythrocytes between the hypertensives and the normotensive controls were abolished by these drugs. These results suggest that the greater changes of the osmotic fragility of the erythrocytes by Ca-loading in essential hypertension might be due to the abnormality of Ca-handling of the cell membranes causing an increase in the intracellular Ca concentration, contributing at least partially to the pathogenesis of hypertension.

Adult↗
PubMed1986

A case of Sjögren's syndrome with valvular diseases.

The case of a 61 year old woman with Sjögren's syndrome with aortic and mitral stenosis is reported. She suffered from rheumatic fever at a young age. Physical and echocardiographic examinations showed findings of mitral and aortic valve stenosis. In addition, she had experienced xerostomia, a gritty sensation in the eyes and Raynaud's phenomenon. Blood examination showed hypergammaglobulinemia, positive rheumatoid factor, antinuclear and anti-Ro (SS-A) antibodies. The diagnosis of Sjögren's syndrome was confirmed by sialography and biopsy of the labial salivary gland. The combination of valvular disease and Sjögren's syndrome is rare and the etiological correlation is discussed.

Antibodies, Antinuclear↗
PubMed1986

Effects of calcium-antagonists on norepinephrine release from sympathetic nerve endings in rat mesenteric vasculature.

The present study was designed to investigate whether Ca-antagonists influence norepinephrine release from the sympathetic nerve endings in resistance vessels. Isolated mesenteric vascular preparations of rats, perfused with Ringer-Locke solution, were used to determine the effects of verapamil or diltiazem on norepinephrine release from sympathetic nerve terminals. Pressor responses to exogenous norepinephrine and electrical nerve stimulation were recorded, and the norepinephrine contents of the perfusate were measured before and after the electrical nerve stimulation, using high pressure liquid chromatography with an electrochemical detector. Pressor responses to exogenous norepinephrine and electrical nerve stimulation were depressed dose-dependently by verapamil and diltiazem. The inhibition of the pressor responses for nerve stimulation was greater than exogenous norepinephrine. Both verapamil and diltiazem reduced norepinephrine release from the mesenteric arterial beds after the electrical nerve stimulation. These results indicate that Ca++-antagonists, such as verapamil and diltiazem, have inhibitory effects on norepinephrine release from the sympathetic nerve endings, in addition to their direct actions on the vascular smooth muscle. It is also suggested that the presynaptic inhibitory action of Ca++-antagonists could be due to the blockade of Ca++-channels in nerve cell terminals, which may be important in the clinical use of Ca-antagonists.

Animals↗
PubMed1986

Neurotransmitter release, vascular responsiveness and their suppression by Ca-antagonist in perfused mesenteric vasculature of DOCA-salt hypertensive rats.

To investigate the role of norepinephrine release from the sympathetic nerve endings and vascular responsiveness in the pathogenesis of hypertension, the perfused mesenteric preparations were used in DOCA-salt hypertensive rats (acute phase: 10 days after operation, chronic phase: 7-8 weeks). In addition, the effects of a Ca-antagonist (verapamil) on the norepinephrine release and vascular responsiveness were also examined. Vasoconstrictor responses to the electrical nerve stimulation were significantly greater in DOCA-salt hypertension in the chronic phase than the age-matched normotensive controls. The pressor responses to exogenous norepinephrine were significantly enhanced in DOCA-salt hypertension both in acute and chronic phases. Endogenous norepinephrine overflow from the sympathetic nerve endings during the electrical nerve stimulation was enhanced in the chronic phase of DOCA-salt hypertension, but not in the acute phase, compared with the age-matched normotensive controls. After infusion of verapamil, the pressor responses and norepinephrine overflow by the electrical nerve stimulation were significantly inhibited, and the suppression was greater in chronic DOCA-salt hypertension than in the normotensive controls. These results demonstrate that the vascular responsiveness was increased in both acute and chronic phases of DOCA-salt hypertensive rats, while the norepinephrine overflow from the adrenergic nerve terminals was enhanced only in the chronic phase. More marked inhibition of the vasoconstrictor responses and norepinephrine overflow in the presence of a Ca-antagonist in chronic DOCA-salt hypertension might represent the higher Ca-dependency in the neurotransmission of the peripheral resistance vessels, especially in the mechanism of presynaptic norepinephrine release, than their normotensive controls, and it could partly contribute to the development and maintenance of DOCA-salt hypertension.

Animals↗