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Biomedical subjects

Y Masuyama

Publications and source records attributed to Y Masuyama.

At least 127 records · Page 7Linked to original sources
PubMed1989

[A case of infective endocarditis (IE) improving with orally administered amoxicillin (AMPC)].

Progress in chemotherapy and cardiosurgery has remarkably decreased the mortality due to infective endocarditis (IE) in recent years. In chemotherapy for IE, parental administration of antibiotics has been used routinely, the patients suffer from the psychological and physiological burden due to frequent injections and long period of therapy, even though the therapy for IE is successful. In this report, we present a case of IE caused by S. mitis, which was remarkably improved by oral administration of AMPC. A case, 69. y.o. female. She felt like a common cold and visited a G.P. Cardiomegaly was pointed out and positive inflammatory findings in serological examination were found. A low grade fever continued, and she was admitted to the hospital. Blood cultures were positive for S. mitis. For further examination, she was transferred to the university hospital. Based on the extensive blood cultures and cardioechogram, she was diagnosed IE caused by S. mitis. Because there were no symptoms of heart failure, we decided to try oral administration of AMPC, 4 g/day or 6 g/day at an interval of 6 hours. On the second day of therapy, the blood culture turned to be negative for pathogens, and on the fourth day body temperature became normal. On about the 60th day, the CRP finding became negative. Concentrations in the serum of AMPC were more than 10 folds of AMPC-MIC (0.5 microgram/ml) for S. mitis. The patient, however, suffer from complications of lung embolism and was operated for exchange of heart valves. After surgery, she has been well without any symptoms from IE.

Administration, Oral↗
PubMed1989

Inhibition of adrenergic transmission by methionine- and leucine-enkephalins is impaired in the mesenteric vasculatures of spontaneously hypertensive rats.

The present study was carried out to investigate the effects of enkephalins (methionine-enkephalin: Met-Enk, leucine-enkephalin: Leu-Enk) on the adrenergic neurotransmission in hypertension. Perfused mesenteric vasculatures were prepared in spontaneously hypertensive rats (SHR, Okamoto and Aoki strain, 7-10 weeks old) and age-matched Wistar Kyoto rats (WKY), and the effects of these peptides on vascular responsiveness as well as norepinephrine release from the sympathetic nerve endings were examined. Pressor responses to electrical nerve stimulation were inhibited in a dose-dependent manner by Met-Enk and Leu-Enk, and the inhibition was antagonized by naloxone. Norepinephrine release during electrical nerve stimulation was also suppressed by these peptides. In SHR, stimulation-evoked pressor responses and norepinephrine release were significantly enhanced compared to those in WKY, while the suppressive magnitudes of the responses by Met-Enk and Leu-Enk were smaller in SHR than in WKY. These results demonstrate that Met-Enk and Leu-Enk affected presynaptic sites of blood vessels and caused a decrease in electrically-stimulated norepinephrine release from the sympathetic nerve endings. The lower reduction in norepinephrine release and vascular responsiveness by Met-Enk and Leu-Enk in SHR suggests an insufficient regulation of the vascular adrenergic neurotransmission by the opioid peptides in this model of hypertension.

Animals↗
PubMed1989

Inhibition of norepinephrine release by presynaptic alpha 2-adrenoceptors in mesenteric vasculature preparations from chronic DOCA-salt hypertensive rats.

This study investigated norepinephrine release during electrical nerve stimulation and inhibitory characteristics of presynaptic alpha 2-adrenoceptors in perfused mesenteric vasculature from deoxycorticosterone acetate (DOCA)-salt hypertensive rats (7-8 weeks after surgery). Electrical stimulation of sympathetic innervation caused a significantly greater release of endogenous norepinephrine into the mesenteric vasculature of DOCA-salt hypertensive rats than in age-matched normotensive controls. Pressor responses to electrical nerve stimulation were also enhanced in DOCA-salt hypertension. Yohimbine, a potent alpha 2-adrenoceptor blocking agent, potentiated the stimulation-evoked release of norepinephrine into the vasculature in normotensive rats. This effect was blunted in DOCA-salt hypertension. These results suggest that increased norepinephrine release from the sympathetic nerve endings in DOCA-salt hypertension might partly reflect an impaired presynaptic alpha 2-adrenoceptor-mediated inhibition, which could enhance vascular sympathetic tone in this model of hypertension.

Animals↗
PubMed1989

Neurotransmitter release and vascular responsiveness in mesenteric vasculatures from two-kidney, one-clip Goldblatt hypertensive rats.

In order to investigate the peripheral neuroeffector functions of renal hypertension, norepinephrine release from the sympathetic nerve endings and vascular responsiveness were evaluated in the mesenteric vasculatures from two-kidney, one-clip Goldblatt hypertensive rats (2K, 1C-HT). Norepinephrine release and pressor responses during periarterial nerve stimulation (40 V, 5 msec rectangular pulses for 1 min, 5, 10 and 15 Hz) were unchanged during the acute phase (3 weeks after surgery), and were rather reduced during the chronic phase (7-8 weeks after surgery) in 2K, 1C-HT compared to sham-operated normotensive control rats. By contrast, the vasoconstrictor responses to exogenously applied norepinephrine were significantly greater in 2K, 1C-HT than in the normotensive controls. From these observations, it seems unlikely that peripheral adrenergic function in the blood vessels plays an important role in the pathogenesis of 2K, 1C-HT. However, the increased sensitivity of vascular smooth muscle cells to norepinephrine may contribute to the maintenance of high blood pressure in the face of reduced vascular sympathetic tone in this form of hypertension.

Animals↗
PubMed1989

Adrenoceptors in experimental hypertension.

Cardiac, aortic and renal alpha- and beta-adrenoceptors were examined in three types of experimental hypertension in rats. In spontaneously hypertensive rats (SHR), cardiac alpha 1-adrenoceptor concentration was increased and cardiac and aortic beta-adrenoceptor concentrations were decreased compared with Wistar-Kyoto rats (WKY). A similar decrease in cardiac beta-adrenoceptor concentration was also shown in two-kidney, one clip (2K, 1C) and deoxycorticosterone acetate(DOCA)-salt hypertensive rats. Renal alpha 1- and alpha 2-adrenoceptor concentrations were increased in SHR, but not in 2K, 1C and DOCA-salt hypertension. In contrast, renal beta-adrenoceptor concentration was increased in 2K, 1C and DOCA-salt hypertension, but unchanged in SHR. The observed increase in cardiac alpha 1- and renal alpha 2-adrenoceptor concentrations may partly contribute to the elevation of blood pressure in SHR.

Aging↗
PubMed1989

Blood pressure and sympathetic activity following responses to aerobic exercise in patients with essential hypertension.

Fourteen untreated patients with essential hypertension (EH) were subjected to mild aerobic exercise with the intensity at 50% of the maximum oxygen uptake (VO2max) twice a week for 12 weeks, as compared with 14 normotensive subjects (NT). Blood pressure and norepinephrine (NE) in plasma, platelet and urine were measured as the indices of sympathetic activity. In EH, a significant fall in both systolic and diastolic blood pressure was observed. In addition, exercise training produced a significant decrease both urinary and platelet NE, but not in plasma NE. Neither significant changes in blood pressure nor NE in plasma, platelet and urine were observed in NT. These results suggest that an inhibition of the sympathetic nervous system might be related to the blood pressure fall in physical exercise training.

Adult↗
PubMed1989

Effects of ketanserin, verapamil and diltiazem on vascular sympathetic nerve activity in hypertension.

This study was carried out to investigate the hypotensive mechanisms of ketanserin and Ca-antagonists (verapamil and diltiazem) in hypertension. Perfused mesenteric vasculatures were prepared in spontaneously hypertensive rats (SHR, Okamoto and Aoki strain) and age-matched Wistar Kyoto rats (WKY), and the effects of these drugs on vascular responsiveness and norepinephrine release from the sympathetic nerve endings were examined. Pressor responses and endogenous norepinephrine release during periarterial nerve stimulation were significantly increased in SHR compared with age-matched WKY. Ketanserin, verapamil and diltiazem inhibited the stimulation-evoked pressor responses and norepinephrine release dose-dependently, respectively. The suppressive magnitudes of these responses by ketanserin, verapamil and diltiazem were greater in SHR than in WKY. The results demonstrate that ketanserin, verapamil and diltiazem might inhibit norepinephrine release from the vascular adrenergic neurons more strongly in hypertension. This sympatho-depressive effect may contribute, at least partially, to the hypotensive mechanisms of these antihypertensive drugs.

Animals↗
PubMed1989

[Echocardiographic features of left ventricular hypertrophy and contractility in malignant hypertension].

To assess the hemodynamic characteristics in malignant hypertension, echocardiography was performed in 18 patients with malignant essential hypertension (MH-I, n = 9) and secondary hypertension (MH-II, n = 9). Patients with benign hypertension with or without left ventricular hypertrophy (n = 8 and 7, respectively), patients with hypertensive heart failure (n = 7) and normotensive volunteers (n = 10) were subjected to controls. Plasma noradrenaline (NA) and renin activity (PRA) were also measured prior to the antihypertensive therapy. There were no significant differences in the durations of hypertension before the malignant phase, and the mean arterial pressure between MH-I and MH-II. Although posterior wall thickness (PWTd) in MH-II was similar to that in MH-I, interventricular septal thickness (IVSTd) was less marked in MH-II. The plasma NA and PRA were markedly increased in both MH-I and MH-II. End-diastolic dimension (Dd) of the left ventricle was within normal range, but end-systolic dimension (Ds) was significantly increased in MH-I, MH-II and hypertensive heart failure. The moderate decreases in ejection fraction (EF) and mean velocity of circumferential fiber shortening (mVcf) were observed in both MH-I and MH-II. Marked decreases in EF and mVcf were also observed in patients with hypertensive heart failure. The relationship between systolic blood pressure and Dd/PWTd was shifted toward the right and upper portion of the normal relation in MH-I and MH-II. The present study demonstrated that the hemodynamic characteristics in malignant hypertension are an inappropriate left ventricular hypertrophy due to a marked increase in systolic stress; dilatation of the left ventricle in systole; and a moderate decrease in ventricular systolic function. It is suggested that a decrease in left ventricular systolic function in malignant hypertension might be due in part to a marked increase in the influence of neurohumoral factors on hemodynamics.

Adult↗
PubMed1989

[Contribution of calmodulin to renin release in spontaneously hypertensive rats].

A comparative study was designed to evaluate the contribution of calmodulin to renin release from isolated glomeruli of spontaneously hypertensive rats (SHR, Okamoto and Aoki). Male 7-week-old SHR and age-matched control Wistar-Kyoto rat (WKY) were used in the present study. Glomeruli were isolated by the method of Beierwaltes et al. Isolated glomeruli were placed within the superfusion chamber and perfused with Krebs-Ringer solution at a constant flow of 0.3 ml/minute at 37 degrees C. Renin release was increased by calmodulin inhibitor, W-7 in both SHR and WKY. SHR showed higher maximal levels of renin release by W-7 compared to WKY. This result indicates that calmodulin plays an inhibitory role in renin release from juxtaglomerular cells. Calmodulin-mediated suppression mechanism in renin release is augmented in SHR.

Animals↗
PubMed1989

[Contribution of hypertension to left ventricular diastolic function in patients with asymmetrical apical hypertrophy].

This study was designed to ascertain the contribution of hypertension to the early diastolic time intervals in asymmetrical apical hypertrophy (AAH). Eighteen patients with untreated AAH were categorized as those with (n = 13) and without (n = 5) hypertension. Isovolumic relaxation time and early diastolic filling were determined in four groups: normotensive subjects (n = 20), patients with essential hypertension (n = 20), AAH with hypertension, and AAH without hypertension. Early diastolic function was measured by the interval from the aortic closure sound (IIA, phonocardiography) to the opening of the mitral valve (MVO, echocardiography) and the interval from MVO to the O point of the apexcardiogram. The IIA-O interval was also calculated. Peak velocities in the rapid filling phase (R) and atrial contraction phase (A) were measured using two-dimensional Doppler echocardiography in the center of the mitral orifice in diastole. The MVO-O/IIA-MVO and A/R ratios were also calculated. 1. In the AAH with and without hypertension groups, the IIA-O, IIA-MVO, and MVO-O intervals were significantly prolonged. The IIA-O and MVO-O intervals in the AAH without hypertension group were more prolonged than were those in the AAH with hypertension group. In patients with essential hypertension, the IIA-O and the IIA-MVO intervals were prolonged, but there was no prolongation of the MVO-O interval. 2. The MVO-O/IIA-MVO ratio was lower in essential hypertension and in the AAH with hypertension groups, and significantly higher in the AAH without hypertension group. 3. There was no significant change of the R, A, and A/R in each group. These results indicated that prolonged left ventricular relaxation was distinguished in essential hypertension. In AAH with hypertension, the same prolongation was observed, but the disturbance of early diastolic filling was mild. It is suggested that apical hypertrophy has a possible association with hypertension, though it may more properly belong to cardiomyopathy.

Adult↗
PubMed1988

Decreased membrane fluidity of erythrocytes and cultured vascular smooth muscle cells in spontaneously hypertensive rats: an electron spin resonance study.

1. Membrane fluidity of erythrocytes and cultured vascular smooth muscle cells was studied in spontaneously hypertensive rats (SHR; Okamoto and Aoki strains) by means of an electron spin resonance (e.s.r.) and a spin-label technique. 2. The values of outer hyperfine splitting (2T') and of the order parameter (S) determined from e.s.r. spectra for a fatty acid spin-label agent (5-nitroxy stearate) were significantly higher in erythrocytes of SHR (4 and 10-13 weeks of age) than in those of age-matched Wistar-Kyoto rats (WKY). This finding suggests that the membrane fluidity of erythrocytes might be decreased in SHR. 3. The fluidity of cultured vascular smooth muscle cells obtained from 10-13-week-old SHR was also reduced compared with that from WKY. 4. These results suggest that the decreased membrane fluidity might be a genetically determined abnormality of the cell membranes in SHR.

Animals↗
PubMed1988

The role of calmodulin in neurotransmitter release and vascular responsiveness in spontaneously hypertensive rats.

This study was designed to investigate the role of calmodulin in adrenergic transmission in hypertension. In perfused mesenteric vasculature from spontaneously hypertensive rats (SHR, 7-9 weeks of age) and age-matched Wistar Kyoto rats (WKY), the effects of a specific calmodulin antagonist (W-7) on norepinephrine overflow and vascular responsiveness to endogenous and exogenous norepinephrine were examined. The vasoconstrictor responses to electrical nerve stimulation and exogenous norepinephrine as well as norepinephrine overflow during electrical nerve stimulation were significantly enhanced in SHR compared with those in age-matched WKY. The calmodulin antagonist, W-7, reduced not only vasoconstrictor responses but also norepinephrine overflow during nerve stimulation. These inhibitory effects of W-7 were significantly greater in SHR than in WKY. The results demonstrate that norepinephrine overflow from the sympathetic nerve endings and vascular responsiveness were increased in SHR. The marked reduction in norepinephrine overflow and pressor responses by W-7 might suggest the greater calmodulin-dependent adrenergic transmission in this model of hypertension.

Animals↗
PubMed1988

Effects of calcium antagonists on membrane fluidity in hypertension--an electron spin resonance study.

We examined alterations in membrane fluidity of hypertension and the effects of calcium antagonists on these changes by means of an electron spin resonance (ESR) and spin-label technique. Washed erythrocytes from spontaneously hypertensive rats (SHRs; aged 4 and 10-13 weeks) and from patients with essential hypertension, or cultured vascular smooth muscle cells from SHRs were examined and compared with those from normotensive controls. Electron spin resonance spectra for a fatty acid spin label-agent (5-nitroxy stearate) in the membranes were obtained. The values of hyperfine splitting and other parameters of the spectra were significantly higher in erythrocytes from hypertensive rats than in normotensive controls. Similar results were obtained in cultured vascular smooth muscles. These findings indicate that the membrane fluidity might be decreased in hypertension. When calcium was loaded to erythrocytes with Ca-ionophore A23187, the fluidity was decreased. The alternative degrees were greater in hypertensive rats than in controls, and these hypertensive changes were antagonized by diltiazem or verapamil. The results revealed that abnormalities of membrane fluidity in hypertension might be more prominent in the presence of calcium. Further, it is suggested that calcium antagonists could correct these membrane abnormalities in hypertension.

Adult↗
PubMed1988

Ketanserin decreases sympathetic nervous activity in hypertension.

This study was performed to investigate whether ketanserin (a serotonergic receptor antagonist) might affect the sympathetic nerve activity in resistance vessels of hypertension. Isolated perfused mesenteric vasculatures were prepared from spontaneously hypertensive rats (SHRS, Okamoto and Aoki, 20-22 weeks old) and age-matched Wistar Kyoto rats (WKY), and effects of ketanserin on norepinephrine overflow from the adrenergic nerve endings as well as on vascular responsiveness were examined. Pressor responses to electrical nerve stimulation or exogenous norepinephrine were inhibited by ketanserin, in a dose-dependent manner. Norepinephrine overflow during electrical nerve stimulation was also suppressed by ketanserin. Inhibitory degrees of pressor responses and norepinephrine overflow during electrical nerve stimulation by ketanserin were significantly greater in SHRs than those in WKY rats. These results suggest that ketanserin could affect presynaptic neurotransmitter release from the adrenergic nerve endings in resistance vessels. These sympatho-depressive actions might contribute, at least partially, to the hypotensive mechanisms of ketanserin.

Animals↗
PubMed1988

Relationship between the sympathetic nervous system and sodium potassium adenosine triphosphatase inhibitor in salt-sensitive patients with essential hypertension.

In order to evaluate endogenous Na+,K+-ATPase inhibitor on sympathetic nerve endings, endogenous Na+,K+-ATPase inhibitor and plasma noradrenaline were determined in patients with essential hypertension under different sodium conditions. Compared with the plasma from non-salt-sensitive patients, that from salt-sensitive patients showed significantly higher Na+,K+-ATPase inhibitor and plasma noradrenaline levels. Salt-induced changes in endogenous Na+,K+-ATPase inhibitor and those in blood pressure or plasma noradrenaline showed positive correlations. These results suggest that the salt-induced increase in endogenous Na+,K+-ATPase inhibitor might induce blood pressure elevation in essential hypertension, at least partly via increased noradrenaline levels.

Blood Pressure↗