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M Ishii

Publications and source records attributed to M Ishii.

At least 19 recordsLinked to original sources
PubMed1992

Enhanced inhibitory effect of alpha 2-adrenoceptor stimulation on the formation of cAMP in glomeruli of spontaneously hypertensive rats.

Renal alpha 2-adrenoceptors are known to be increased in spontaneously hypertensive rats (SHR) compared with Wistar-Kyoto rats (WKY). To investigate whether this difference affects the second messenger system, we examined the effect of alpha 2-adrenoceptor stimulation on the formation of cAMP in microdissected glomeruli and proximal convoluted tubules obtained from the kidneys of SHR and WKY. The formation of glomerular cAMP, which was stimulated by parathyroid hormone (PTH), was inhibited by alpha 2-adrenoceptor stimulation. In contrast, the inhibitory effect of alpha 2-adrenoceptor stimulation on PTH-induced cAMP formation in proximal convoluted tubules was not significantly different between SHR and WKY. These results confirm the inhibitory action of alpha 2-adrenoceptors on the formation of cAMP in glomeruli and proximal tubules and suggest that the greater inhibitory effect on glomerular cAMP formation in SHR may reflect an increase in alpha 2-adrenoceptor density in SHR kidneys.

Animals↗
PubMed1992

Pharmacokinetics and pharmacodynamics of benazepril in hypertensive patients with normal and impaired renal function.

The pharmacokinetics and pharmacodynamics of benazepril, an angiotensin converting enzyme (ACE) inhibitor, were investigated after administration of a single oral 5-mg dose and 7 more doses on consecutive days to hypertensive patients with normal renal function (NRF) and those with impaired renal function (IRF). The antihypertensive effect of benazepril was observed as early as 30 min after a single dose, and those effects during consecutive dosing were also sustained for 24 h with a lesser diurnal variation in blood pressure (BP). The time to peak (Tmax) and the apparent elimination half-life (t1/2) for benazepril were 0.6-0.7 h and 0.4-0.8 h, respectively. Tmax for its diacid was 1.5-2.4 h in both groups. The area under the plasma concentration-time curve to 24 h (AUC0-24h) for the diacid was significantly greater in the IRF group than in the NRF group. After consecutive dosing of benazepril, AUC0-24h and plasma peak level (Cmax) were significantly increased in the IRF group. Serum ACE activity was markedly suppressed for 24 h after administration, and the inhibition was closely related to plasma diacid levels. A significant inverse correlation was observed between creatinine clearance and the AUC for the diacid. These results suggest that benazepril is rapidly bioactivated to diacid and exhibits rapid onset and long-lasting antihypertensive effects. Dosage reduction might be required to minimize unnecessary drug accumulation in patients with severe IRF.

Administration, Oral↗
PubMed1992

Diastolic mitral regurgitation in patients with first-degree atrioventricular block.

Diastolic mitral regurgitation has been observed in patients with DDD pacemakers when the atrioventricular (AV) delay was prolonged. However, diastolic mitral regurgitation associated with first-degree AV block has not been fully studied. We examined transmitral blood flow in 24 patients with first-degree AV block and normal cardiac function (ages 35.3 +/- 17.4 years), and in nine patients with DDD pacemakers and normal cardiac function (ages 73.1 +/- 8.1 years), using pulsed Doppler echocardiography. Diastolic mitral regurgitation was observed in 19 of 24 patients with first-degree AV block. Although PQ interval was shortened from 0.32 +/- 0.06 to 0.20 +/- 0.05 seconds (P < 0.01) after 1 mg atropine sulfate IV, the interval between P wave (ECG) and the beginning of diastolic mitral regurgitation did not change, while the duration of diastolic mitral regurgitation was shortened from 0.15 +/- 0.03 to 0.05 +/- 0.03 seconds (P < 0.01). There was a significant correlation between changes in PQ interval and changes in the duration of diastolic mitral regurgitation (r = 0.92, P < 0.001). Although cardiac output (3.9 +/- 0.05 L/min) and pulmonary capillary wedge pressure (5.1 +/- 1.5 mmHg) were normal in all patients with pacemakers, diastolic mitral regurgitation was observed when the AV delay was prolonged. The critical PQ interval for the appearance of diastolic mitral regurgitation was 0.23 +/- 0.01 seconds. In patients with prolonged PQ intervals, delayed ventricular contraction following atrial contraction may be associated with mitral regurgitation in the presence of a reversed AV pressure gradient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Non-invasive evaluation of pulmonary arterial and right ventricular pressures with contrast enhanced Doppler signals of tricuspid regurgitation flow using sonicated albumin solution.

To determine the feasibility of the non-invasive determination of systolic pressure of the pulmonary artery and the right ventricle in pediatric patients, the velocity of tricuspid regurgitation was measured in 30 patients using a contrast enhanced Doppler echocardiography. After sonicated albumin injection, trivial tricuspid regurgitation signals were enhanced in 27 patients (90%). Peak systolic velocity was not altered by before and after sonicated albumin injection in 2 patients. Right ventricular (RV) systolic pressure obtained by continuous wave Doppler during sonicated albumin enhancement corresponded very closely to that measured by catheter in 27 patients (r = 0.96). In 27 patients, difference of estimation of RV systolic pressure by non-enhanced Doppler and enhanced Doppler with sonicated albumin was statistically significant (32.3 +/- 27.6 mmHg versus 2.9 +/- 7.7 mmHg p < 0.001). Systolic pressure of pulmonary artery was estimated by RV systolic pressure measurement (by enhanced Doppler method) minus peak pressure gradient across the pulmonary valve (non-enhanced Doppler method). Pulmonary arterial systolic pressure measured by enhanced Doppler method and that by catheter method were highly significant (sonicated albumin method, r = 0.95). This technique may be a valuable non-invasive method for determining an accurate right ventricular and pulmonary arterial systolic pressures in this setting.

Adolescent↗
PubMed1979

[Basic fetoprotein].

Explore the source record for details and available documents.

Carcinoembryonic Antigen↗
PubMed1979

Arachnoid villi affected by subarachnoid pressure and haemorrhage. Scanning electron microscopic study in the dog.

The arachnoid villi of 18 dogs were studied. The authors confirmed the pressure gradient changes of the morphology of arachnoid villi of dogs with the scanning electron microscope (SEM). A subarachnoid infusion with 5--10 times higher pressure gradient than the physiological one, tore the superficial endothelial layer from the villi, and the inner part could also be observed stereoscopically. On the surface of the arachnoid villi, the authors observed microvilli, openings of vacuoles and intercellular gaps, but did not find openings of performed channels. After subarachnoid haemorrhage (SAH) generally the villi were blocked but the authors have observed a red blood cell escaping from a villus intercellularly.

Animals↗
PubMed1979

Post-haemorrhagic subarachnoid fibrosis in dogs. Scanning electron microscopic observation and dye perfusion study.

Scanning electron microscopic observations of the subarachnoid space were made in dogs focussing upon the fibre components in both the normal subarachnoid space and in areas of post-haemorrhagic fibrosis. It was concluded that the fibrous tissue originates from the arachnoid membrane itself, while organized haematoma is considered to form a component of the fibrosis. Perfusion of the subarachnoid space of dogs with a solution of 0.1% Toluidine Blue was also done. This showed that cerebrospinal fluid (CSF) is carried from the subarachnoid space directly to the dural sinuses through a fine string-like structure, which is conceivably one of the collateral CSF absorptive pathways.

Animals↗
PubMed1979

Scanning electron microscopy of the subarachnoid macrophages after subarachnoid haemorrhage, and their possible role in the formation of subarachnoid fibrosis.

Sixty dogs with experimental subarachnoid haemorrhage (SAH), repeated SAH, and subarachnoid fibrosis (examined three weeks and three months after SAH, and treated with urokinase or dexamethasone) were examined by scanning electron microscope (SEM). The authors observed the resting and activated macrophages, the erythrophagocytosis, and giant cells in the subarachnoid space after SAH. They consider that the macrophages play an important role in the formation of subarachnoid fibrosis, similar to the role of macrophages in fibrosis in other sites.

Animals↗
PubMed1979

Stimulation by catecholamine of purine catabolism in rats and chickens.

The effect of catecholamine in vivo was studied on purine catabolism in rats and chickens. Catecholamine, administered intraperitoneally in a high dose, markedly increased plasma uric acid and allantoin in rats, and an increase was also observed with intravenous infusion of a lower dose of catecholamine. The effects of catecholamine were characterized by inhibition with alpha and beta adrenoceptor antagonists. Regarding the mechanism of this catecholamine action on purine catabolism, it was shown that catecholamine stimulated degradation of tissue ATP into the end-product. Plasma allantoin, the final purine catabolite in rats, elicited by catecholamine could be maintained under conditions of renal failure, although the action of catecholamine in intact rat was short lasting. The effect of catecholamine was potentiated and/or prolonged by angiotensin-II and aminophylline, and a hyperuricemic state could be induced by catecholamine treatment in chickens. In addition, increase of plasma purine catabolite by immobilization stress in rats suggested the involvement of endogenous catecholamine. From these experimental results, it is considered that catecholamines probably play a important role in the pathogenesis of hyperuricemia.

Adrenergic alpha-Antagonists↗
PubMed1979

The effect of angiotensin-converting enzyme inhibition on regional blood flow in salt-depleted and salt-loaded normotensive conscious rats.

The effect of angiotensin-converting enzyme inhibition on regional blood flow was studied in a total of 21 normotensive Wistar rats fed on either low or high salt diet. A new potent angiotensin-converting enzyme inhibitor (CEI), SQ 14,225 was administered intravenously in a dose of 2 mg/Kg to the conscious animals, and changes in fractional distribution of cardiac output were determined with a microsphere method. Prior to administration of CEI, there was no significant difference in mean arterial pressure (MAP) or regional blood flow between salt-depleted and salt-loaded rats. With CEI, MAP did not change significantly in either group. Fractional distribution of cardiac output increased to the kidneys (p less than 0.002), and decreased to the stomach, spleen, and skeletal muscle (p less than 0.02, p less than 0.002, and p less than 0.01, respectively) in the salt-depleted group, while a pattern of blood flow distribution was not changed in the salt-loaded group. These results suggest that angiotensin II plays an important role in regulating regional blood flow in salt-depleted conscious animals, but not in salt-loaded ones.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1979

Immunopathologic studies of pneumonitis in systemic lupus erythematosus.

We performed immunohistopathologic studies on biopsied lung tissue obtained from two patients with lupus pneumonitis using immunofluorescence, immunoperoxidase, electron microscopy, and acid-microelution. In both patients, immunofluorescence showed granular deposits of IgG, the third component of complement (C3), and DNA in the alveolar walls. The immunoperoxidase technique in both and electron microscopy in one showed that these deposits were in the interstitium of the alveolar walls and in the alveolar capillary walls. The eluates obtained from cryostat sections of the biopsied lungs contained antinuclear factor of IgG class in one patient and showed anti-DNA antibody activity in both. We suggest that the deposits are immune complexes composed of DNA, anti-DNA antibody, and complement and that deposits of DNA-anti-DNA immune complex may play a role in lupus pneumonitis.

Adolescent↗
PubMed1979

[Subarachnoid hemorrhage and circulatory disturbance of cerebrospinal fluid--scanning electron microscopid study in clinical and autopsy cases (author's transl)].

The scanning electron microscopy (SEM) gives intersting information about the changes of the subarachnoid space. In this study, specimens from 16 patients (one during surgery and others at autopsy) were examined by SEM: 11 cases of subarachnoid hemorrhage, 2 of posterior fossa brain tumor operated and 3 of control cases without CNS diseases. In cases of subarachnoid hemorrhage, there seemed to be three stages of the obstruction in the subarachnoid space: a) obstruction by blood clots mainly consisted of red blood cells, b) obstruction by subarachnoid fibrosis with thickening of arachnoid, c) obstruction by arachnoid adhesion obliterating subarachnoid space. Specimens from parietal parasagittal area, lateral cerebral fissure and temporal base on both sides were systematically examined by SEM, and the degree of the obstructive changes of the subarachnoid space were classified into five grades: 0) no changes 1) minimal changes--slight thickening of arachnoid and perivascular fibrosis in subarachnoid space 2) moderate changes--thickening of arachnoid and fibrosis in subarachnoid space with patent meshwork 3) severe obstruction of subarachnoid meshwork 4) complete obstruction of subarachnoid space--no space for CSF circulation. We found high incidence of communicating hydrocephalus after SAH in those cases in which epicortical CSF circulation was obstructed more than grade 3 in the parasagittal area bilaterally.

Adult↗