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Biomedical subjects

S Yagi

Publications and source records attributed to S Yagi.

At least 181 records · Page 10Linked to original sources
PubMed1992

Interferon gamma attenuates hypertensive renal injury in salt-sensitive Dahl rats.

Evidence has been provided that the immunological mechanism is involved in the genesis or maintenance of hypertension. In the present study, we investigated the effects of interferon gamma, a potent immunomodulator derived from lymphocytes, on hypertension and organ damage in Dahl salt-sensitive rats and in spontaneously hypertensive rats. Subcutaneous injection of interferon gamma (5 x 10(4) units/kg body wt once a week for 10 weeks) reduced blood pressure in Dahl salt-sensitive rats fed a 4% high salt diet (174 versus 194 mm Hg, p less than 0.025). This blood pressure reduction was associated with an improvement of renal functions, an increase in glomerular filtration rate (690 versus 569 ml/day/100 g body wt, p less than 0.05), and decreases in urinary protein excretion (48 versus 78 mg/day/100 g body wt, p less than 0.025) and urinary N-acetyl-beta-D-glucosaminidase excretion (143 versus 183 milliunits/day/100 g body wt, p less than 0.05). Morphological investigation showed a marked resolution of the vascular injuries seen in untreated Dahl salt-sensitive rats, e.g., intimal and medial hyperplasia, with infiltration of inflammatory cells, and significant amelioration of the glomerular sclerotic changes. In contrast, interferon gamma affected neither blood pressure nor renal functions in spontaneously hypertensive rats. These data indicate that interferon gamma ameliorates the development of hypertension and vascular and renal injuries in Dahl salt-sensitive rats. The resolution of vascular and renal injuries contributes, in part, to the antihypertensive action of interferon gamma.

Acetylglucosaminidase↗
PubMed1992

Effect of alpha 1-adrenoceptor blockade on the left ventricular force-length relationship in dogs.

We used the left ventricular (LV) end-systolic force-diameter (Fes-Des) relation to evaluate the effect of an alpha1-adrenoceptor antagonist (bunazosin hydrochloride) on the contractility of the beta-blocked left ventricle. Nine adult mongrel dogs were instrumented with ultrasonic crystals to measure LV diameter and a micromanometer to measure LV pressure. Beta-adrenergic and vagal blockade was induced with intravenous propranolol (2 mg/kg) and atropine (0.2 mg/kg), respectively, and preload was decreased by inferior vena caval occlusion. The slope (Ec) and extrapolated diameter intercept (Do) of the LV Fes-Des relation were derived from end-systolic data obtained in the control state (after beta-blockade) and after bunazosin infusion (1 mg/kg). Ec was used as a new index of LV contractility. After bunazosin infusion, the heart rate and Ec were decreased by 7 and 22%, respectively, in comparison with the control state, whereas Do did not change. These results indicate that alpha1-adrenoceptor blockade significantly reduces myocardial contractility in the beta-blocked canine heart, perhaps by decreasing the intracellular calcium concentration and/or myosin ATPase activity.

Adrenergic alpha-Antagonists↗
PubMed1992

[The effect of propranolol on the myocardial force-length relationship in the in situ canine left ventricle].

The effect of beta-adrenoceptor blockade on the wall performance of the in situ canine left ventricle (LV) was evaluated based on the LV end-systolic force-diameter (Fes-Des) relation in 10 healthy mongrel dogs. LV diameter was measured with ultrasonic crystals, and LV pressure was measured with a micromanometer. Preload was altered by inferior vena caval (IVC) occlusion. In the control contractility state, the IVC was occluded for 7 sec. Blockade of the cardiac beta-adrenergic nerves was induced with 2 mg/kg propranolol i.v.. Slopes (Ec) and extrapolated diameter intercepts (D(o)) of the LV Fes-Des relation were obtained from end-systolic data of the control contractility state and after the infusion of propranolol. Ec was used as an index for the inotropic state of the myocardium of the LV wall. IVC occlusion during 7 sec under the control contractility state produced little change in the heart rate. Thus, IVC occlusion for 7 sec avoided the major reflex change of autonomic tone. After the infusion of propranolol, the heart rate and Ec both decreased by 24 and 43% of the control value, respectively; whereas, D(o) was not significantly altered. Therefore, it was suspected that the cardiac beta-adrenergic nerve played an important role in maintaining myocardial contractility state of the in situ canine LV wall.

Adrenergic Fibers↗
PubMed1992

[A case of endobronchial fibroma associated with recurrent pneumonia].

We present a case of endobronchial fibroma in a 59-year-old man admitted for repeated pneumonia, successfully treated by endoscopic Nd-YAG laser. His chest X-ray showed an infiltrative shadow in the right lower lung field and a mass shadow within the truncus intermedius. Bronchoscopy revealed a polypoid mass with lobulated whitish surface, obstructing 90% of the lumen. A biopsy taken from the tumor was suggestive of fibroma histologically. Two previous case reports stated that endobronchial fibroma readily detaches from the bronchial wall during removal. The tumor was successfully removed without dropping any tumor fragment to obstruct the distal bronchus by means of biopsy forceps manually attached to an endoscope with endoscopic Nd-YAG laser. The resected tumor was mainly composed of collagen fibers with scanty spindle-shaped fibroblastic cells, which was considered consistent with endobronchial fibroma. Endobronchial fibroma is a rare benign lung tumor, and only seven cases have been reported in the Japanese literature. There was no recurrence at three years and nine months.

Bronchial Neoplasms↗
PubMed1992

[A case of acute renal failure in a patient with idiopathic hypouricemia].

This report is a 17-year-old man with an acute renal failure who complained of nausea, vomiting, bilateral loin pain and abdominal pain after scuffle. Renal biopsy specimen obtained from the left kidney revealed acute tubular necrosis. After recovering renal function he showed extreme hypouricemia (serum uric acid, 0.6 mg/dl) and elevated uric acid clearance (62-78 ml/min). The fractional excretion of uric acid (CUA/Ccr) could not be influenced by either oral pyrazinamide or probenecid. As no other renal tubular or metabolic abnormalities were detected, it is suggested that presecretory reabsorption defect or subtotal defect in uric acid transportation was responsible for the hypouricemia in this patient.

Acute Kidney Injury↗
PubMed1991

Calcium signal and histamine secretion induced by aggregation of immunoglobulin E receptors in rat basophilic leukemia (RBL-2H3) cells.

The changes in cytosolic Ca concentration in rat basophilic leukemia cells (RBL-2H3) were determined using a fluorescent Ca probe, fura-2, after aggregation of IgE receptors. By means of a superfusion system, both histamine secretion and changes in cytosolic Ca concentration were determined simultaneously. In addition, the microscopic observation revealed the oscillatory Ca signal after stimulation with an antigen.

Animals↗
PubMed1991

A double-blind comparative study of doxazosin and prazosin in the treatment of essential hypertension.

Two hundred sixty-six patients took part in a multicenter comparative study of doxazosin and prazosin. Both drugs produced a significant reduction (p less than 0.001) in blood pressure and no increase in heart rate. Blood pressure was considered "markedly decreased" or "decreased" in 70.8% of patients treated with doxazosin and 70.0% of patients treated with prazosin. No statistically significant between-group differences in antihypertensive efficacy were observed. Both doxazosin and prazosin were well tolerated; seven patients (5.6%) in each group had the therapy withdrawn.

Antihypertensive Agents↗
PubMed1991

Inhibitory effects of beta adrenoceptor antagonist, atenolol, on the thromboxane system in the kidney of spontaneously hypertensive rats.

We attempted to investigate the alterations in the vasoconstrictor thromboxane (TXA2) system in the kidney when spontaneously hypertensive rats (SHR) were treated subchronically with atenolol, a beta 1-adrenoceptor antagonist. Atenolol treatment (30 mg/kg body weight per day for 2 weeks) reduced systolic blood pressure by 11%, being accompanied by a decrease in heart rate. This treatment strikingly decreased thromboxane content in the renal cortex by 48% (p less than 0.05), whereas the tissue content was unaltered for prostaglandin E2 (PGE2) or slightly decreased for prostacyclin (PGI2). These alterations in the eicosanoid system led to an increase in the ratio of PGE2/TXA2 and of PGI2/TXA2. Similarly, thromboxane content in the renal papilla was lowered significantly with atenolol treatment, which raised the ratio of PGE2 to TXA2. Thromboxane reduction was not observed in the aortic walls and heart. However, in the vascular walls, PGI2 synthesis was markedly stimulated with atenolol treatment, resulting in an increase in the ratio of PGI2 to TXA2. Thus, these data indicate that subchronic atenolol-treatment inhibits the thromboxane system in the kidney, thereby shifting the eicosanoid system towards a vasodilator state. These alterations contribute, in part, to the anti-hypertensive properties of atenolol in genetic hypertension.

Animals↗
PubMed1991

Stimulating effects of atenolol on vasodepressor prostaglandin generation in spontaneously hypertensive rats.

1. To assess the role of the vasodepressor prostaglandin system in the antihypertensive properties of beta-adrenoceptor antagonist, we investigated the alterations of prostaglandin generation in the kidney and in the aorta when spontaneously hypertensive rats were treated with atenolol for 2 weeks. 2. The blood pressure reduction was associated with an increase in urinary sodium excretion and urinary prostaglandin E2 excretion. The sodium excretion was positively related to the prostaglandin E2 excretion. 3. Basal release of prostaglandin E2 from the sliced renal cortex was enhanced by the atenolol treatment. Prostacyclin-generating capacity in the aortic wall was also significantly increased. 4. Atenolol treatment stimulated prostaglandin synthesis in the kidney and vascular wall in a dose-dependent manner. However, atenolol per se did not directly stimulate prostaglandin synthesis in the vascular wall. 5. Inhibition of prostaglandin generation by a cyclooxygenase inhibitor, indomethacin, was associated with attenuation of the antihypertensive effects of atenolol. 6. Thus these data indicate that sub-chronic atenolol treatment stimulates vasodepressor prostaglandin generation in the kidney and in the aortic vessels, and this shares the antihypertensive effects of this drug with the mechanism of beta-adrenergic antagonism probably mediated through vasorelaxation and natriuresis.

Animals↗
PubMed1991

Possible role of prostacyclin synthase in altered prostacyclin generation in DOCA-salt hypertensive rats.

Prostacyclin (PGI2) synthase is one of the key enzymes for vasodepressor PGI2 biosynthesis in the vascular wall. In this study, we attempted to define the alterations in PGI2 synthase and its role in the PGI2 generation in the vascular wall of deoxycorticosterone acetate (DOCA)-salt rats. The PGI2-generating capacity was enhanced significantly when DOCA-salt rats established hypertension, whereas the generation of other arachidonate metabolites, eg, PGE2, PGF2 alpha, and thromboxane, was unaltered. Moreover, the increase in PGI2 generation was associated with an increase in PGI2 synthase activity in the vascular wall. Indeed, the averaged PGI2 generating capacity was closely correlated to the averaged PGI2 synthase activity in DOCA-salt hypertensive rats and three lines of control rats. Incontrast, phospholipase C and phospholipase A2, both of which liberate arachidonate for PGI2 synthesis, were rather lowered in DOCA-salt hypertensive rats. These data clearly indicate that vascular PGI2 generation is increased in the development of DOCA-salt hypertension and that PGI2 synthase is mainly responsible for this enhancement. The increased PGI2 synthase may be relevant to the blood pressure elevation and is expected to have beneficial effects on the vascular protection in hypertension.

Animals↗
PubMed1991

Antihypertensive effects of cicletanine and renal protection in Dahl salt-sensitive rats.

We designed experiments to reveal the antihypertensive properties of cicletanine, a novel antihypertensive drug, in Dahl salt-sensitive (Dahl-S) rats. Cicletanine (39 mg/kg body weight per day for 6 weeks) ameliorated the development of hypertension in Dahl-S rats fed a high-salt (4% NaCl) diet. This blood pressure reduction was associated with a decrease in heart weight and vascular wall thickness. Moreover, urinary prostacyclin (PGl2) excretion was increased with cicletanine treatment, being inversely related to systolic blood pressure. Proteinuria and urinary excretion of n-acetyl-beta-D-glucosaminidase were decreased and glomerular filtration rate was increased with this treatment. Morphological investigation revealed an improvement in glomerulosclerosis, renal tubular damage and intrarenal arterial injury in the salt-induced hypertensive rats. In contrast, trichloromethiazide, which decreased blood pressure to the same extent as cicletanine, lowered urinary PGl2 excretion and generally did not ameliorate the deteriorated renal functions and morphological abnormalities. Thus, these data indicate that cicletanine ameliorates the development of hypertension in Dahl-S rats and protects the cardiovascular and renal systems against the injuries seen in the hypertension. The enhanced vasodepressor PGl2 synthesis probably participates, to some extent, in these beneficial properties of long-term cicletanine treatment.

Animals↗
PubMed1991

Evidence for medial-mass regression in the vascular wall of Dahl hypertensive rats by cicletanine treatment.

We designed experiments to investigate the effects of cicletanine, a novel antihypertensive drug, on medial hypertrophy in Dahl rats susceptible to salt-induced hypertension (Dahl S rats). Cicletanine treatment (500 mg of cicletanine/kg of chow) for 6 weeks lowered blood pressure by 19% in Dahl S rats challenged with a high-salt (4%) diet. The blood pressure reduction was associated with a significant decrease in weight of the aortic vessels. Morphological examination revealed that this treatment decreased medial hypertrophy and expansion of intimal tissue, in concert with resolution of the periarteritis in the intrarenal arteries. In fact, the content of actin in the aortic wall, analyzed by SDS-PAGE, was decreased significantly with this treatment and myosin content was reduced to the same extent as well. Moreover, cicletanine per se lowered protein synthesis in randomly cycling cultured vascular smooth muscle cells (VSMCs) from Sprague-Dawley rats. Actin formation by VSMCs was decreased with cicletanine. Thus, these data indicate that chronic cicletanine treatment produces regression of the medial hypertrophy in Dahl S rats. Direct inhibitory effects on cytoskeleton protein synthesis, as well as its antihypertensive action, are partly responsible for this regression in vivo.

Animals↗
PubMed1991

Antiproliferative effects of the serotonin type 2 receptor antagonist, ketanserin, on smooth muscle cell growth in rats.

We defined the role of a serotonin type 2 receptor antagonist, ketanserin, in the growth of aortic vascular smooth muscle cells (VSMCs) from Wistar rats, using cell culture and cell synchrony methods. Deoxyribonucleic acid (DNA) replication in the G0/G1- or G1/S-synchronized VSMCs was assessed by [3H]thymidine uptake into DNA. Ketanserin at 2 x 10(-5) M significantly decreased the thymidine uptake by 48% in the proliferating VSMCs, whereas methysergide, a nonspecific serotonin inhibitor, unaffected the thymidine uptake. Ketanserin at 10(-5) M did not influence the duration of the G1 resting period. However, this dose of ketanserin significantly lowered DNA replication in the DNA synthetic (S) period in a dose-dependent manner. Neither methysergide nor the alpha 1-adrenoceptor antagonist, prazosin, affected DNA synthesis in the S period. Ketanserin exhibits antiproliferative effects on rat VSMC growth probably through the suppression of DNA replication in the S phase. This property would also contribute to the vascular protective effects of ketanserin with its well-documented antihypertensive action.

Animals↗
PubMed1991

[An optimum dose-finding study of HR810 (CPR) in chronic respiratory tract infections].

In order to determine the optimal dose of cefpirome sulfate (HR810, CPR) against respiratory tract infections (RTI), an optimal dose-finding study was conducted on cases of chronic RTI, and the clinical properties of the drug were compared with those of ceftazidime (CAZ). Inpatients with chronic RTI were randomly assigned to 3 groups: an HR 0.5 g group, receiving 0.5 g X 2/day of CPR an HR 1.0 g group, receiving 1.0 X 2/day of CPR and a CAZ group, receiving 1.0 g X 2/day of CAZ. As a rule, the drugs were administered by intravenous drip infusion for 14 days, after which period clinical efficacy, bacteriological response, safety, and utility were investigated. Of the total 121 cases, 106 were subject to analysis of clinical efficacy, including 38 cases in the HR 0.5 g group, 32 in the HR 1.0 g group, and 36 in the CAZ group. Efficacy rates in the assessment by the committee were 84.2% for the HR 0.5 g group, 75.0% for the HR 1.0 g group, and 86.1% for the CAZ group, without any significant difference between the 3 groups. The bacterial elimination rates were 73.9%, 75.0% m and 88.5%, respectively, without any significant difference between the 3 groups. Associated reactions were noted in 2 of 36 cases in the HR 1.0 g group (eruption and diarrhea), but not in the other 2 groups. The incidence of abnormal clinical laboratory findings was 23.1% in the HR 0.5 g group, 22.2% in the HR 1.0 g group, and 22.5% in the CAZ group, without any significant difference between the 3 groups. Utility rates were 84.2% for the HR 0.5 g group, 74.2% for the HR 1.0 g group, and 86.1% for the CAZ group, without any significant difference between the 3 groups. The HR 0.5 g and 1.0 groups showed no difference in clinical efficacy, bacteriological response, safety, and utility against RTI, and the results of both groups were about equal to those of the CAZ group.

Adolescent↗
PubMed1991

Slope of human left ventricular end-systolic force-length relation is independent of myocardial length.

We have introduced a new contractility index (Ec), i.e., the slope of the left ventricular (LV) end-systolic force-length (Fes-Les) relation. To examine whether Ec was dependent on the LV wall myocardial length, 16 normal hearts of human subjects were evaluated to determine the LV end-systolic force-dimension (Fes-Des) and pressure-dimension (Pes-Des) relations (dimension denotes the distance between the LV septum and posterior wall). LV end-systolic pressures and dimensions were estimated simultaneously by intra-arterial cannulation and LV echocardiography. In seven subjects, the effect of a dobutamine infusion was also assessed. The Fes-Des relation was found to be nearly linear. Slopes and extrapolated dimension intercepts were obtained for the LV Fes-Des and Pes-Des relations [Ec, slope of LV Pes-Des relation (Es), and extrapolated dimension intercept of LV Fes-Des (Do), and of Pes-Des relation (D'o), respectively]. Es showed a hyperbolic relation to the baseline LV Des, whereas Ec was unrelated to it. The average variation for Ec (9.5%) was smaller than that for Es (22.5%). Dobutamine infusion increased Ec, Es, and D'o, whereas Do was not changed. Thus the assumption of linearity of the LV Fes-Les relation was found to be reasonable in normal human hearts. Do appears to provide a more accurate parameter than D'o for estimating the actual unstressed myocardial length, whereas Ec could possibly serve as an index of LV wall performance in the normal human heart that is independent of myocardial length and nearly constant between individuals.

Adult↗