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Biomedical subjects

O Iimura

Publications and source records attributed to O Iimura.

At least 37 records · Page 2Linked to original sources

[The role of the renal dopaminergic and the prostaglandin systems in renal uric acid metabolism in patients with essential hypertension].

The present study aimed to elucidate the role of renal dopaminergic and prostaglandin (PG) systems in renal uric acid metabolism in essential hypertension. Mean arterial pressure (MAP), heart rate (HR), endogenous creatinine clearance (Ccr), serum uric acid (SUA), urinary excretions of uric acid (UUAV) and sodium (UNaV), fractional excretions of uric acid (FEUA) and sodium (FENa), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were measured before and after intravenous injection of a dopamine receptor antagonist, metoclopramide (MCP: 8 mg/m2.BSA), or before and after a single oral administration of prostaglandin synthesis inhibitor, indomethacin (IM: 75 mg), in 34 mild-to-moderate essential hypertensives (EHT). MCP injection or acute oral administration of IM caused significant decreases of UNaV and FENa in each group, whereas MAP, HR and SUA did not change in either group. Significant decreases in Ccr, UUAV and FEUA and increases in PRA and PAC were demonstrated by MCP injection, while no significant changes in these parameters were revealed by IM administration. There was a significant positive correlation between delta UUAV and delta Ccr or delta FEUA in both groups. In addition, a close positive correlation between delta UUAV and delta UNaV as well as between delta FEUA and delta FENa was found in the MCP group, but not in the IM group. On the other hand, no significant correlation was observed between delta UUAV and delta PRA or delta PAC in either MCP or IM administration. The decreases of UUAV and FEUA were significantly greater in MCP than in IM administration, despite similar changes in Ccr, UNaV and FENa between the two procedures. These data suggest that the endogenous renal dopaminergic system may contribute to renal uric acid metabolism, which is rather closely related to sodium handling in essential hypertension than the prostaglandin system. Furthermore, the attenuated renal dopaminergic activity may contribute to the elevation of serum uric acid level in patients with essential hypertension.

Adult

[The role of hyperinsulinemia on the renal mechanism of hyperuricemia in overweight patients with essential hypertension].

The aim of the present study was to investigate the role of insulin on the renal mechanism of hyperuricemia in overweight patients with essential hypertension. Thirty-four essential hypertensives(EHT), receiving a regular diet containing 120mEq of sodium, 75mEq of potassium and 2000 kilocalories daily, were divided into two groups of non-obese(NHT) and obese(OHT) EHT. NHT as categorized as a body mass index (BMI) less than, and OHT as a BMI equal to or more than, 25 kg/m2 in male patients and 24 kg/m2 in female patients. In the early morning after overnight fast, renal uric acid and sodium clearance were examined while the patients remained in a supine position. During the two-hour clearance period, mean arterial pressure(MAP), heart rate(HR), endogenous creatinine clearance(Ccr), immunoreactive insulin(IRI), serum uric acid(SUA), fractional excretion of uric acid(FEUA) and sodium(FENa) were measured. Although there were no significant differences in age, MAP, HR, Ccr, nor SUA between the two groups, a higher ratio of female to male patients was found in OHT than in NHT. On the other hand, higher SUA and IRI and lower FEUA and FENa were observed in OHT than in sex-and Ccr-matched NHT. SUA was negatively correlated with FEUA in all patients (r = -0.392, p less than 0.05) and in NHT (r = -0.553, p less than 0.05), unlike in OHT. A significant negative correlation between BMI and FEUA was revealed in all EHT (r = -0.441, p less than 0.01) and in OHT (r = -0.597, p less than 0.01) but not in NHT. FEUA was positively correlated with FENa in all EHT (r = 0.554, p less than 0.001) as well as in NHT (r = 0.548, p less than 0.05) and OHT (r = 0.507, p less than 0.05). Moreover, there was a significant negative correlation between IRI and FENa in all EHT (r = -0.361, P less than 0.05) and in OHT (r = -0.470, p less than 0.05). However, no significant relation was demonstrated between IRI and SUA or FEUA in NHT or OHT. From these results, it is concluded that an attenuated renal excretion of uric acid related to natriuretic ability may play an important role in hyperuricemia in EHT. However, the role of hyperinsulinemia, which contributes to the blunting of natriuresis, might be relatively small in the renal mechanism of hyperuricemia in EHT, particularly in OHT.

Female

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

Adenosine infusion during early reperfusion failed to limit myocardial infarct size in a collateral deficient species.

STUDY OBJECTIVE: Intracoronary or intravenous adenosine during reperfusion in combination with lignocaine may attenuate "reperfusion injury" and limit myocardial infarct size in the canine heart. The aim of this study was to test whether intravenous adenosine also protects myocardium in the rabbit heart, which lacks xanthine oxidase and significant coronary collaterals in contrast to the canine heart. DESIGN: Five groups of rabbits underwent a 30 min occlusion of the circumflex coronary artery, followed by reperfusion. In adenosine treated groups, either a high dose of adenosine (0.37 mg.kg-1.min-1) with lignocaine treatment (5 mg intravenously 1 min before coronary occlusion and before reperfusion) or a low dose (0.15 mg.kg-1.min-1) of adenosine with or without lignocaine was infused for 60 min starting 5 min before the onset of reperfusion. Group 1 was untreated, while group 2 received a high dose of adenosine with lignocaine. These groups were reperfused for 3 h. Group 3 was untreated, group 4 received a low dose of adenosine, and group 5 a low dose of adenosine and lignocaine. These groups were reperfused for 72 h. EXPERIMENTAL MATERIAL: 60 anaesthetised open chest rabbits were used. Groups 1 and 2 were killed after 3 h coronary reperfusion. Groups 3, 4, and 5 recovered from surgery for 72 h and were then killed for further study. MEASUREMENTS AND MAIN RESULTS: The high dose of adenosine reduced mean blood pressure to 44% of baseline value and diminished reactive hyperaemia in the area at risk by "coronary steal". The low dose of adenosine did not significantly alter systemic blood pressure or heart rate. Infarct size did not differ between groups 1 and 2, at 39.7(SD 20.1)% of area at risk v 33.2(15.9)% (by tetrazolium staining), nor between groups 3, 4, and 5: 50.3(12.6)% v 52.7(15.6)% v 47.8(9.3)% (by histology). CONCLUSION: Neither a high dose nor a low dose of adenosine limited myocardial infarct size in the rabbit heart even when adenosine was combined with lignocaine treatment.

Adenosine

Myocardial infarct size-limiting effect of ischemic preconditioning was not attenuated by oxygen free-radical scavengers in the rabbit.

BACKGROUND: The limiting effect of ischemic preconditioning on infarct size has been reported in canine hearts, which contain considerable amounts of xanthine oxidase, a free radical-producing enzyme. Furthermore, a recent study suggested that free radicals generated during preconditioning may contribute to the cardioprotective effect of preconditioning. The present study examined 1) whether preconditioning limits infarct size in rabbits, which, like humans, lack myocardial xanthine oxidase and 2) whether the cardioprotective effect of PC is mediated by free radicals. METHODS AND RESULTS: A branch of the circumflex coronary artery in rabbits was occluded for 30 minutes and then reperfused for 72 hours. Myocardial infarct size and area at risk were determined by histology and fluorescent particles, respectively. Five groups were studied: an untreated control group, a preconditioned group (PC group), a high-dose superoxide dismutase (SOD)-treated preconditioned group (high-dose SOD-PC group), a low-dose SOD-treated preconditioned group (low-dose SOD-PC group), and a SOD-plus-catalase-treated preconditioned group (SOD/CAT-PC group). Preconditioning was performed with four episodes of 5 minutes of ischemia and 5 minutes of reperfusion. The free radical scavengers (30,000 units/kg SOD for high-dose SOD-PC group, 15,000 units/kg SOD for low-dose SOD-PC group, and 30,000 units/kg SOD plus 55,000 units/kg catalase for SOD/CAT-PC group) were infused intravenously over 60 minutes starting 20 minutes before preconditioning. Infarct size as the percentage of area at risk was 45.1 +/- 3.5% (mean +/- SEM) in the control group (n = 11), 13.3 +/- 3.0% in the PC group (n = 12), 9.7 +/- 1.8% in the high-dose SOD-PC group (n = 8), 11.9 +/- 2.2% in the low-dose SOD-PC group (n = 6), and 9.6 +/- 2.3% in the SOD/CAT-PC group (n = 6) (p less than 0.05 versus control for the last four values). The differences in infarct size as the percent of area at risk among the PC, high-dose SOD-PC, low-dose SOD-PC, and SOD/CAT-PC groups were not significant. CONCLUSION: Ischemic preconditioning delays ischemic myocardial necrosis regardless of myocardial xanthine oxidase content. Free radicals are unlikely to have a major role in the mechanism of the preconditioning in rabbits.

Animals

Does myocardial stunning contribute to infarct size limitation by ischemic preconditioning?

BACKGROUND: The mechanism through which ischemic preconditioning causes cardioprotection is unknown. The present study investigated the role of stunning in preconditioning. METHODS AND RESULTS: We studied three different protocols of preconditioning: two cycles of 2-minute ischemia separated by 5-minute reperfusion (2'PC), one cycle of 5-minute ischemia by 5-minute reperfusion (5'PC1), and two cycles of 5-minute ischemia separated by 5-minute reperfusion (5'PC2). In the first series of experiments, the stunning associated with 2'PC, 5'PC1, or 5'PC2 was assessed using an epicardial Doppler transducer in anesthetized open-chest rabbits. The thickening fraction (percent baseline) of the preconditioned region was 76.8 +/- 7.2% (mean +/- SEM) after 2'PC but 31.4 +/- 9.2% and 34.3 +/- 9.7% after 5'PC1 and 5'PC2, respectively, which were significantly lower, thus indicating more severe stunning than that after 2'PC. In the second series of experiments, a branch of the left circumflex artery was occluded for 30 minutes and then reperfused for 72 hours in four groups of rabbits. One group was not preconditioned and three groups were preconditioned with 2'PC, 5'PC1, or 5'PC2 protocols before the 30-minute ischemia. In contrast to the differences observed in the stunning in the first series of experiments, histological infarct size was similar in the three preconditioned groups (21.1 +/- 3.0% of area at risk after 2'PC, 20.1 +/- 3.4% after 5'PC1, 16.4 +/- 4.2% after 5'PC2), all of which were significantly smaller than that in the unpreconditioned group (43.9 +/- 5.0%). The third series of experiments examined the degree of stunning by 2'PC, 5'PC1, or 5'PC2 and the size of infarct (tetrazolium staining) in the same animal after 30-minute ischemia/3-hour reperfusion; again, the results showed no significant correlation between degree of stunning and infarct size. CONCLUSIONS: The myocardial infarct size-limiting effect of preconditioning did not correlate with the degree of myocardial stunning accompanying preconditioning. Thus, it is unlikely that myocardial stunning contributes to the cardioprotective effect of ischemic preconditioning.

Animals

Inhibition of thromboxane A2 synthetase failed to limit myocardial infarct size in a rabbit ischemia-reperfusion model.

The role of thromboxane A2 (TXA2) in myocardial necrosis during coronary occlusion and reperfusion was investigated by using a new long-acting TXA2 synthetase inhibitor, DP1904. A rabbit coronary branch was occluded for 30 min and then reperfused for 72h. Infarct size and area at risk were determined histologically and by fluorescent particles, respectively, for 4 groups; a saline receiving control group (C group), a DP1904 treated group (DP group), a heparin treated group (H group), and a DP1904 plus heparin treated group (DP-H group). The H group and DP-H group were included to examine the influence of heparinization on the effect of DP1904. In the DP and DP-H groups, 10 mg/kg of DP1904 was injected i.v. 2h before coronary occlusion, as well as 24 and 48h after reperfusion. This dose of DP1904 (10 mg/kg i.v.) was able to inhibit serum thromboxane B2 formation ex vivo to 1.1% of the control level 2h after its administration, and to 39.5% at 24h, in the rabbit (n = 5). The H and DP-H groups received 1000 units of heparin i.v. 3 min prior to coronary occlusion. The size of the area at risk, heart rate, blood pressure, and rate-pressure products were comparable between the 4 groups. Mortality was not significantly different in any group. Myocardial infarct size as the percentage of area at risk was 43.6 +/- 3.9% in C group (n = 10), 41.1 +/- 4.4% in DP group (n = 9), 47.8 +/- 3.0% in H group (n = 13), and 44.7 +/- 4.0% in DP-H group (n = 10), which were not significantly different. These findings suggest that TXA2 does not contribute directly to myocardial necrosis during coronary occlusion and reperfusion in the rabbit.

Animals

A case of congenital left ventricular diverticulum with pulmonary stenosis and its scintigraphic characteristics.

We encountered a 31-year-old female patient with mild valvular pulmonary stenosis who had no abnormality in the electrocardiogram but pulmonary dilatation in the chest radiograph. Two-dimensional echocardiography and magnetic resonance imaging demonstrated two small protrusions at the interventricular septum indicating diverticula. Large perfusion defects were observed at the anterior wall in the thallium-201 myocardial tomograms. Short axial and vertical long axial images by ECG-gated blood pool tomography revealed an out-pouching best seen during diastole and a good contraction during systole in the corresponding areas. These findings suggested the presence of thin but normal myocardium in the anterior wall, i.e. a muscular type of left ventricular diverticulum. The presence of the muscular type of left ventricular diverticulum at the anterior and septal walls was confirmed by contrast left ventriculography. A congenital diverticulum at the anterior and septal walls with pulmonary stenosis is very rare. Furthermore, its scintigraphic images were quite characteristic and useful for its diagnosis.

Adult

[The coefficient of variation of RR intervals (CVRR) on electrocardiogram in patients with essential hypertension with reference to aging, hemodynamics and sympatho-adrenomedullary function].

To evaluate the significance of parasympathetic nerve activity in essential hypertension, we measured the coefficients of variation of RR intervals (CVRR) on electrocardiogram and examined the relationships between CVRR and aging, hemodynamics and sympatho-adrenomedullary function in normotensive subjects (NT) and in patients with essential hypertension (EHT). Mean arterial pressure (MAP), heart rate (HR), plasma noradrenaline concentration (pNA), plasma adrenaline concentration (pAd) and CVRR resting in a supine position were simultaneously measured in 37 NT (33.8 +/- 2.0 years) and 47 mild-to-moderate EHT (51.3 +/- 1.5 years). In both NT and EHT, significantly negative correlations between CVRR and age (NT: r = -0.54, p less than 0.001, EHT: r = -0.41, p less than 0.005) were observed, however, CVRR correlated with neither MAP, HR nor pAd. CVRR tended to correlate negatively with pNA (r = -0.27, p less than 0.1) in NT, unlike in EHT. The mean value of CVRR in EHT (n = 10, age: 38.3 +/- 1.6 years, CVRR: 3.61 +/- 0.37%) was significantly (p less than 0.005) lower than in age-matched NT (n = 10, age: 38.3 +/- 2.5 years, CVRR: 5.76 +/- 0.45%). These results indicate that the parasympathetic tone suggested by CVRR may be related to aging and sympathetic nerve activity, and that parasympathetic function might be impaired in EHT.

Adolescent

[Shy-Drager syndrome: its autonomic function, alpha 2 receptor density and mechanism of postprandial hypotension].

The autonomic function, platelet alpha 2 receptor (alpha 2R) density, and mechanism of postprandial hypotension were examined in a 58-year-old man with Shy-Drager syndrome (SDS). His chief complaints were orthostatic syncope and impotence. His blood pressure was kept within normal limits in a supine position, but severe hypotension and fainting occurred when he assumed an upright posture. There were diminished sweating response to warm stress, abnormal pupil reactions to drugs, lack of blood pressure elevation at phase IV during the Valsalva maneuver, and a lack of pressor response to hyperventilation and cold stress. The plasma norepinephrine levels (pNE) were very low in a supine position at rest and in a head-up tilt position. Severe blood pressure fall (hypotension) associated with a lack of pNE elevation occurred during an oral glucose tolerance test (oGTT). Platelet alpha 2R density increased and the pressor response to infused norepinephrine (NE-R) was pronounced. The heart rate response to injected atropine was clearly attenuated. The coefficient of the R-R interval variation in the ECG (CVRR), which may reflect parasympathetic activity, was markedly low at rest. In addition, a decrease in a head-up tilt position and increase during oGTT also resolved. These results indicate that a dysfunction of the parasympathetic and sympathetic nervous systems and the up-regulation in the alpha 2R system that leads to an increase in alpha 2R density in SDS are involved in this disease and that the mechanism of postprandial hypotension in SDS may be different from that in normal elderly subjects.

Atropine

Normalized left ventricular filling indexes to detect diastolic dysfunction in hypertension and in hypertrophic cardiomyopathy.

In order to establish a normalizing method for left ventricular filling indexes, peak filling rate (PFR) and time to peak filling rate (TPFR), derived from resting radionuclide ventriculography using Fourier analysis with third-order harmonics, were analyzed in 45 normal subjects, 40 hypertensive patients, and 29 patients with hypertrophic cardiomyopathy. PFR was significantly negatively correlated with age (r = -0.62) and significantly positively correlated with peak ejection rate (PER) (r = 0.58) in normals. TPFR normalized for heart rate (N-TPFR) was correlated positively with age in normals (r = 0.60) and hypertensives (r = 0.49) but not in patients with hypertrophic cardiomyopathy. N-TPFR was not significantly correlated with systolic parameters. A significant relationship between PFR normalized to PER (PFR/PER) and age was observed in normals (r = -0.58) but not in patients with hypertension or hypertrophic cardiomyopathy. To cancel the ageing effect, individual data of PFR/PER and N-TPFR were expressed as a percentage of the predicted regression value in normal subjects (%PFR/PER and %N-TPFR, respectively). Per cent PFR/PER was significantly lower and %N-TPFR was significantly greater in patients with hypertension and hypertrophic cardiomyopathy compared to normals. When normal limits of these indexes were defined as %PFR/PER greater than 80% and %N-TPFR less than 120%, the sensitivity, specificity and diagnostic accuracy of differentiating normals from patients with hypertension or hypertrophic cardiomyopathy were 41 of 45 (91%), 44 of 68 (65%), and 85 of 113 (75%), respectively. These findings indicate that %PFR/PER and %N-TPFR might be more reasonably normalized parameters for describing diastolic filling and its abnormality.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent

Myocardial accumulation of monoclonal antimyosin Fab in hypertrophic cardiomyopathy and postpartum cardiomyopathy.

Indium-111-antimyosin Fab scan was performed in patients with hypertrophic and postpartum cardiomyopathies to assess whether or not myocardial damage can be delineated. In two patients with hypertrophic cardiomyopathy, intense and diffuse antimyosin uptake was observed, although there was no evidence of acute myocardial damage or wall motion abnormality. A patient with postpartum cardiomyopathy showed a dense and relatively localized accumulation in the left ventricular anterior wall in association with thallium perfusion and wall motion abnormalities. Thus, antimyosin scanning can delineate not only manifested but also subclinical myocardial damage in hypertrophic and postpartum cardiomyopathies which may not be detectable by other techniques.

Adult

Effect of prednisolone on myocardial infarct healing: characteristics and comparison with indomethacin.

OBJECTIVE: To characterize retardation of myocardial infarct healing by corticosteroid administration, and to examine the role of suppression of prostaglandin production in its effect. DESIGN: The left circumflex coronary artery of the rabbit was occluded for 30 mins and reperfused for 72 h. Rabbits were divided into four groups: a control group, a low dose prednisolone group (L-PSL) that was treated with 5 mg/kg/24 h prednisolone, a high dose prednisolone group (H-PSL) that was treated with 10 mg/kg/24 h prednisolone, and an indomethacin group that received a 5 mg/kg intravenous bolus of indomethacin followed by 10 mg/kg/24 h. The status of infarct healing and infarcted wall thinning was assessed 72 h after ischemia by the percentage of infarct mass organized (%O/I) and the ratio of infarcted wall thickness to noninfarcted wall thickness (thinning ratio). MAIN RESULTS: The %O/I was 61.4 +/- 4.2% (mean +/- SEM) in the control group. The L-PSL and H-PSL groups had %O/Is of 48.3 +/- 3.7% and 29.1 +/- 2.1%, respectively, which were significantly lower than the control value. The difference in %O/I between the H-PSL and L-PSL groups was also significant. However, the %O/I of the indomethacin group (55.1 +/- 3.3%) was not significantly different from control. When the myocardial infarcts were retrospectively subgrouped into small infarcts (infarct volume less than 0.31 cm3) and large infarcts (greater than or equal to 0.31 cm3), infarct healing delay in large infarcts was evident only for H-PSL and not for L-PSL, while both L-PSL and H-PSL treatment retarded healing of small infarcts. No significant difference was observed in the thinning ratio for any group. CONCLUSION: Infarct healing delay by prednisolone is dosage dependent, and smaller infarcts may be more sensitive to its effect. Retardation of infarct healing by prednisolone is unlikely to be mediated by suppression of prostaglandins from the cyclo-oxygenase pathway.

Animals

Acute thrombocytopenia after intravenous infusion of radiographic contrast medium.

Acute thrombocytopenia due to intravenous infusion of radiographic contrast media is extremely rare. We report the first such case in Japan. A 52-year-old male was admitted to hospital because of right ureteral stone. Two hours after drip infusion pyelography, the patient experienced chills and fever. It was shown that his platelet count had decreased abruptly from 233,000 to 8000/mm3. Platelet associated immunoglobulin was not detected. An in vitro test for platelet aggregation by contrast media was negative. Following infusion of hydrocortisone, the platelet count recovered to a normal level within several days.

Blood Platelets

[Correlations between the coefficient of variation of RR intervals and sympathetic nerve activity following superior tilting in normotensive subjects and in patients with essential hypertension].

The relationship between changes in sympathetic nerve activity and those in parasympathetic tone with a change in position was investigated in patients with essential hypertension using the coefficient of variation of RR intervals on electrocardiograms (CVRR). Mean arterial pressure (MAP), heart rate (HR), plasma noradrenaline concentration (pNA) and CVRR were measured in a supine position at rest and 20 min after having the head tilted 60 degrees superiorly in 10 normotensives (NT: 51.9 +/- 3.0 yrs) and 7 essential hypertensive patients (EHT: 51.0 +/- 2.8 yrs). After changing the position, CVRR decreased significantly in the NT, but not in the EHT; whereas, significant increases of both HR and pNA without significant changes in MAP were shown in both groups. A significant negative correlation between percentage changes in CVRR (% delta CVRR) and pNA (% delta pNA) were observed in the NT, but not in the EHT. However, there was no relationship of % delta CVRR to % delta MAP or to % delta HR in either group. It was suggested from the changes in CVRR that suppression of the parasympathetic tone, which occurs in the NT group corresponding to sympathetic augmentation to present a decrease in blood pressure with a change in position, may be impaired in the EHT group.

Blood Pressure