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Biomedical subjects

O Iimura

Publications and source records attributed to O Iimura.

At least 109 records · Page 6Linked to original sources
PubMed1992

Bartter's syndrome with gouty arthritis.

A 45-year-old woman with Bartter's syndrome complicated with gouty arthritis is reported. Bartter's syndrome was diagnosed from hypokalemia, metabolic alkalosis, high plasma renin activity, normal blood pressure and attenuated pressor response to exogenous angiotensin II infusion. Serum uric acid was 11.8 mg/dl, the renal clearance of uric acid was low (3.0 ml/min) and fractional excretion of uric acid (FEUA) was 7.0%, being the lower limit of the normal range. Fractional excretion of phosphate was low (5.3%) and fractional free water clearance per fractional distal sodium delivery was 0.51. The mechanism of hyperuricemia in this case is discussed.

Arthritis, Gouty↗
PubMed1992

Hypocalcemic cardiomyopathy in a patient with idiopathic hypoparathyroidism.

An idiopathic hypoparathyroidism-induced cardiomyopathy patient had severe long-lasting hypocalcemia. The dramatic improvement of cardiac function with correction of only the serum calcium concentration could be quantitatively demonstrated on both echocardiogram and ventriculogram. The concentration of the extracellular calcium ion was considered to have a direct effect on the strength of the myocardial contraction through excitation-contraction coupling. Furthermore, elevated serum creatine phosphokinase and lactate dehydrogenase levels which were thought to be delivered from skeletal muscle returned to the normal range concomitant with the correction of hypocalcemia. The serum calcium concentration and these enzyme level showed significant inverse correlations.

Cardiomyopathies↗
PubMed1992

Isolated post exercise delayed ST depression as a sign of severe ischemia: the influence of percutaneous transluminal coronary angioplasty.

The clinical implications of isolated late recovery ST depression were tested in patients with scintigraphically defined ischemia (coronary artery disease [CAD], n = 18) compared with patients without ischemia (n = 25). Spontaneous (78.4 versus 12.0%, P < 0.008) and exercise-induced angina (44.4 versus 0%, P < 0.0001) were more frequently seen in patients with CAD. Histories of unstable angina (33.3%), prior myocardial infarction (27.8%), ST elevated angina (22.2%) and significant stenosis in the left anterior descending artery (17 of 18, 94.4%) were almost exclusively seen in the CAD group. There was no significant difference between the two groups in capacity for exercise, maximum deviation of ST level or TV2 amplitude. Balloon angioplasty abolished late recovery ST changes in 63.6% of CAD patients. These results suggest that isolated late recovery ST depression, when accompanied with typical chest pain, may be considered as an indicator of myocardial ischemia, but this phenomenon is difficult to distinguish electrocardiographically.

Adult↗
PubMed1992

The renal kallikrein-kinin system at the prehypertensive stage of hypertension.

In essential hypertension, renal dopaminergic activity and PGE2 was suppressed as was the renal kallikrein-kinin system. The suppression of the renal depressor systems may play an important role in the etiology of hypertension through sodium and body fluid retention. At the prehypertensive stage of essential hypertension, renal dopaminergic activity was suppressed, which induced the retention of body fluids and sodium. On the other hand, the renal prostaglandin E2 was augmented, and it seemed to be a compensatory mechanism for sodium retention. We could not confirm the suppression of the renal kallikrein-kinin system at the prehypertensive stage of hypertension. Although all renal depressor systems are suppressed in essential hypertension, the suppression of the renal kallikrein-kinin system and PGE2 seem to be very important in the etiology of hypertension. Further study is necessary to clarify when both systems are suppressed.

Animals↗
PubMed1992

Activation of kinins on myocardial ischemia.

In experimental ischemic dog heart with coronary-constriction, no increase of coronary blood flow, Max dP/dt or MVO2 with no change of kinin in arterial blood were exhibited. Following sympathetic nerve stimulation, remarkable increases of kinin in coronary sinus blood were observed with a significant elevation of left ventricular end-diastolic pressure and an augmented production of lactate from the heart as well as an ischemic change of ECG-ST. Infusion of kinin into the left main coronary artery resulted in no change in the mean systemic blood pressure, coronary blood flow, coronary vascular resistance, cardiac function, myocardial metabolism or ECG-ST in the control and coronary-constricted groups. These data suggest that kinin was released significantly from the ischemic heart, however, such a level of kinin has no significant effect on coronary circulation or myocardial metabolism. In ischemia-reperfusion rabbit hearts, no significant influence of the ACE inhibitors, captopril and ramiprilat, were observed. Species differences may be responsible for the beneficial role of ACE inhibitors in the limitation of infarct size in the dog hearts, possessing collateral flow, that are not seen in the rabbit heart with poor collateral flow.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

[Effects of intravenously infused magnesium on renal calcium metabolism and plasma parathyroid hormone in patients with essential hypertension].

This study aimed to elucidate the effects of intravenously infused magnesium on renal calcium and sodium metabolism in patients with essential hypertension. Mean arterial pressure (MAP), heart rate (HR), urine volume (UV), endogenous creatinine clearance (Ccr), urinary excretion of calcium (UCaV) and sodium (UNaV), fractional excretion of calcium (FECa) and sodium (FENa), plasma ionized calcium (pCa2+) and parathyroid hormone(PTH) were measured before and after intravenous infusion of 10% magnesium sulfate (initial dose: Mg 13.5mg/m2.BSA/15 min.: maintenance dose: Mg 2.7mg/m2.BSA/105min) in 6 normotensive subjects (NT) and 13 mild-to-moderate essential hypertensives (EHT). After the magnesium infusion, significant increases of UV, UCaV, UNaV, FECa and FENa, and a significant decrease of PTH were observed in both NT and EHT while MAP and HR did not change in either group. PCa2+ significantly decreased and Ccr tended to increase only in EHT. Although no significant difference was found in the change in Ccr (delta Ccr) or PTH (delta PTH) between NT and EHT, the changes of UCaV (delta UCaV), UNaV (delta UNaV), FECa (delta FECa) and FENa (delta FENa) were greater in EHT than each in NT. A positive correlation was found between delta UCaV and delta FECa, as well as delta UCaV and delta Ccr, but the former was more remarkable in both groups. In addition, delta UCaV was positively correlated with delta FENa in EHT, but not in NT. No significant relationship was observed between delta UCaV and delta PTH in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium↗
PubMed1992

[A case of idiopathic chronic interstitial nephritis progressed to renal failure without proteinuria nor hematuria].

A case of idiopathic interstitial nephritis who underwent to chronic renal failure without history of hematuria nor proteinuria is discussed. A 46 years old woman who showed gradually elevation of serum creatinine (1.3-2.5 mg/dl) admitted on our hospital. On occasions of pregnancy, health examination or hospital visit, she has never been pointed out hematuria nor proteinuria. Immunological disorders such as SLE, metabolic diseases, urinary tract obstruction and chronic urinary tract infection were excluded by the examinations after admission. Because of the severe enzymuria (beta 2-microglobulin, N-acetyl glucosaminidase), chronic interstitial nephritis was considered, and renal biopsy was performed. Severe tubulointerstitial changes were observed histologically, however, glomerular damage was comparatively mild. From these results, she was diagnosed idiopathic chronic tubulointerstitial nephritis. In this case, hematuria and proteinuria were absent until severe renal dysfunction. This may be caused by that inflammation was located to the tubulointerstitial area. The observation of enzymuria seemed to be important to diagnosis and follow-up of the interstitial nephritis.

Chronic Disease↗
PubMed1991

[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↗
PubMed1991

[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↗
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

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↗
PubMed1991

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↗
PubMed1991

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↗