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Biomedical subjects

O Iimura

Publications and source records attributed to O Iimura.

At least 91 records · Page 5Linked to original sources
PubMed1990

Does verapamil limit myocardial infarct size in a heart deficient in xanthine oxidase?

1. The delay of ischaemic myocardial necrosis by verapamil has been reported in the dog heart, which contains a high level of xanthine oxidase, a potential source of cytotoxic free radicals. To test whether the retardation of ischaemic myocyte death by verapamil is not an isolated phenomenon in the xanthine oxidase rich heart, we assessed the effect of verapamil in the rabbit heart, which lacks xanthine oxidase. 2. Verapamil (200 micrograms/kg, i.v. bolus plus 40 micrograms/kg per min) was administered in a group of rabbits (n = 5) to test the haemodynamic response to this agent. The heart rate, blood pressure and left ventricular dp/dt max were reduced by 11, 25 and 57%, respectively, and the plasma concentration of verapamil was maintained at 300-400 ng/mL during the infusion. 3. In other groups of rabbits, the effect of the same dosage of verapamil on the size of myocardial infarct after 20 or 30 min ischaemia and 72 h reperfusion was examined. The verapamil was administered for 45 min, starting 15 min prior to ischaemia. The percentage of area at risk infarcted (%I/AAR) was 15.2 +/- 3.9% in the 20 min ischaemia control group and 15.4 +/- 4.5% in the 20 min ischaemia verapamil group, 49.1 +/- 3.4% in the 30 min ischaemia control group and 41.2 +/- 3.3% in the 30 min ischaemia verapamil group. The %I/AAR was significantly smaller in the 20 min ischaemia control groups and 15.4 +/- 4.5% in the 20 min ischaemia there was no difference in %I/AAR between the control and verapamil treated animals in either the 20 or the 30 min ischaemia groups. 4. These results suggest that verapamil does not delay the transition from reversible to irreversible myocardial injury during coronary occlusion in the rabbit, which like the human, lacks myocardial xanthine oxidase.

Animals↗
PubMed1990

A malignant mixed mesodermal tumor of the uterine corpus with hypercatecholaminemia.

We report an unusual case of malignant mixed mesodermal tumor of the uterine corpus associated with various symptoms related to overproduction of catecholamine by the tumor cells. Histologically, the tumor was dominated by carcinomatous epithelium with foci of malignant mesenchyma. The type of epithelium was endometrioid with papillary adenocarcinomas containing foci of malignant squamous epithelium. The malignant mesenchyma consisted mainly of a fibrous stroma with many large and bizarre cells and spindle cells mimicking leiomyosarcoma, many of which were pleomorphic and contained large bizarre hyperchromatic nuclei. Foci of atypical adult-type cartilage and neoplastic osteoid formation were noted. In the tumor tissue, membrane-bound neurosecretory-type cytoplasmic granules were demonstrated by electron microscopy and polypeptide hormone synthesis was demonstrated by immunohistochemistry. Furthermore, the patient suffered frequent attacks of sudden hypertension with hypercatecholaminemia.

Carcinoembryonic Antigen↗
PubMed1990

Suppressed dopaminergic activity and water-sodium handling in the kidneys at the prehypertensive stage of essential hypertension.

1. In this study, the question of whether the suppression of the renal dopaminergic system is primary or not was investigated. 2. Renal dopaminergic activity was compared between young healthy normotensive subjects without a family history of hypertension (FH(-] and those with a family history of hypertension (FH(+]. 3. A significant decrease in urinary free dopamine excretion was noted, and the responses of urine volume, urinary sodium excretion, and fractional excretion of sodium to infused dopamine were significantly augmented in FH(+). In addition, a normal level of l-dopa delivery at the renal proximal tubules and a significant reduction in the conversion of l-dopa to dopamine in the kidney were found in FH(+). 4. These findings suggest that renal dopaminergic activity is already suppressed at the prehypertensive stage, and that the reduction in the conversion of l-dopa to dopamine in the proximal tubules may contribute to the attenuation of renal dopaminergic activity in FH(+).

Adult↗
PubMed1990

Angiotensin-converting enzyme inhibitors and the kallikrein-kinin system.

The role of plasma kinin in the hypotensive mechanism of angiotensin-converting enzyme (ACE) inhibitors in essential hypertensive patients and in a dog myocardiac ischemic model is discussed. Both an increase in plasma kinin and a decrease in plasma angiotensin II might contribute to the hypotensive effects of ACE inhibitors in a normal-renin group. In a low-renin group, the hypotensive mechanism of this drug may be mainly the increase in plasma kinin levels. The augmentation of urine volume and urinary sodium excretion may also be related to the hypotensive effects of ACE inhibitors, and this mechanism might be explained by the renal blood flow increase and augmented activity in the renal kallikrein-kinin system. In a dog myocardial ischemia model, when an apparent myocardial ischemia occurred in the constricted group, plasma kinin levels in coronary sinus blood increased significantly. Following infusion of kinin into the left main coronary artery, 0.1 ng/kg/min of kinin for 5 min did not cause any change in plasma kinin levels in the artery or coronary sinus. A dose of 10 ng/kg/min of kinin for 5 min produced a significant elevation in plasma kinin in the coronary sinus from 12.8 to 142 pg/ml without any change in plasma kinin in the artery. However, such a level of kinin had no significant effect on coronary circulation, myocardial metabolism, or ECG ST segment in either group. Thus, the role of increased kinin in this dog model still remains unclear. Further studies including the administration of ACE inhibitors or bradykinin antagonist will be necessary to reach conclusions about the role of kinin in the heart.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

Dopaminergic activity and water-sodium handling in the kidneys of essential hypertensive subjects: is renal dopaminergic activity suppressed at the prehypertensive stage?

To investigate whether the suppression of the renal dopaminergic system in hypertension is primary or secondary, renal dopaminergic activity was compared between young healthy normotensive subjects without a family history of hypertension [FH(-)] and those with a family history of hypertension [FH(+)]. A significant decrease in urinary dopamine excretion was recognized, and the responses of urine volume, urinary sodium excretion, fractional excretion of sodium, and urinary kallikrein and kinin activity to infused dopamine were significantly augmented in FH(+) subjects. In addition, a normal level of L-dopa delivery into the kidney and at the renal proximal tubules and a significant reduction of the conversion from L-dopa to dopamine in the kidney were found in FH(+) subjects. These findings suggest that renal dopaminergic activity is already suppressed at the prehypertensive stage, and a reduction in the conversion from L-dopa to dopamine in the proximal tubules may contribute to the attenuation of renal dopaminergic activity in FH(+) subjects.

Adult↗
PubMed1990

Hypertension and cardiovascular diseases in an epidemiological study in Hokkaido, Japan.

The present study describes the results from the 10-year follow-up data of a prospective epidemiological study for hypertension and cardiovascular diseases in two communities of rural agricultural districts in Hokkaido, Japan. The number of incidences of cerebrovascular accidents (CVAs) in persons who were normotensive, borderline hypertensive (BHT), untreated hypertensive (HT), well-controlled HT [blood pressure (BP) less than 150/90 mm Hg], and poorly controlled HT (BP greater than or equal to 150/90 mm Hg) were 0.46, 3.24, 4.17, 3.49, and 12.76 per 1,000 person-years. respectively: CVAs were markedly high in poorly controlled HT persons. The winter-summer mean BP differences in the first year were significantly and positively correlated with the differences in mean BP between the tenth and the first year, and were significantly higher in the progression to hypertension group than in the nonprogression group in both towns. Multivariate analysis indicated that the winter-summer mean BP difference was a significant variable for indication of progression to hypertension. From these results, we concluded that (a) good control of hypertension could considerably prevent CVA, (b) cold environment may contribute to the progression to hypertension, and (c) winter-summer variation in BP may predict the future course of BP.

Acute Disease↗
PubMed1990

Tissue-type plasminogen activator alone or in combination with thromboxane A2 synthetase inhibitor for ischemic myocardium.

Although the efficacy of tissue-type plasminogen activator (t-PA) for coronary thrombolysis is well established, its direct cardioprotective effect - independent of its thrombolytic effect - is still controversial. In addition, the potentiation of t-PA's direct cardioprotective effect by thromboxane A2 synthetase inhibitor has recently been reported. In this study, the authors examined whether t-PA alone or in combination with DP1904, a thromboxane A2 synthetase inhibitor, is able to salvage ischemic myocardium via a direct action on myocardium. In addition, the effect of these interventions on intramyocardial hemorrhage in reperfused infarcts was assessed. A branch of the coronary artery of the rabbit was occluded for 30 mins and then reperfused for 72 h. Myocardial infarct size and 'area at risk' were determined by histology and fluorescent particles, respectively. The extent of intramyocardial hemorrhage was graded using scores. Rabbits were divided into three groups: control, t-PA and DP1904 plus t-PA. The t-PA was administered intravenously at 500 iu/kg/min for 30 mins starting 5 mins prior to reperfusion. DP1904 was injected intravenously at a dosage of 10 mg/kg every 24 h starting 2 hr prior to coronary occlusion. Mortality was similar and hemodynamic parameters and area at risk were comparable between all three groups. The myocardial infarct size as a percentage of area at risk was 44.5 +/- 3.8% (mean +/- standard error) (n = 9) in the control group, 41.6 +/- 4.6% in the t-PA group (n = 8) and 51.3 +/- 5.2% in DP1904 plus t-PA group (n = 8), not significantly different (ANOVA). Neither were the hemorrhage scores significantly different between the groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

[Assessment of infarct-related coronary arteries using the bull's eye view method and unfolded surface mapping in thallium-201 myocardial tomography].

Infarct-related coronary lesions and collaterals were assessed by the bull's eye view and the unfolded surface map derived from thallium-201 myocardial tomography (Tl-201 SPECT) in 25 patients with anterior myocardial infarction. The patients were categorized in six groups according to their cine-angiographic findings: locations of stenosis (proximal or distal portions of the first diagonal branch or distal site of the first septal branch), and the presence or absence of collaterals. The anterior half of the left ventricle on the bull's eye view map was divided into eight regions from the anterior septum to the lateral wall and from the apex to the cardiac base. Tl-201 SPECT images were expressed as functional maps using maximum-count circumferential profile analysis: an "extent image" showing the extent of perfusion defect, and a "severity image" demonstrating the degree of hypoperfusion. The following results were obtained: 1. Perfusion defect of the "extent image" at the basal portion of the anterior septum reflected poor collaterals, with a sensitivity of 81.3%, a specificity of 77.8%, and a diagnostic accuracy of 80.0%. 2. Coronary stenosis at segment 6 (AHA classification) was differentiated from that at segment 7 by detecting hypoperfusion at the basal septum on the "severity image", with a sensitivity of 71.4%, a specificity of 77.8%, and a diagnostic accuracy of 75.0%. 3. Perfusion defect at the basal section of the proximal portion of the anterior wall on the "extent image" indicated stenosis at the proximal segment 6, with a sensitivity of 57.1% and a specificity of 88.9%.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

In vivo concentrations of kinins and angiotensins.

In the investigation of hypotensive mechanisms for the converting enzyme (ACE) inhibitor, precise methods for plasma kinin and angiotensin II measurement are essential. We describe here determination methods of plasma kinin and angiotensin II, and their applications to converting enzyme inhibitor administration. In our kinin RIA system, a high titered antiserum (final dilution 1:640,000) was used. Sensitivity was 0.25 pg/tube. Regarding plasma kinin measurement, an inhibitor mixture including aprotinin, hexadimethrine, SBTI, phenanthroline and EDTA, was used to collect the plasma sample. The determined plasma kinin levels in normal subjects were below 10 pg/ml. A very sensitive and simplified direct RIA system for plasma angiotensin II was also developed in our laboratory using the very high titered antiserum (final dilution 1:1,500,000). The sensitivity was 0.1 pg/tube, and cross-reactivity of angiotensin I was less than 0.1%. These data suggest that plasma angiotensin II level can be determined directly in very small plasma samples, such as 0.1 ml by this RIA system even in the ACE inhibitor administration. The plasma angiotensin II levels in normal subjects were 12.0 pg/ml. Both of these RIAs which were applied to the clinical experiments of ACE inhibitor administration.

Angiotensin II↗
PubMed1989

Physiological role of renal kallikrein-kinin system in human.

The physiological role of renal kallikrein-kinin system in human is discussed by the three following topics. Localization of each component of renal kallikrein-kinin system: Kallikrein is localized in the apical site of the distal tubular epithelial cells and collecting ducts by the immunostaining method. Following the stop-flow method in dog kidney, kallikrein and kinin are recognized in the distal tubules. Kininase I, II and neutral endopeptidase (enkephalinase) are localized not only in the proximal tubules, but also in the distal tubules. The localization of kininases is further confirmed by the stop-flow method pretreated with specific inhibitors for each of the kininases. Sodium metabolism and renal kallikrein-kinin system: In normal subjects, fractional excretions of sodium and inorganic phosphorus which reflect the total and proximal sodium reabsorption, show significantly positive correlations for both urinary kallikrein and kinin excretions. In the case of 0.9% saline infusion, the activity of renal kallikrein-kinin system is augmented following the infusion as shown in the increases of urinary kallikrein and kinin excretions and the decreases of urinary kininases excretions. Relation to other renal depressor systems: The close relations among renal dopamine, kallikrein-kinin and prostaglandin systems have been suggested by a dopamine infusion study. Dopamine may augment the activity of the renal kallikrein-kinin system through both the increases of renal prekallikrein synthesis and kallikrein specific activity. From these studies reported up to the present, it is suggested that the renal kallikrein-kinin system produced in the distal nephron in the kidney may play a role in the sodium metabolism with other renal depressor systems in addition to its own action.

Amino Acid Sequence↗
PubMed1989

The pathophysiological role of kinin and chemical mediators on experimental allergic rhinitis.

In order to clarify the pathophysiological role of the chemical mediators, the releases of kinins, histamine and leukotriene C4(LTC4) into the nasal cavity were measured following nasal allergic challenge in ovalbumin(OA)-sensitized guinea pigs, or following nasal stimulation with one of these chemical mediators in OA-non-sensitized animals. In sensitized animals, an increased vascular permeability of nasal mucosa was recognized immediately after antigenic stimulation and lasted for 60-90 minutes. Releases of kinins and LTC4 into the nasal lavage fluid augmented not only immediately after the antigenic challenge, but also during 60 to 90 minutes after the stimulation. Release of histamine into the nasal lavage fluid was observed only immediately after the antigenic stimulation. In non-sensitized guinea pigs, nasal stimulation with bradykinin accelerated nasal vascular permeability. Nasal stimulation with histamine or LTC4 resulted in increase of nasal vascular permeability and of kinins concentration in the nasal lavage fluid. These results suggest that kinins might be concerned with the immediate and later vascular permeability during the allergic response.

Animals↗
PubMed1989

Significance of kallikrein-kinin and renin-angiotensin systems in the hypotensive mechanism of angiotensin-I converting enzyme inhibitors in essential hypertensives.

This study was undertaken to further clarify the role of kallikrein-kinin and renin-angiotensin systems in the hypotensive mechanisms of the angiotensin-I converting enzyme inhibitor by using highly sensitive and specific radioimmunoassays in patients with essential hypertension. Captopril was administered for 14 days (chronic effect), and the acute effects of captopril, alacepril and ramipril were also studied in the in-patients with essential hypertension. All of these converting enzyme inhibitors rapidly decreased the blood pressure and plasma angiotensin II levels, and increased plasma and urinary kinin and plasma renin activity in the acute effect. Following the administration of captopril for 14 days, these decreases and increases were maintained. The change of blood pressure was significantly correlated negatively with that of plasma kinin levels and positively with that of plasma angiotensin II levels in both the acute and chronic effect of converting enzyme inhibitors. Urine volume and urinary sodium excretion were markedly augmented, while both the change of urine volume and that of urinary sodium excretion were negatively correlated with the change of blood pressure in the chronic effect. These findings suggest that the hypotensive effect of converting enzyme inhibitors might be caused by an increase of plasma kinin and a decrease of plasma angiotensin II, and in part by an augmentation of urine volume and urinary sodium excretion. In this drug treatment, the renal kallikrein-kinin system may also play some role in the increase of urine volume and urinary sodium excretion through the increased kinin in the kidney.

Angiotensin II↗
PubMed1989

Relationship between human seminal kallikrein-kinin system and spermatogenesis.

The concentration of kallikrein and the activity of angiotensin converting enzyme (ACE) in the semen specimens mainly from patients with male sterility and from those who were subjected to vasoligation, and in the prostatic fluid specimens from normal controls were determined by radioimmunoassay (RIA) and the modified Cushman's method, respectively. The kallikrein level in the semen from normal control was 40.4 +/- 21.3 ng/ml which was more than 10 times that in the blood. The value tended to increase with the decrease of the number of sperm. But there was no significant correlation between the kallikrein level and the sperm motility. The seminal kallikrein level from the patients subjected to vasoligation and that in the prostatic fluid from the normal male were 20-28 ng/ml. Therefore, that amount was considered to be secreted from the prostate gland. The results of column chromatography suggested that kallikrein combined with the other substances to form a high molecular compound in the semen. The ACE activity was 94.9 +/- 10.9 nmol/ml/min in the semen from the normal control, which was about three times that in the blood. Similar to kallikrein, it tended to decrease with the increase of the number of vasoligation and that in the prostatic fluid from the normal males was higher than that in the semen from the normal control and patients with male sterility, it was estimated that the considerable amount of ACE was secreted from the prostate gland.

Humans↗
PubMed1989

The renal kallikrein-kinin system in renoparenchymal hypertension.

In order to investigate the pathophysiological role of renal kallikrein (KK)-kinin system in renoparenchymal hypertension (RHT), urinary excretion of KK was measured in 15 patients with RHT and compared with that in 16 normotensive subjects (NT). The urinary kininase excretion was also determined in some subjects. KK quantity and activity was measured by direct radioimmunoassay and kininogenase assay, respectively. Kininase activity was determined as a bradykinin-degradating activity. The urinary excretion of KK quantity and activity as well as the fractional excretion of KK were significantly lower in RHT than in NT. Significantly positive correlations were observed between urinary excretion of KK quantity or KK activity and creatinine clearance. The fractional excretion of kininase was significantly higher in RHT than in NT while no significant difference was found in the urinary kininase excretion between these groups. These results suggest that renal KK-kinin system is suppressed not only in the whole kidney but in each nephrone which is still functioning, and the suppression of this system may contribute to the pathophysiology of RHT.

Adult↗
PubMed1989

Renal kininases in primary aldosteronism.

In order to further clarify the role of renal kallikrein-kinin (K-K) system in primary aldosteronism (PA), daily urinary excretions of renal K-K system components including kallikrein (KAL), kinin (KIN), total kininase (K-ase), K-ase I, K-ase II and neutral endopeptidase (NEP) were measured in PA and normotensives (NT). In this study, a new method for the simultaneous determination of human urinary K-ase I, II and NEP was established and employed. The daily excretions of KAL was significantly higher in PA than that in NT, while no difference was found in KIN between PA and NT. On the other hand, total K-ase in PA (897 +/- 258 micrograms/min/day) was significantly higher than that in NT (209 +/- 6). NEP was also significantly higher in PA (262 +/- 22 micrograms/min/day) than that in NT (127 +/- 6), whereas there were no differences in K-ase I and K-ase II between PA and NT. The relative contributions of K-ase I, II and NEP to total K-ase in NT were 14, 27 and 59%, while those in PA were 12, 17 and 36%, respectively. As a result, these three K-ase contributed only 64% to the total K-ase in PA. These findings suggested that 1) NEP may play a major role in the catabolism of renal KIN in human, 2) NEP is accelerated in PA, 3) unknown K-ase, different from K-ase I, II or NEP, may exist in PA, and 4) accelerated renal K-ase activity may play some role on the disorder of renal water-sodium metabolism and high blood pressure in PA.

Humans↗
PubMed1989

Localization of kallikrein in human male genital organ.

Male genital organs (testis, epididymis, seminal vesicle and vas deferens) were stained by the peroxidase-antiperoxidase (PAP) method to clarify the localization of kallikrein. Sertoli cells of the testis, epithelial cells of the epididymis, and adenocytes of the prostate gland were specifically stained showing that endogenous kallikrein was localized in these cells.

Epididymis↗
PubMed1989

Availability of 111In-labeled platelet scintigraphy in patients with postinfarction left ventricular aneurysm.

Eighteen patients with postinfarction left ventricular aneurysms (LVAs) were examined with Indium-111-labeled autologous platelet scintigraphy to identify intracardiac thrombi and to investigate the effect of antithrombotic agents on thrombogenesity within their LVAs. Left ventriculography (LVG), and two-dimensional echocardiography were also carried out to assess the diagnostic ability of the platelet imaging. Indium-111-platelet scintigraphy for the detection of LVA mural thrombi had a sensitivity of 60% and a specificity of 100%. Four of six patients with false-negative scintigraphic studies had been under antiplatelet therapy. Eight of the nine patients who had showed active platelet deposition on initial examination had not received antiplatelet therapy. Thereafter, five of these nine were treated with tichlopidine (300 mg/day) for 29.8 +/- 5.0 days. On the second platelet study, two had resolution and the other three had interruption of intra-aneurysmal deposition, which remained positive. In only one patient of the three, the third platelet study was performed after warfarin therapy. It took two weeks after beginning the therapy to completely interrupt platelet deposition within the LVA in this patient. ECG gated radionuclide ventriculography and Thallium-201-myocardial scintigraphy were also performed to assess left ventricular wall motion of left ventricular ejection fraction (LVEF) and myocardial blood perfusion. Thallium-201-SPECT showed apical or anteroapical perfusion defects and the radionuclide ventriculography correctly identified all 18 apical and anteroseptal aneurysms which were confirmed by LVG methods. The comparison between the thrombus positive group and the thrombus negative group was carried out on both the LVEF and the period from the last myocardial infarction to the initial platelet scanning study. There were no statistical differences in the LVEF and the interval (34.5 +/- 12.5% vs 37.3 +/- 14.6%, 39.6 +/- 52.6 days vs 89.6 +/- 108.3 days) between the two groups. These results suggest that Indium-111-labeled platelet scintigraphy can be a reliable method for the identification of active left ventricular mural thrombi and a practical method of judging antiplatelet and anticoagulant therapy.

Adult↗