Search PubMedSearch

Biomedical subjects

O Iimura

Publications and source records attributed to O Iimura.

At least 55 records · Page 3Linked to original sources

Myocardial distribution of indium-111-antimyosin Fab in acute inferior and right ventricular infarction: comparison with technetium-99m-pyrophosphate imaging and histologic examination.

In a postmortem study of a 69-yr-old female patient who had suffered 2 yr previously a non-Q-wave anterior infarction and who had sustained just seven days earlier a left inferior and right ventricular infarction, the distribution of 111In-antimyosin Fab was compared to the results of 99mTc-pyrophosphate imaging and histologic examination. Indium-111-antimyosin Fab imaging could not be performed because of cardiogenic shock. However, postmortem gamma scintillation counting revealed increased activities of antimyosin Fab in the inferoapical and right ventricular infarcted regions in which 99mTc-pyrophosphate positive imagings were observed; in contrast, a histologically confirmed old subendocardial anterior infarction had no definite activity. Thus, the myocardial distribution of 111In-antimyosin Fab corresponded well to the results of 99mTc scintigrams and histologic examinations in a human heart, suggesting that this technique could be useful in vivo for detecting several-day-old myocardial infarction of the right ventricle as well as the left ventricle. Tissue from the 2-yr-old infarction was not identified by this technique.

Aged

[Scintigraphic diagnosis of postinfarction left ventricular aneurysm and the prediction of the residual left ventricular function after aneurysmectomy using ECG gated blood pool SPECT].

The diagnostic accuracy of ECG gated blood pool SPECT (blood pool SPECT) for detecting and quantify postinfarction left ventricular aneurysm (LVA) was assessed in 49 patients with myocardial infarction and 15 control subjects. LVA, which was detected in 35 of 49 patients, was defined as a regional protrusion through a cardiac cycle in contrast ventriculography and as a non-contracting segment with a markedly delayed phase angle in the tomographic functional images derived from phase analysis. The blood pool SPECT technique showed a high sensitivity (100%), specificity (78.6%) and accuracy (93.3%) for detecting LVA and was very useful for precisely determining LVA location and sizing contractile and non-contractile volume of left ventricle in patients with LVA. Furthermore, left ventricular ejection fraction (LVEF) after the excision of LVA was predicted using preoperative pool SPECT images in 9 patients. The predicted LVEF was closely correlated with the measured LVEF after the operation (y = 1.09x-4.37, r = 0.87, p less than 0.01). Thus, gated blood pool SPECT can be a useful non-invasive technique not only for detecting and quantifying left ventricular aneurysm but also for predicting a residual left ventricular function after aneurysmectomy.

Adult

[Usefulness of high resolution transesophageal echocardiography for diagnosis of ruptured chordae tendineae of the mitral valve: clinical and echocardiographic characteristics].

Transesophageal echocardiography with high resolution (TEE; 5 MHz, convex type probe) revealed ruptured chordae tendinae of the mitral valve (RCT) in seven patients. However transthoracic echocardiography (TTE) was diagnostic only in two patients. These all seven patients had mitral valve prolapse and mitral regurgitation documentated by TTE. Six of seven patients were 59 years or older, and four patients had only mild symptoms. TEE showed the systolic appearance of an edge echo, suggesting an edge of ruptured chordae tendineae within the left atrium. These results show that TEE is a useful method for detecting RCT of the mitral valve, especially in the aged patients with MVP and mitral regurgitation. It is because of the availability of high resolution and nearfield in TEE.

Adult

Effects of early and later reperfusion on healing speed of experimental myocardial infarct.

The effects of reperfusion on myocardial infarct healing in the rabbit were analyzed using two morphometric indexes: the ratio of the volume of the organized portion of infarct to the volume of the whole infarct (%O/I), and the ratio of the minimal thickness of the infarct zone to the normal zone thickness (thinning ratio). In the nonreperfused infarcts, %O/I increased from 43.8 +/- 3.1% (mean +/- SEM) at 48 h to 85.7 +/- 2.5% at seven days, which supported the validity of this index. The thinning ratio was 0.50 +/- 0.03 at 48 h and did not change during the following five days. In other groups of rabbits, the coronary artery was temporarily occluded for 30 mins (early reperfusion) or 60 mins (late reperfusion), and the hearts were analyzed at 72 h or seven days. Early reperfusion limited infarct size as a percentage of the area at risk (%I/AAR) by approximately 50%, but late reperfusion did not. In both nonreperfused and reperfused infarcts, %O/I correlated significantly with absolute infarct size. Furthermore, the regression lines of the relationship of infarct size to %O/I of early and late reperfused infarcts shifted towards higher %O/I values compared with that of nonreperfused infarcts at seven days, which suggested accelerated organization. However, such a regression line shift by reperfusion was not detected at 72 h after infarction. The thinning ratio was higher in early reperfused infarcts compared to nonreperfused or late perfused infarcts, and there was a weak inverse correlation between thinning ratio and %I/AAR when the data of reperfused and nonreperfused infarcts were pooled.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

The transient increase of urinary digitalis-like substance excreted during excess sodium intake in reduced renal mass rats.

Urinary immunoreactive endogenous digitalis-like substance (EDLS) excretion was studied in gradually reduced renal mass rats (RRM). Urinary EDLS increased immediately after the start of 1% NaCl ingestion, then it returned to the basal level 2 weeks later. Both urinary sodium excretion and urinary EDLS were significantly higher in 3/6 and 4/6 RRM than in control until 2 weeks after starting 1% NaCl. However, there was no difference in blood pressure between the groups. Transient EDLS increase may play an important role in maintaining sodium and water homeostasis, but its transient increase apparently does not contribute to blood pressure elevation.

Animals

The role of Na,K-ATPase inhibitor on pressor responsiveness in patients with benign essential hypertension.

To clarify the role of Na,K-ATPase inhibitor in the enhanced pressor response to infused noradrenaline (NA-R) in patients with benign essential hypertension (EHT), NA-R, plasma noradrenaline concentration (PNA), and blood ionized calcium (Ca2+) were investigated before and after intravenous injection of ouabain in 15 normotensive subjects (NT) and 13 EHT. NA-R was enhanced by ouabain in both NT and EHT. The augmentation of NA-R following ouabain injection (delta NA-R) and % delta NA-R were significantly lower in EHT than in NT. Following ouabain injection, no significant change in PNA and blood Ca2+ was observed in both NT and EHT. NA-R negatively correlated with PNA and blood Ca2+, which were estimated just prior to noradrenaline infusion, before ouabain injection as well as after. After ouabain, the regression line between NA-R and PNA or blood Ca2+ shifted toward higher NA-R level in NT, unlike in EHT. These results suggest that an exogenous Na,K-ATPase inhibitor brings about a blunted enhancement of NA-R in EHT consistent with the presence of an endogenous Na,K-ATPase inhibitor in EHT.

Adult

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

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

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

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

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

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

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

[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

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

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