Search PubMed⌕ Search

Biomedical subjects

O Iimura

Publications and source records attributed to O Iimura.

At least 73 records · Page 4Linked to original sources
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↗
PubMed1989

Scintigraphic imaging of a case of congenitally corrected transposition of the great vessels and an adult case of single atrium and single ventricle.

We report on the clinical utility of radionuclide angiography and gated blood pool single emission computed tomography (gated blood pool SPECT) in two patients having congenital heart disease. Both conventional equilibrium radionuclide angiography and gated blood pool SPECT demonstrated the connection of the great vessels with both ventricles in a 15-year-old male patient with a congenitally corrected transposition of the great vessels. In particular, the latter procedure could provide very useful information about the ventricular morphology and inversion which is important for diagnosing this disorder. The second case is an extremely rare 42-year-old female patient with a single atrium and single ventricle. She underwent first-pass and multiple gated blood pool angiography from the anterior, right and left oblique views. The combination of these scintigraphic techniques revealed an insufficiency in anatomical correlations among the single atrium, atrioventricular valve, single ventricle and the great vessels in addition to the connection of superior vena cava with the single atrium, and the atrioventricular valve. Thus, conventional equilibrated angiography from multiple views and gated blood pool SPECT seems to be very reliable not only for anatomical evaluation but also for clinical course observation in patients with complicated congenital heart disease.

Abnormalities, Multiple↗
PubMed1989

The influence of cold temperatures on the progression of hypertension: an epidemiological study.

In order to clarify the relationship between cold temperatures and the progression of hypertension, a prospective epidemiological study was carried out in a cold area of Hokkaido, Japan. We analysed the findings in 909 subjects, who were followed up for 8 years (1977 to 1985). The difference between the mean blood pressure in winter and in summer in the first year was significantly and positively correlated with the difference between the mean blood pressure in the first and in the eighth year. The winter/summer difference was significantly higher in the group with progressive hypertension than in the other groups. The pressor response to exposure to cold was significantly greater in hypertensives, and tended to be higher in borderline hypertensives compared with normotensives. From these results, we conclude that a cold environment might increase the inhabitants' blood pressure levels, and the difference between a subject's blood pressure in winter and summer may predict future hypertension.

Adult↗
PubMed1989

Role of kallikrein-kinin system in the hypotensive mechanisms of converting enzyme inhibitors in essential hypertension.

Patients with essential hypertension were studied to clarify the role of the kallikrein-kinin system in the hypotensive actions of angiotensin I converting enzyme inhibitors. Captopril, alacepril, ramipril, and altiopril administered in single doses rapidly decreased blood pressure and plasma angiotensin II levels, and increased plasma and urinary kinins as well as plasma renin activity. Following administration of captopril for 14 days, similar effects were observed. Urine volume and urinary sodium excretion were augmented after acute and chronic administration of captopril. The patients who received ramipril and altiopril were divided into renin subgroups. In the normal-renin group, the change in blood pressure was accompanied by an increase in plasma kinin level and a decrease in plasma angiotensin II level. However, in the low-renin group, although these drugs reduced blood pressure and increased plasma kinin, no significant change was observed in plasma angiotensin II levels. These findings suggest that (a) in patients with normal renin activity, the hypotensive effect of converting enzyme inhibitors might be caused by an increase in plasma kinin and a decrease in plasma angiotensin II, but in the low-renin group, the increase in plasma kinin levels may be more important; and (b) the augmentation of urine volume and urinary sodium excretion may also be related to the hypotensive effects of the converting enzyme inhibitors during long-term administration.

Adult↗
PubMed1989

Mechanisms of suppression of renal kallikrein activity in low renin essential hypertension and renoparenchymal hypertension.

The mechanism of suppression of renal kallikrein activity in low renin essential hypertensive and renoparenchymal hypertensive patients was investigated in this study. From Sephadex G-200 column chromatography studies, a single kallikrein peak was observed in both kallikrein radioimmunoassay and kininogenase activity in all samples from normal subjects, low renin essential hypertensive and renoparenchymal hypertensive patients, and in purified kallikrein solution. The enzyme-specific activity around the kallikrein peak in all urine samples from each group was significantly lower than that in purified kallikrein, and a significantly lower specific activity was found in both patient groups than was found in normal subjects. Moreover, it was also recognized that the specific activity of kallikrein decreased in all cases with the increase of the molecular weight of kallikrein, and this tendency was observed more obviously in the low renin essential hypertensive and renoparenchymal hypertensive patients than in the normal subjects. These results suggest the presence of a kallikrein-specific inhibitor with a low molecular weight in human urine, although the possibility of a variant form of kallikrein cannot be excluded.

Female↗
PubMed1989

The effect of inotropic dose of dobutamine during reperfusion on myocardial infarct size.

We examined whether dobutamine infusion during reperfusion modifies myocardial infarct size in a rabbit ischemia-reperfusion model. Prior to the infarct size study, the hemodynamic response to dobutamine 5, 10, and 15 micrograms/kg/min i.v. was evaluated in the rabbit model. Ten micrograms/kg/min of dobutamine increased the left ventricular dp/dt max by 34.0 +/- 4.9% (n = 7) and the myocardial blood flow from 0.86 +/- 0.16 to 2.19 +/- 0.57 ml/min/g without change in the collateral blood flow (n = 4). The heart rate, systolic and diastolic blood pressures were elevated by only 4.7 +/- 1.0%, 9.4 +/- 3.0%, and 8.0 +/- 3.7%, respectively (n = 7). In the infarct size study, a coronary branch was occluded for 30 min and then reperfused. Seventy-two hours after reperfusion, the myocardium supplied by the occluded artery (area at risk, AAR) and the infarcted area were determined by fluorescent particles and histology (hematoxylin-eosin and modified Mallory's staining), respectively. In the dobutamine treated group (DB group), 10 micrograms/kg/min of dobutamine were infused for 30 min starting immediately after reperfusion, and a comparable volume of saline was infused in the control group. Hemodynamic parameters and the size of AAR were comparable in the control and DB groups. Myocardial infarct size, expressed as the percentage of AAR, was 45.1 +/- 3.9% in the control (n = 11) and 40.2 +/- 2.4% in the DB group (n = 10), which was not significantly different. These findings indicated that the inotropic dose of dobutamine administered during reperfusion did not cause myocardial necrosis by disturbing the recovery process of the myocardium from ischemic injury.

Animals↗
PubMed1989

Endogenous and exogenous catecholamines can accentuate myocardial ischemia only when coronary blood flow is below a critical level.

Seventy-eight dogs with graded constriction of the left main coronary artery were studied to determine the coronary blood flow at which the heart is vulnerable to catecholamine induced ischemia. The left main coronary artery was cannulated with a Griggs' type self-perfusing cannula. The coronary blood flow (CBF) was reduced by graded constriction of the extra-corporeal circuit connected with this cannula. Blood flow rates between 12 and 117 ml/min/100 g were studied. Cardiac activation was achieved by either intracoronary administration of a physiological dose of catecholamine (noradrenaline; 0.4 microgram/kg/min or adrenaline; 0.2 microgram/kg/min), or by electrical stimulation of the left stellate ganglion (4 Hz, 2 msec, 10 V for 5 min). When CBF was below 30 ml/min/100 g, accentuated myocardial ischemia was always indicated by lactate production, myocardial creatine phosphate depletion, ischemic ST segment changes, and elevated left ventricular end diastolic pressure (LVEDP) during these stimulations. When CBF was above 50 ml/min/100 g, catecholamine clearly accelerated the cardiac function and myocardial metabolism with no signs of ischemia. When CBF was between 30 and 50 ml/min/100 g signs of accentuated myocardial ischemia appeared during catecholamine activation in only 1/2 of the dogs. This study indicated that the critical level for CBF at which endogenous or exogenous catecholamine can produce ischemia is between 30 and 50 ml/min/100 g.

Adrenergic Fibers↗
PubMed1989

Tuberculosis on regular hemodialysis--a case of pericardial tamponade.

The patient presented in this paper had been stable for 3 months after the induction of hemodialysis, when nausea, vomiting and hepatomegaly suddenly developed. A chest film revealed rush cardiomegaly, and massive pericardial effusion was demonstrated by echocardiography. One liter of hemorrhagic fluid was removed by pericardiocentesis and subsequent pericardial drainage under echocardiography. The patient received chemotherapy against pulmonary tuberculosis 30 years ago and calcification on chest film was apparent. Although sputum smear and pericardial effusion was negative for acid-fast organisms, combination therapy was initiated for suspected tuberculosis. The patient recovered completely and 2 months later it was demonstrated that cultures of sputum grew mycobacterium tuberculosis. Tuberculin skin test (PPD), which was negative 2 months previously, converted to positive. Tuberculosis must be considered as a potential cause of pericardial tamponade in patients on regular hemodialysis, and prompt therapy for both cardiac tamponade and the occult infection is warranted.

Aged↗
PubMed1989

Human superoxide dismutase failed to limit the size of myocardial infarct after 20-, 30-, or 60-minute ischemia and 72-hour reperfusion in the rabbit.

The effect of superoxide dismutase (SOD) on the size of the myocardial infarct resulting from various durations of ischemia and a 72-hour reperfusion was examined in the rabbit. A coronary branch of the circumflex artery was occluded for 20, 30, or 60 min and then reperfused. Seventy-two hours after the coronary occlusion, the infarct size and the size of the area at risk (vascular bed of occluded coronary artery) were determined by histology (hematoxylin-eosin and Mallory's staining) and by fluorescent particles, respectively. Human SOD (45,000 units/kg) was injected intravenously as a bolus in SOD-treated rabbits, while only saline was administered to control rabbits. The percentage of the area at risk which actually infarcted (%I/AAR) was 25.5 +/- 12.9% (mean +/- S.D.) in the 20-min ischemia control group (n = 9), 19.7 +/- 10.2% in the 20-min ischemia SOD group (n = 9), 44.8 +/- 9.0% in the 30-min ischemia control group (n = 9), 41.0 +/- 6.3% in the 30-min ischemia SOD group (n = 9), 74.2 +/- 13.8% in the 60-min ischemia control group (n = 9), and 76.6 +/- 8.2% in the 60-min ischemia SOD group (n = 7). The %I/AAR was not significantly different between the control and SOD groups for any duration of ischemia. Heart rate, blood pressure, and the size of area at risk were comparable in all six groups. These findings suggested that oxygen-free radicals produced during initial moments of reperfusion were unlikely to contribute to myocardial necrosis regardless of the duration of ischemia in the rabbit.

Animals↗
PubMed1989

A case of primary aldosteronism with chronic renal failure undergoing hemodialysis treatment.

A 56-year-old man with primary aldosteronism and chronic renal failure undergoing hemodialysis is described. He complained of numbness of the extremities and showed persistent hypopotassemia in spite of anuria. In the endocrinological examination, a very high plasma aldosterone concentration was observed, while plasma renin activity was within the normal range. From the abdominal Computed Tomography (CT), adrenal scintigraphy, and segmental venous sampling data, he was diagnosed as primary aldosteronism due to left adrenocortical adenoma. In this case, hypopotassemia could not be explained by potassium loss through the kidneys, which suggests potassium excretion in the gastrointestinal tract as the mechanism of hypopotassemia. This was clearly shown from a potassium-balance study and the results of spironolactone administration. Our report is on the first case showing hypopotassemia due to primary aldosteronism in spite of anuria. If a patient treated with maintenance dialysis should have persistent hypopotassemia, as in the present report, it is necessary to consider an association with primary aldosteronism.

Humans↗
PubMed1989

Progression of myocardial infarction in a collateral flow deficient species.

The effect of a varying period of ischemia on the development of myocardial infarction was investigated in the rabbit. Radiomicrosphere measurements confirmed that the collateral blood flow is almost zero (0.02 +/- 0.01 ml/min/g) and without a significant transmural gradient in the rabbit heart (n = 15). A coronary branch of the left circumflex artery was occluded for 5, 10, 15, 30 or 60 min and then reperfused. The coronary branch was occluded permanently in another group of rabbits. Three days after the coronary occlusion, the infarct size was determined by hematoxylin-eosin and Mallory's staining and the ischemic zone size was determined by fluorescent particles. The results showed that the percentage of the ischemic zone infarcted (% infarction) vs the log of duration of ischemia yielded a sigmoid curve which could be linearized by probit analysis: Probits of % infarction = 3.05 x log (ischemic duration in minutes) + 0.33, r = 0.83, p less than 0.01. The regression equation indicated that 50% of the ischemic myocytes necrotized after 34 min of coronary artery occlusion. Unlike in the dog heart, the infarct of the rabbit heart first appears in the midmyocardium and then progresses towards both the endocardium and epicardium.

Animals↗