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Biomedical subjects

K Kanmatsuse

Publications and source records attributed to K Kanmatsuse.

At least 181 records · Page 10Linked to original sources
PubMed1992

Blood pressure response to hyperinsulinemia in salt-sensitive and salt-resistant rats.

We investigated the role of insulin in salt-sensitive hypertension in Dahl salt-sensitive and salt-resistant rats. The rats were kept in metabolic cages, and sodium intake and urinary sodium excretion were measured. In salt-sensitive rats receiving a 0.3% NaCl diet, sodium retention was significantly greater at weeks 1 and 2 in rats that received an insulin infusion than in those receiving a saline infusion. Mean arterial blood pressure and plasma norepinephrine levels were significantly higher at week 3 in insulin-treated rats than in saline-treated rats (mean arterial pressure, 137 +/- 3 mm Hg versus 119 +/- 3 mm Hg, p < 0.05; plasma norepinephrine, 0.40 +/- 0.02 ng/ml versus 0.27 +/- 0.01 ng/ml, p < 0.05). Insulin did not influence sodium retention, mean arterial pressure, or plasma norepinephrine in salt-resistant rats. Coadministration of an alpha-blocker (bunazosin, 10 mg/kg per day for 3 weeks) in salt-sensitive rats abolished the insulin-induced elevations in mean arterial pressure and sodium retention. When salt-sensitive rats were fed a low salt diet (0.03% NaCl), insulin did not raise mean arterial pressure. Thus, insulin elevated blood pressure only in the salt-sensitive model. The sympathetic nervous system and sodium retention in the early phase of insulin overload may contribute to elevation of mean arterial pressure in this model.

Animals↗
PubMed1992

[Anthracycline cardiotoxicity evaluated by digitized M-mode echocardiography].

Ten patients with malignant diseases whose mean age was 20.0 +/- 13.2 years received anthracycline derivatives therapy and were evaluated for their left ventricular systolic and diastolic functions by computer-assisted digitized M-mode echocardiography. Fractional shortening (%FS), a parameter of systolic function, was measured. The first derivative of left ventricular dimension change (peak LV dD/dt), posterior wall thinning (peak LVPW thinning rate) and interventricular septum thinning (peak IVS thinning rate) were used as indices of diastolic function. Blood pressure (BP) was measured noninvasively at the end of the echocardiographic examination and hemoglobin concentration (Hb) was measured on the same day. These examinations were performed immediately before administration of anthracycline and one week and one month after the last administration. Statistical analyses were performed using the Student's t-test. The mean BP, HR, LVDd, LVDs, LVPW and IVS remained unchanged following the drug administration. %FS did not change significantly; 36.8 +/- 6.3%, before the administration, 35.3 +/- 6.5%, one week after the administration, and 36.5 +/- 5.1%, one month after the administration. Peak LVdD/dt and the peak LVPW thinning rate decreased appreciably from 4.46 +/- 1.10 to 3.76 +/- 1.08, and from 7.99 +/- 1.55 to 6.41 +/- 1.04, respectively, one week after the administration. The peak IVS thinning rate decreased from 3.54 +/- 0.81 to 2.99 +/- 0.79 after one week (p < 0.01). All of these values returned to the control levels in one month after the drug administration. We concluded that the indices of left ventricular diastolic function were more sensitive for detecting cardiac impairment than those of systolic function during the course of anthracycline therapy.

Adolescent↗
PubMed1989

Complete atrioventricular block associated with regional myocardial scarring in a patient with Coxsackie B2 myocarditis.

Transient atrioventricular (A-V) conduction abnormalities are often experienced in patients with evolving acute viral myocarditis, but persistent complete A-V block requiring permanent cardiac pacing is rare. We describe a case who developed irreversible complete A-V block during the long-term course of Coxsackie B2 myocarditis. The endomyocardial biopsy revealed inflammatory cellular infiltrates and myocyte necrosis. A left ventriculogram and echocardiogram consistently demonstrated an aneurysm in the basal portion of the interventricular septum. It was speculated that the extensive myocardial scar caused by acute myocarditis resulted in the ventricular aneurysm of this particular myocardial region involving the A-V conduction system.

Adult↗
PubMed1988

Randomized, double-blinded multicenter study. Comparison of intracoronary single-chain urokinase-type plasminogen activator, pro-urokinase (GE-0943), and intracoronary urokinase in patients with acute myocardial infarction.

Coronary recanalization rates and changes in the coagulation and fibrinolysis system were evaluated in a randomized fashion in patients with acute myocardial infarction after intracoronary administration of single-chain urokinase-type plasminogen activator (pro-urokinase: GE-0943) or urokinase. Three groups of patients were studied: group H (n = 50), 6,000 units pro-urokinase i.c.; group L (n = 44), 3,000 units pro-urokinase i.c.; and group U (n = 54), 960,000 IU urokinase i.c. Coronary recanalization rates determined angiographically after 45 minutes of intracoronary infusion averaged 90% in group H, 59% in group L, and 61% in group U. The differences were statistically significant between group H and the latter two groups. Pro-urokinase affected plasma proteins of the fibrinolytic system to a lesser degree than urokinase. Bleeding complications were present in one patient in group L, in none in group H, and in five in group U. Thus, intracoronary administration of 6,000 units pro-urokinase is more effective in coronary thrombolysis and causes less systemic fibrinogenolysis than intracoronary administration of urokinase.

Adult↗
PubMed1988

Experimental and clinical investigations for the time interval from onset of symptoms to the coronary reperfusion.

To clarify the relationship between time interval from the onset of coronary occlusion to the reperfusion and reperfusion rates or left ventricular function, an experiment with 113 mongrel dogs was carried out. Coronary thrombi experimentally induced within 4 hours in 63 dogs were rapidly lysed by intracoronary thrombolytic agent (Experiment 1). Infarct size was investigated in 17 dogs. The infarct size (% of left ventricle) in 9 dogs with 4-hour reperfusion following 2-hour coronary occlusion was significantly smaller than that in 8 dogs with 6-hour occlusion (12.0 +/- 7.9 vs 19.1 +/- 8.7% respectively p less than 0.05) (Experiment 2). The infarct size in 8 dogs with 7-day reperfusion following 2-hour occlusion was also significantly reduced compared to that in 7 dogs with 7-day occlusion (16.3 +/- 7.4 vs 28.5 +/- 8.9%, respectively p less than 0.02) (Experiment 3). The infarct size in 11 dogs with 4-hour reperfusion with verapamil administration following 2-hour occlusion was significantly reduced compared to that in 7 dogs with 6-hour occlusion without verapamil (5.5 +/- 1.9 vs 20.3 +/- 3.3%, respectively p less than 0.01) (Experiment 4). In experiment 3, anterior wall motion also was assessed by contrast ventriculography and infarct related areas in reperfused group was found to be improved compared to non-reperfused group at 7 days after infarction. In clinical studies, 121 patients who were admitted within 12 hour of onset of symptoms, were investigated to evaluate reperfusion rates and left ventricular function. The reperfusion rate of young age thrombus within 3 hours was 89% of 18 patients with completely occluded coronary artery. It was 77% of the 52 patients with 3 to 6 hour occlusion and 72% of the 18 patients with over 6 hour occlusion. There was a tendency towards high reperfusion rates in younger thrombus. In patients who were recanalized within 3 hours from the onset of symptoms ejection fraction of left ventricle at the chronic stage had a significantly higher percentage when compared to the unsuccessful group. Wall motion of infarct-related areas in patients who were thrombolysed within 6 hours was improved compared to the unsuccessful group. Administration of verapamil during reperfusion in patients with acute myocardial infarction suppressed rapid CK release and sigma CK. Thus, young age thrombus can be lysed easily, earlier recanalization after coronary occlusion can reduce infarct size and improve left ventricular function. Reinforced administration of verapamil during reperfusion can also reduce infarct size.

Adult↗
PubMed1985

Indications for and limitations of coronary thrombolysis.

Experimental studies in dogs with coronary thrombi induced by copper wire confirmed the optimal method of intracoronary thrombolysis, and showed that a high-dose, brief intravenous infusion of urokinase can lead to recanalization. The thrombolytic effects of intracoronary thrombolysin at a rate of 50 IU/kg over 10 minutes are similar to the effects of intracoronary urokinase at a rate 500 IU/kg over 20 minutes. Overall reperfusion rates of 83-86% have been achieved. These results indicate that the thrombolytic effect of thrombolysin is 20 times stronger than that of urokinase. The effect of a brief intravenous infusion of urokinase was less than that of intracoronary urokinase. The reperfusion rate in the same experimental model was 40%. Later, a clinical trial of intracoronary urokinase was performed in 47 patients with acute myocardial infarction who were admitted within 12 hours of the onset of symptoms. In 25 of 33 (75.8%) patients with complete occlusion, selective or ostial infusion of urokinase 500 IU/kg over 20 minutes was successful. When given intravenously, recanalization was achieved in 11 of 15 (73%) patients with complete occlusion who were admitted within 6 hours. Both reperfusion rates were similar except for dosage and the duration of infusion.

Aged↗
PubMed1984

Effects and limitation of CCU--prevention of evolving myocardial infarction.

Emergency coronary angiography and intracoronary thrombolysis were performed on 47 patients who were hospitalized within 12 hours from onset of chest pain. It revealed either a severe stenosis (14 pts: stenosed group) or complete occlusion (33 pts) of infarct-related coronary artery. In 25 out of 33 patients (76%) with complete occlusion, reperfusion was achieved after 10 to 20 minutes of intracoronary urokinase (UK) infusion at a rate of 500IU/kg/min (thrombolysed group). The failure to open coronary artery in remaining 8 patients may have been caused by the occlusion of atheroma itself (unsuccessful group). Left ventricular angiography was performed at one month after attack. In unsuccessful group, the mean age was younger and infarct-nonrelated vessel disease was lower frequency compared to other two groups. Ejection fraction in stenosed, thrombolysed and unsuccessful groups were 56.6 +/- 12, 47.5 +/- 14 and 44.3 +/- 5.1%, respectively. Wall motion assessed by point-score system were 6.7, 5.9 and 3.6, respectively (p less than 0.05 in each group). These facts suggest that early recanalization may result in greater reversal of cardiac function. The time to the peak CPK was shortened in stenosed and thrombolysed groups, but, the values of CPK was maximum in thrombolysed group. Rethrombosis was recognized in 2 patients during 1 to 30 months follow-up. No death and no remarkable complications were seen during this intervention, but 4 late deaths were recognized. Thus, early reperfusion by intracoronary UK infusion is effective therapy to improve cardiac function and reduction of death in AMI.

Adult↗