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K Kanmatsuse

Publications and source records attributed to K Kanmatsuse.

197 records · Page 11Linked to original sources

[Intracoronary thrombolysis in acute myocardial infarction].

To lyse intracoronary (IC) thrombi, coronary angiography was performed for 36 patients with acute myocardial infarction who were admitted within 12 hours of the onset of symptoms. Their average age was 59.6 years. Twenty-four patients (66.7%) had total occlusions of the infarct-related coronary artery, and 12 patients (33.3%) had severe atherosclerotic stenosis without occlusion (group A = Stenosis). In 19 of the 24 patients (79.2%) with total occlusion, IC infusion of urokinase (UK) at a rate of 500 units/kg/min during 10 to 20 min resulted in reperfusion of the distal coronary artery (group B = Thrombolysis). In the remaining five patients, IC thrombolysis was not successfully performed (group C = No effect). The degree of coronary artery stenosis immediately after reperfusion was 88.7 +/- 18.8% in group B. Long-term follow-up (four weeks) coronary angiography in groups A and B revealed improved patency to 79.2 +/- 19.3% and 79.4 +/- 27.8%, respectively. By contrast, total occlusion remained in group C. The ejection fraction measured four weeks later was slightly greater in group B than in group C, and was significantly greater in group A than in group C. If the average ages and complications of the other coronary vessels were considered, a significant difference was recognized among these three groups. The amplitude of the anterior wall motion of the patients with anterior infarction in each group assessed by a point score system was significantly increased in groups A and B as compared to group C. Peak CPK, GOT and LDH rose rapidly immediately after reperfusion and the time interval from the onset of symptoms to peak enzyme production was significantly shortened after reperfusion. These data supported the following concept: 1) coronary thrombus formation frequently occurs in acute myocardial infarction and can be rapidly lysed by IC infusion of UK with a total dose of 250,000 to 600,000 units, 2) reperfusion by lysis of IC thrombi in patients with acute myocardial infarction improves left ventricular wall motion, 3) peak enzyme rises rapidly after reperfusion, 4) the time interval from the onset of symptoms to peak enzyme production is remarkably shortened after repeat perfusion and that 5) no fatal arrhythmia nor bleeding are recognized. Thus, IC infusion of UK in the early stage of acute myocardial infarction was effective and useful.

Adult↗

Divergent effects of inotropic stimulation on the ischemic and severely depressed reperfused myocardium.

Mechanical function remains depressed for hours and days after even brief periods of ischemia. To determine whether the depressed function of the reperfused myocardium could be improved y inotropic stimulation, we studied segmental function during ischemia and after reperfusion using mercury-in-Silastic length gauges in 15 dogs. During coronary artery occlusion, segmental function could not be improved by inotropic stimulation with dopamine. Release of occlusion after 30 minutes of ischemia resulted in only slight improvement in segmental function (systolic shortening at 20% of control). After reperfusion, segmental function could be markedly enhanced by inotropic stimulation. The response to inotropic stimulation was similar after reperfusion after 3 hours of ischemia if the myocardium remained viable (nine dogs). When the myocardium was necrotic (five dogs), there was no improvement after reperfusion, either spontaneously or in response to inotropic stimulation. If applicable to humans, these results suggest that intractable pump failure caused by extensive but reversible ischemia could be effectively treated by reperfusion and inotropic stimulation.

Animals↗

Early phase acute myocardial infarct size quantification: validation of the triphenyl tetrazolium chloride tissue enzyme staining technique.

Gross histochemical delineation of myocardium which has lost dehydrogenase enzyme activity has been shown to facilitate macroscopic recognition of necrotic myocardium. The present study was undertaken to assess the accuracy of the triphenyl tetrazolium chloride (TTC) technique for quantitating myocardial infarct size very early after coronary occlusion. In 16 closed-chest dogs the left anterior descending coronary artery was occluded with an intra-arterial balloon. Twelve dogs were killed 6 hours after occlusion, their hearts excised, cut from apex to base into 1 cm thick slices, and incubated in TTC. Whole-mount histologic sections of each slice were prepared. Myocardial infarct size was measured by planimetry of photographs of each gross slice and histologic section using classical criteria of necrosis. Myocardial infarct size determined in 54 slices by the TTC technique and histologically was similar (25 +/- 16% vs 27 +/- 16% of the left ventricular mass, mean +/- SD) with close correlation between the two methods (r = 0.91). Four dogs were killed 3 hours after occlusion and TTC stained and unstained myocardium was studied by electron microscopy. When the TTC technique identified necrosis so did electron microscopy. Areas identified by the TTC technique as non-necrotic were either normal or only ischemic by electron microscopy. Thus, using TTC, necrosis can be quantitated reliably 6, and even 3 hours after coronary occlusion, before histologic changes are clearly diagnostic. This technique represents a reliable, practical means for quantitation of recent infarction and for studying the evolution of ischemic injury in its early phase.

Acute Disease↗

The relationship of vascular injury and myocardial hemorrhage to necrosis after reperfusion.

Early reperfusion may salvage ischemic myocardium; late reperfusion often intensifies morphologic changes of necrosis and causes hemorrhage. To determine whether hemorrhage after reperfusion increases the extent of myocardial infarction, six closed-chest, anesthetized dogs underwent balloon occlusion of the left anterior descending coronary artery for 5.5 hours, followed by 30 minutes of reflow. Colloidal carbon was injected distal to the balloon before reperfusion to label injured vessels. After sacrifice, the area of myocardial necrosis was measured by planimetry of 1-cm-thick serial slices of left ventricle stained with triphenyl tetrazolium chloride. Areas of hemorrhage and vascular injury were also measured. In all hearts, the extent of hemorrhage and vascular injury was less than the extent of necrosis (10.2 +/- 4.6% vs 19.8 +/- 8.6% [mean +/- SD], p < 0.01). Further, hemorrhage was always within the area of necrosis, primarily in the subendocardial portion. Hemorrhage after reperfusion occurred only in necrotic tissue where carbon labeling indicated severe vascular injury before reperfusion, suggesting that the hemorrhage was the consequence of preexisting microvascular injury, not its cause.

Animals↗

Augmented interleukin-18 production by peripheral blood monocytes in patients with minimal-change nephrotic syndrome.

BACKGROUND/AIM: The etiology of minimal-change nephrotic syndrome (MCNS) is poorly understood. It has been proposed that cell-mediated immunity and T-cell activation are key features of this glomerular disease. Interleukin (IL)-18, a novel interferon-gamma-stimulating factor, may act as an important effector molecule involved in various immune responses. To our knowledge, very little is known about the involvement of IL-18 in NCNS. The aim here was to define further the involvement of IL-18 in MCNS. METHODS: To understand the role of this cytokine, in vitro IL-18 levels were analyzed by a sensitive enzyme-linked immunosorbent assay (ELISA) method in 16 patients with MCNS who were either in a stable or active condition. The disease controls included 16 patients with IgA nephropathy (IgAN). The IL-18 levels were compared with values in healthy controls. RESULTS: Significantly increased spontaneous and lipopolysaccharide (LPS)-stimulated production of IL-18 was detected in peripheral blood monocyte (PBM) cultures of MCNS patients with the nephrotic syndrome (NS) as compared with those of normal controls. Moreover, when individual MCNS patients were followed through their clinical illness, IL-18 levels were increased during the active phase and normalized as the patients went into remission. The amounts of IL-18 are significantly correlated with the levels of vascular permeability factor (VPF) in MCNS patients. CONCLUSIONS: Thus, in MCNS patients, the level of IL-18 was increased and this increase was related to the activity of this disease. The data provide circumstantial evidence for a role of IL-18 in MCNS.

Adult↗

Increased production of macrophage migration inhibitory factor by T cells in patients with IgA nephropathy.

BACKGROUND/AIM: Several studies have demonstrated an upregulation of macrophage migration inhibitory factor (MIF) synthesis in experimental glomerulonephritis. To our best knowledge, no investigation of MIF production by T cells from patients with IgA nephropathy (IgAN) has been reported so far. MIF is one of the immunoregulatory cytokines involved in T-cell activation and delayed-type hypersensitivity. In this study, we examined MIF production of T cells from patients with IgAN to investigate the contribution of the cells to elevated serum MIF content and to its pathologic characteristics. METHODS: We measured MIF production by T cells from the peripheral blood of 20 healthy controls and 20 patients with IgAN before and approximately 10 days after the beginning of steroid therapy. The disease controls included 20 patients with minimal-change nephrotic syndrome (MCNS) before therapy. MIF concentrations in the supernatants of T-cell cultures were measured with a specific enzyme-linked immunosorbent assay (ELISA). We also investigated the relationship between MIF levels and disease activity. RESULTS: The mean level for MIF in patients with IgAN was significantly elevated compared with that of healthy controls and also higher than that of patients with MCNS. When T cells were stimulated by concanavalin A, MIF production by T cells of patients with IgAN was more enhanced than in control subjects or patients with MCNS. We also investigated the relationship between MIF levels and pathological features in IgAN patients. Our findings reveal that MIF levels correlated with the grade of glomerular crescent formation and immunofluorescent C3 deposits in the glomeruli. Moreover, MIF overproduction was significantly related to the acute exacerbation stage of IgAN patients. Elevated MIF levels during the acute phase or exacerbations were found to be decreased during spontaneous or steroid therapy-induced remission in all IgAN patients examined. CONCLUSIONS: We provide data indicating that a T-cell population isolated by negative selection from peripheral blood mononuclear cells shows increased in vitro production of MIF in IgAN, and a reduction in that production when patients are treated with corticosteroids. In this paper, we describe the hypothetical role of MIF in the pathophysiology of IgAN.

Acute Disease↗

A C2077T polymorphism of the type B human natriuretic peptide receptor gene is not associated with myocardial infarction.

INTRODUCTION: We examined previously the genomic structure of the human natriuretic peptide receptor type B (hNPRB) gene and reported a C2077T polymorphism located in exon 11 of the gene. We now have studied the C2077T polymorphism in myocardial infarction [MI] patients and non-MI [control] subjects to evaluate the value of this polymorphism as a marker for MI. MATERIAL AND METHODS: 302 subjects (163 MI patients and 139 non-MI age-matched control subjects) were studied. PCR-restriction fragment length polymorphism analysis (PCR-RFLP) was developed to detect the C2077T transition. RESULTS: The distribution of C2077T polymorphism genotypes in the MI patients (CC:CT:TT, 47.2%:41.1%:11.7%) was not significantly different from that in the control patients (CC:CT:TT, 53.2%:40.3%:6.5%) (chi 2 = 2.73, p = NS). Allele frequencies of the C2077T polymorphism were f(C/T) 68.2%/31.8% in the MI group and 73.4%/26.6% in the control group. However, no association was found between this polymorphism and clinical diagnosis of MI. CONCLUSION: Our data indicate that the C2077T polymorphism is not a useful marker of the relation between the hNPRB gene and MI in the Japanese and variations of the hNPRB gene that may be in linkage disequilibrium with this polymorphism do not play a causative role in MI.

Aged↗

Case of spinocerebellar ataxia type 1 showing high intensity lesions in the frontal white matter on T2-weighted magnetic resonance images.

We report a case of genetically confirmed spinocerebellar ataxia type 1 (SCA1) in which magnetic resonance imaging (MRI) demonstrated a high signal intensity on T2-weighted images in the white matter of the frontal lobes. The patient was a 60-year-old Japanese man who complained of gait instability and speech difficulties. He was diagnosed as having spinocerebellar ataxia at the age of 46. A CAG repeat number of the patient was 48/26. Brain MRI showed marked atrophy of the cerebellum and brain stem. The high-signal intensity lesions on T2-weighted MRI in the white matter of the frontal lobes were evident in the periventricular regions. Such MRI abnormalities have not been described in SCA1 previously.

Base Sequence↗

Isolation of the 5'-flanking region of genes by thermal asymmetric interlaced polymerase chain reaction.

BACKGROUND: Isolation of the 5'-flanking region of gene segments adjacent to known sequences is a tedious task. Thermal asymmetric interlaced (TAIL)-PCR developed in 1995 uses nested sequence-specific primers together with a shorter arbitrary degenerate primer so that the relative amplification efficiencies of specific and nonspecific products can be thermally controlled. In the present study, we modified the TAIL-PCR method to isolate the 5'-flanking region of two human genes, human natriuretic peptide receptor type A (NPRA) and type B (NPRB) genes. MATERIAL AND METHODS: We improved upon the original TAIL-PCR method in some aspects: three different series of eight AD primers were used simultaneously; a high denaturing temperature was used; and a Taq DNA polymerase developed for long and accurate PCR was used. RESULTS: We succeeded in isolating the 5'-flanking region of the NPRA and NPRB genes directly from human genomic DNA. CONCLUSION: Our TAIL-PCR method is applicable not only to be human genome but also to the genome of other life forms.

Guanylate Cyclase↗