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Biomedical subjects

M Kawase

Publications and source records attributed to M Kawase.

At least 19 recordsLinked to original sources
PubMed1998

Overexpression of SOD1 in transgenic rats protects vulnerable neurons against ischemic damage after global cerebral ischemia and reperfusion.

Transient global cerebral ischemia resulting from cardiac arrest is known to cause selective death in vulnerable neurons, including hippocampal CA1 pyramidal neurons. It is postulated that oxygen radicals, superoxide in particular, are involved in cell death processes. To test this hypothesis, we first used in situ imaging of superoxide radical distribution by hydroethidine oxidation in vulnerable neurons. We then generated SOD1 transgenic (Tg) rats with a five-fold increase in copper zinc superoxide dismutase activity. The Tg rats and their non-Tg wild-type littermates were subjected to 10 min of global ischemia followed by 1 and 3 d of reperfusion. Neuronal damage, as assessed by cresyl violet staining and DNA fragmentation analysis, was significantly reduced in the hippocampal CA1 region, cortex, striatum, and thalamus in SOD1 Tg rats at 3 d, as compared with the non-Tg littermates. There were no changes in the hippocampal CA3 subregion and dentate gyrus, resistant areas in both SOD1 Tg and non-Tg rats. Quantitative analysis of the damaged CA1 subregion showed marked neuroprotection against transient global cerebral ischemia in SOD1 Tg rats. These results suggest that superoxide radicals play a role in the delayed ischemic death of hippocampal CA1 neurons. Our data also indicate that SOD1 Tg rats are useful tools for studying the role of oxygen radicals in the pathogenesis of neuronal death after transient global cerebral ischemia.

Animals↗
PubMed1998

The development of a new mouse model of global ischemia: focus on the relationships between ischemia duration, anesthesia, cerebral vasculature, and neuronal injury following global ischemia in mice.

A new model for mouse global ischemia is presented, and the relationship of ischemia duration, cerebral vasculature, and ischemic neuronal injury has been determined. CD-1 mice anesthetized by chloral hydrate were subjected to global ischemia by bilateral common carotid artery occlusion under controlled ventilation for 3, 5, and 10 min. After evaluating the patency of the posterior communicating artery (PcomA) as hypoplastic or normoplastic, neuronal injury was independently determined in the striatum, cortex, and hippocampus in each hemisphere. Ischemic injury was strongly correlated with not only ischemia duration, but also with the patency of the PcomAs. Furthermore, neuronal injury developed in a delayed fashion after 3-min ischemia, while it was maximized at 24 h after 10-min ischemia. Physiological studies showed the induction of slight hypotension as compared with inhalation anesthesia, and improvement of blood gas data relative to spontaneous respiration. These data demonstrate the usefulness of this method to induce selective vulnerability and delayed neuronal cell death in mice, and to provide a useful model to study the detailed mechanism of global ischemia using transgenic or knockout mutant mice.

Anesthesia↗
PubMed1998

Mitochondrial susceptibility to oxidative stress exacerbates cerebral infarction that follows permanent focal cerebral ischemia in mutant mice with manganese superoxide dismutase deficiency.

Mitochondrial injury has been implicated in ischemic neuronal injury. Mitochondria, producing adenosine triphosphate by virtue of electron flow, have been shown to be both the sites of superoxide anion (O2-) production and the target of free radical attacks. We evaluated these mechanisms in an in vivo cerebral ischemia model, using mutant mice with a heterozygous knock-out gene (Sod2 -/+) encoding mitochondrial manganese superoxide dismutase (Mn-SOD). Sod2 -/+ mice demonstrated a prominent increase in O2- production under normal physiological conditions and in ischemia, as evidenced by specific oxidation of a fluorescent probe, hydroethidine, reflecting decreased activity of Mn-SOD. A mitochondrial viability assay that used rhodamine 123, which is accumulated by transmembrane potential of viable mitochondria, demonstrated accelerated development of mitochondrial injury. This rapid progress of ischemic injury resulted in exacerbation of infarct size and hemisphere enlargement, causing advanced neurological deficits but without altering DNA fragmentation induction. The present study suggests that O2- overproduced in a mitochondrial compartment, when uncoupled from antioxidant defenses, induces impairment of mitochondrial function and causes exacerbation of cerebral infarction after ischemia.

Animals↗
PubMed1998

Intraoperative TEE during mitral valve repair: does it predict early and late postoperative mitral valve dysfunction?

BACKGROUND: Intraoperative transesophageal echocardiography (TEE) using color Doppler flow mapping can accurately measure residual mitral regurgitation (MR), but it is unknown to what extent such measurements correlate with those obtained with postoperative transthoracic echocardiography (TTE). METHODS: We used intraoperative TEE (based on direct planimetry of the maximal regurgitant jet area) to measure residual MR in 42 patients who underwent mitral valve reconstruction for MR and compared these measurements with those obtained with early and late postoperative TTE. RESULTS: Residual MR as measured by intraoperative TEE correlated significantly with values obtained with both early (r = 0.66; p < 0.0001) and late (r = 0.71; p < 0.0001) postoperative TTE. Forty patients with no or trivial MR (< or =2 cm2) as measured by intraoperative TEE also had no or trivial MR as measured by early (probability of 87.5%) and late (probability of 80.0%) postoperative TEE. Of the 40 patients, 6 had clinically insignificant mild MR (< or =4 cm2) when measured by late postoperative TTE. Two other patients in whom intraoperative TEE showed mild MR developed moderate regurgitation about 3 months later. CONCLUSIONS: Intraoperative TEE correlates with early and late postoperative TTE in measurement of residual MR, suggesting it can reliably predict early and late postoperative mitral valve dysfunction.

Echocardiography, Doppler, Color↗
PubMed1998

Cyanoglycosylation products of 17-O-acetyl-testosterone.

17-O-Acetyl testosterone, which has no susceptible hydroxyl or carboxyl group for glycosylation, was glycosylated with 2,3,4,6-tetra-O-acetyl-alpha-D-glucopyranosyl bromide in the presence of a mixed catalyst, Hg(CN)2 and HgBr2, in benzene-nitromethane. Reaction occurred on the alpha, beta-unsaturated ketone on the six-membered A-ring to give six 3-O-glycosides, each bearing a cyano group at the 3- or 5-position of the aglycon, and a 3-O-glycoside bearing a CONH2 group at the 3-position. Structural analyses of these products were carried out by various NMR (1H, 13C NMR, 1H-1H and 1H-13C COSY, HMBC, and DEPT), FABMS and X-ray analyses. The mechanisms of the formations of the products are discussed. It was determined that mercuric cyanide was essential as a catalyst for the progress of the cyanoglycosylation.

Bromides↗
PubMed1998

Cellular accumulation of extravasated serum protein and DNA fragmentation following vasogenic edema.

Accumulation of serum protein has been demonstrated in injured brain cells following vasogenic brain edema. The present study was conducted to test whether this phenomenon is also observed in apoptotic cells as well as in necrotic cells. Apoptotic cell death has been implicated in a variety of brain injuries, including ischemia and trauma. Cold injury and focal cerebral ischemia-reperfusion were used to induce both vasogenic edema and apoptotic cell death. Evans blue extravasation was used to determine the cellular accumulation of serum albumin. Apoptotic cell death was evaluated by both morphological alterations and by terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end labeling (TUNEL) staining. Evans blue accumulation in cells was observed not only in the surrounding zone of the lesion after cold injury and in the entire ischemic area after focal ischemia, but was also detected in the regions remote from the primary injury site. Some of these cells demonstrated nuclei fragmentation. TUNEL staining confirmed that apoptosis was induced in the region where apoptotic cells were morphologically detected. These observations suggest that accumulation of the extravasated serum component is accompanied by apoptotic cell death following vasogenic brain edema.

Animals↗
PubMed1998

Cytosolic redistribution of cytochrome c after transient focal cerebral ischemia in rats.

Recent in vitro cell-free studies have shown that cytochrome c release from mitochondria is a critical step in the apoptotic process. The present study examined the expression of cytochrome c protein after transient focal cerebral ischemia in rats, in which apoptosis was assumed to contribute to the expansion of the ischemic lesion. In situ labeling of DNA breaks in frozen sections after 90 minutes of middle cerebral artery (MCA) occlusion showed a significant number of striatal and cortical neurons, which were maximized at 24 hours after ischemia, exhibiting chromatin condensation, nuclear segmentation, and apoptotic bodies. Cytosolic localization of cytochrome c was detected immunohistochemically in the ischemic area as early as 4 hours after 90 minutes of MCA occlusion. Western blot analysis of the cytosolic fraction revealed a strong single 15-kDa band, characteristic of cytochrome c, only in the samples from the ischemic hemisphere. Western blot analysis of the mitochondrial fraction showed a significant amount of mitochondrial cytochrome c in nonischemic brain, which was decreased in ischemic brain 24 hours after ischemia. These results provide the first evidence that cytochrome c is being released from mitochondria to the cytosol after transient focal ischemia. Although further evaluation is necessary to elucidate its correlation with DNA fragmentation, our results suggest the possibility that cytochrome c release may play a role in DNA-damaged neuronal cell death after transient focal cerebral ischemia in rats.

Animals↗
PubMed1998

[A study of minimally invasive direct coronary artery bypass (MIDCAB): comparison of low risk group and high risk group].

We started to perform MIDCAB for the cases of markedly low cardiac function from June, 1996 and obtained satisfactory results. So we expanded the indications to include only left anterior descending artery (LAD) lesion from June, 1997 and have since performed this operation on 14 cases. The 14 cases of MIDCAB were divided into two groups, Group L consisting of 6 low risk cases: 1 lesion alone without any complications involving other organ before operation and Group H made up of 8 high risk cases: multi branch lesion but rated as high risk because of the extracorporeal circulation being used. Both Group L and Group H were free of operation death and hospital death. In Group L, all the cases underwent operation without blood transfusion, the period of postoperative stay in ICU was not longer than 1 day, on catecholamine was required after operation and complications were not found either. The patency of the graft was 100 percent. The patients were discharged 13.7 days after operation. In Group H, 2 cases required blood transfusion and 3 cases required catecholamine after operation. Complication arising from operative wound were noted in 3 cases. One GEA graft to the right coronary artery and one LITA to the LAD buried in the muscle were occluded. After operation, hospital stay for 23.9 days was required. In Group L, the postoperative course was excellent, so MIDCAB was considered indicated well for this group. In Group H too, the selection of MIDCAB was considered adequate that the risk of conventional CABG is considered much higher.

Adult↗
PubMed1998

[Coronary artery bypass grafting with arterial graft alone: radial artery and inferior epigastric artery used in combination].

UNLABELLED: We experienced 8 cases in which Coronary Artery Bypass Grafting (CABG) was performed by the arterial graft alone with radial artery (RA) and inferior epigastric artery (IEA) used in addition to internal thoracic artery (ITA) and right gastroepiploic artery (RGEA). All the patients were male ranging in age from 50 to 66 years (mean 57.5 year). The number of anastomosis was 3 to 5 branches (mean 3.6 branches). IEA was anastomosed with LITA and used as a composite graft in all cases. As for the proximal anastomosis of RA it was anastomosesd with ascending aorta. On postoperative radiography of graft, LITA, RITA, IEA and RA were all patent and RGEA was occluded only in one anastomosis where it was sequentially used (96.6%). All the patients followed a satisfactory postoperative course, and no case developed any major complications. CONCLUSION: The use of IEA and RA made it possible to perform CABG using only the artery with excellent postoperative results and early patency rate of the graft.

Aged↗
PubMed1998

[Pitfalls in echocardiographic diagnosis of mitral bileaflet prolapse].

Preoperative echocardiography provides good planning information for successful repair of mitral valve regurgitation, but identifying the prolapse of both the anterior and posterior leaflets is sometimes difficult. To clarify the cause of this problem, preoperative echocardiographic findings and intraoperative observations of the prolapse were analyzed in 124 patients with non-rheumatic pure mitral regurgitation. In 48 patients with final diagnoses of bileaflet prolapse, 16 (33%) were considered to have only single leaflet prolapse before the operation. Anterior leaflet prolapse was overlooked in 14, and prolapse of either of its commissural segments was the least detectable by echocardiography. Chordal rupture was seen more in the posterior leaflet than in the anterior leaflet. Movement of the anterior leaflet may be influenced by a prolapsed and hypermobile posterior leaflet and/or regurgitant jet flow caused by the posterior leaflet prolapse.

Chordae Tendineae↗
PubMed1998

[Hemorrhage exerts different effects on variabilities of heart rate and blood pressure in dogs].

The aim of the present study was to evaluate the effects of hemorrhage on heart rate variability (HRV) and blood pressure variability (BPV) as indicators of autonomic nervous system (ANS) and hypovolemia. We induced hemorrhagic hypovolemia in 7 dogs by removing blood in graded stages (0%, 10%, 20%, 30%, 40% of the estimated blood volume; EBV). HR was unchanged during hemorrhage, while mean BP decreased significantly after 30% EBV hemorrhage. Low frequency component (LF: 0.04-0.15 Hz) of HRV significantly increased after 20% EBV hemorrhage but high frequency component (HF: 0.15-0.4 Hz) of HRV was not altered. LF of BPV increased significantly stepwise after 20% EBV hemorrhage and HF of BPV increased significantly after 30% EBV hemorrhage, showing that both LF and HF of BPV might indicate the degree of hypovolemia. During hemorrhage LF of HRV and BPV increased and HF of HRV was unchanged, indicating the shift of the autonomic balance toward sympathetic dominance. An excellent quantitative correlation between LF of BPV and the degree of hypovolemia was demonstrated during graded hemorrhage, while LF of HRV plateaued at its maximum value at 20% EBV hemorrhage. In conclusion, our study suggests that the spectral analysis of HRV and BPV during graded hemorrhage shows different characteristics in the quantitative evaluation of ANS and hypovolemia.

Animals↗
PubMed1997

Attenuation of nitric oxide synthase induction in IRF-1-deficient glial cells.

Nitric oxide (NO) produced by inducible nitric oxide synthase (iNOS) exerts inhibitory and cytotoxic effects on various cells including neuronal cells. Glial NO production, mediated via induction of iNOS, is thought to facilitate neuronal damage during cerebral ischemia. Recently, interferon regulatory factor-1 (IRF-1) has been reported to be an essential transcription factor for iNOS mRNA induction in murine macrophages. However, expression of IRF-1 and its role in the central nervous system have not been examined. In the present study, by using primary glial cell cultures from mice with targeted disruption of the IRF-1 gene, we investigated whether IRF-1 is involved in iNOS mRNA induction in glial cells. After stimulation with lipopolysaccharide and interferon-gamma, IRF-1 mRNA was strongly induced in wild-type (IRF-1 +/+) glial cells. iNOS mRNA induction and nitrite production in IRF-1 -/- glial cells were reduced as compared with those observed in IRF-1 +/+ glial cells. Diethyldithiocarbamate, a selective inhibitor of nuclear transcription factor kappa B (NF-kappa B), completely inhibited iNOS mRNA induction. These results suggest that not only NF-kappa B but also IRF-1 play important roles in iNOS mRNA induction in the central nervous system.

Animals↗
PubMed1997

Effectiveness of fructose-modified chitosan as a scaffold for hepatocyte attachment.

Free amino groups of chitosan, a substance which has previously been shown to be a good scaffold for hepatocyte attachment, were covalently modified with fructose. The modification significantly increased the number of cells that could be attached on the surface of chitosan gel. Rat hepatocytes cultivated on fructose-chitosan behaved similarly to those on unmodified chitosan, i.e., they retained the spherical shape they have in vivo, and released much less lactate dehydrogenase than cells attached on a collagen-coated surface. The modification with fructose did not alter the important characteristics of chitosan for hepatocyte culture: liver-specific functions such as urea synthesis and drug metabolism were stably maintained for 5 d in the hepatocytes cultured on fructose-chitosan. In sharp contrast, hepatocytes attached on a collagen-coated surface underwent a severe morphological change, from spherical to flat, and lost almost all their lidocaine-removal activity within 5d. A very thin fructose-chitosan layer was also applied onto the collagen-coated surfaces of polystyrene plates and a dextran microcarrier by crosslinking free amino groups in the chitosan and collagen with glutaraldehyde to fix the thin layer. Hepatocytes on the fructose-chitosan-coated surface retained their spherical shape, masking the cell-flattening effect of the collagen layer. Perfusion culture was then carried out using a hollow-fiber cartridge in which hepatocytes attached on fructose-chitosan-coated microcarriers were suspended in the extracapillary space: the liver-specific functions were stably maintained during 4d of the culture. A fructose-chitosan-coated surface thus appears to be a very promising scaffold for hepatocyte attachment which can be used in cellular biological studies of liver functions, especially in relation to cytochrome P450, as well as in bioartificial liver support systems.

Animals↗
PubMed1997

Application of glutaraldehyde-crosslinked chitosan as a scaffold for hepatocyte attachment.

The effectiveness of chitosan, a biocompatible polymer derived by the deacetylation of chitin, as a scaffold of hepatocyte attachment, was examined. Since chitosan gel was too fragile to use for cell culture, its free amino groups were crosslinked by glutaraldehyde to increase its strength. Rat hepatocytes seeded onto glutaraldehyde-crosslinked chitosan (GA-chitosan) gel could stably attach to the surface, retaining its spherical form, the same as in vivo, and then release a very small amount of lactate dehydrogenase during the 5 d culture period. By contrast, hepatocytes on a collagen-coated surface spread flat, and they released much more lactate dehydrogenase than those on the GA-chitosan gel. Hepatocytes on GA-chitosan also retained higher urea synthesis activity, a liver-specific function, than those on the collagen-coated surface. These results indicate that chitosan is a promising biopolymer as a scaffold of hepatocyte attachment, which can be applied to an effective bioartificial liver support system.

Animals↗
PubMed1997

Severe hemolysis due to artificial chordae displacement.

Hemolytic anemia is a well-recognized complication of mechanical heart valve prosthesis but, as yet, has not been reported after mitral valve repair with chordal replacement. We report a case of severe hemolytic anemia after mitral valve repair with chordal replacement and Carpentier-Edwards annuloplasty ring insertion. Progressive prolapse of the anterior leaflet due to the artificial chordae being too long caused recurrent regurgitation which was responsible for the hemolysis. The patient also had idiopathic thrombocytopenic purpura, but successful second mitral valve repair was performed after high-dose gamma-globulin therapy.

Anemia, Hemolytic↗