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Biomedical subjects

K Takeuchi

Publications and source records attributed to K Takeuchi.

At least 739 records · Page 41Linked to original sources
PubMed1993

Endogenous sulfhydryls in healing gastric mucosal injury induced by HCl in the rat.

The role of endogenous sulfhydryls (SH) in the healing of HCl-induced gastric injury was investigated in the rat. The animals fasted for 18 h were given 1 ml of 0.6 N HCl by gavage, and they were fed normally from 1 h later and killed various days after HCl treatment. Gastric lesions induced by HCl healed to quiescent states within 7 days both macroscopically and histologically. Mucosal SH levels were markedly reduced after induction of damage by HCl, but recovered gradually to or above normal values within 5 days. Gastric acidity was also significantly reduced after administration of 0.6 N HCl (induction of lesions), followed by a return to normal values within 5 days, although the volume of gastric contents remained unchanged before and after HCl treatment. The healing of HCl-induced gastric lesions was significantly impaired by diethylmaleate (DEM 0.3 ml/kg x 2) when this drug was given subcutaneously for 5 days. Glutathione (GSH: 100 mg/kg x 2) alone did not affect the healing of gastric lesions, but the combined administration of GSH with DEM significantly antagonized the delayed healing caused by DEM. Administration of DEM caused a marked and persistent reduction in the mucosal SH contents, while GSH by itself significantly increased the mucosal SH levels and partially reversed the reduced SH contents caused by DEM. Gastric acid secretion was not significantly altered by either DEM or GHS. These results suggest that endogenous SH may play some roles in the healing process of gastric mucosal lesions. DEM caused a deleterious effect on the healing of gastric lesions, probably by reducing the mucosal SH.

Animals↗
PubMed1993

Angiographic-pathologic correlations after elective percutaneous transluminal coronary angioplasty.

BACKGROUND: The local effect of coronary angioplasty is evaluated on the basis of postangioplasty angiograms. Smooth-walled dilation is considered to represent minimal or no injury, whereas intraluminal haziness corresponds with wall laceration. This study correlates the preangioplasty and postangioplasty angiograms with the histopathology of the target sites. METHODS AND RESULTS: The study includes 12 patients, each undergoing an elective procedure, and covers 19 angioplasty sites. Smooth-walled dilation and intraluminal haziness were not mutually exclusive. The angiograms were interpreted as smooth-walled dilation (n = 3), smooth-walled dilation with intraluminal haziness (n = 4), intraluminal and extraluminal haziness (n = 5), extraluminal dissection (n = 5), spiraltype dissection (n = 1), and aneurysm (n = 1). The histology of the arterial segments revealed wall laceration in all. Smooth-walled dilation without intraluminal haziness correlated with laceration limited to the intima in two, but with medial injury in one. Smooth-walled dilation with intraluminal haziness correlated with laceration limited to the intima in two and with medial injury in two. Intraluminal and extraluminal haziness corresponded with extensive laceration with deep involvement of the media in each. Extraluminal dissection correlated with a dissection along the shoulder area of the plaque, creating a broad-based flap. The spiral-type dissection corresponded with a true dissection into the plaque-free media. The aneurysm correlated with partial washout of an atherosclerotic plaque. CONCLUSIONS: The angiographic image of intraluminal and extraluminal haziness indicates extensive medial laceration. Smooth-walled dilation, with or without intraluminal haziness, is not a reliable indicator. The study emphasizes the need to reconsider the interpretations of postangioplasty coronary angiograms.

Aged↗
PubMed1993

Molecular structure and transcriptional function of the rat vascular AT1a angiotensin receptor gene.

Rat vascular angiotensin receptors (AT1a receptors) are encoded by two mRNA transcripts sharing an identical receptor coding sequence but differing in their 5' and 3' untranslated sequences. We screened male Sprague-Dawley rat genomic libraries to clone the vascular AT1a receptor gene. Two sets of overlapping clones were isolated that encode over 90 kb of genomic sequence around the AT1a receptor gene. Four overlapping clones were identified from the 5' flanking portion of the gene. These contain the promoter region and two exons, 141 bp and 89 bp in size, respectively, encoding the alternatively spliced 5' untranslated mRNA sequence. Six additional clones overlap each other but do not overlap the set of clones from the 5' flanking region of the gene. These contain a single 1977-bp exon that encodes 900 bp of the 5' and 3' untranslated sequences in addition to a 1077-bp open reading frame identical to that found in vascular smooth muscle cell AT1a receptor cDNAs. Primer extension and RNase protection studies indicate that the transcription start site for this gene begins 9 bp upstream from the most 5' sequence found within the AT1a receptor cDNAs. Our mapping studies of the cloned gene, which so far includes an uncloned gap within the second intron, indicate that the transcription start site is no less than 67 kb upstream from the receptor coding exon. Promoter-reporter assays were performed by transfection of vascular smooth muscle cells with deletions of a 3.2-kb promoter region fused to a luciferase cDNA reporter plasmid. Relatively strong basal transcriptional activity is observed from the 5'-most 2 kb of the promoter and diminishes markedly with deletions within 1 kb of the early promoter region, suggesting strong promoter elements in the more upstream regions of the gene. Deletion of a 53-bp early promoter region containing the transcription start site and a putative TATA box completely abolishes the ability of upstream elements to drive transcription of the luciferase cDNA. These results indicate that we have isolated the AT1a receptor gene and its functional promoter.

Animals↗
PubMed1993

Estimation of infarct size using serum troponin T concentration in patients with acute myocardial infarction.

To estimate the size of myocardial infarction, serum troponin T concentration was measured in 34 patients with acute myocardial infarction. Left ventriculography, 2-dimensional echocardiography and resting 201thallium myocardial single photon emission computed tomography (SPECT) were performed about 4 weeks after the onset of myocardial infarction and used for correlation with the late serum troponin T peak concentration which occurred on the 3rd to 5th day after onset. Both left ventricular ejection fraction (LVEF) obtained from left ventriculography and wall motion index (WMI) obtained from 2-dimensional echocardiography were inversely related to late troponin T peak value (LVEF: r = 0.68, p < 0.001, WMI: r = 0.70, p < 0.001). Extent score (ES) and severity score (SS), which were estimated from the initial resting 201thallium SPECT image, showed excellent linear correlations with late troponin T peak concentrations (ES: r = 0.77, p < 0.001, SS: r = 0.66, p < 0.001). This correlation was present both in patients with an early troponin T peak on day 1 (group A-16 patients) and in those without an early peak (group B-10 patients). Thus, late troponin T peak concentration can be used to predict infarct size regardless of the kinetics of its appearance in serum.

Adult↗
PubMed1993

Role of nitric oxide in the vasodilatory responses to acetylcholine and bradykinin in perfused hearts.

The role of nitric oxide in the coronary vasodilation caused by acetylcholine or bradykinin in perfused guinea-pig hearts was investigated by using 1 mM L-NG-nitro arginine (L-NNA), a specific inhibitor of the formation of nitric oxide from L-arginine. L-NNA increased coronary perfusion pressure and inhibited the vasodilator responses to acetylcholine and bradykinin. The extent of vasodilation was evaluated in terms of the reduction of perfusion pressure from the initial baseline that had been induced by U-46619. L-NNA markedly attenuated coronary vasodilation caused by 5 x 10(-11) mol of acetylcholine from 15 +/- 1 to 4 +/- 1 mmHg (p < 0.01), and that caused by 1 x 10(-11) mol bradykinin from 21 +/- 2 to 8 +2- 1 mmHg (p < 0.01). On the other hand, L-NNA only weakly inhibited coronary vasodilation caused by 5 x 10(-7) mol of acetylcholine from 40 +/- 3 to 27 +/- 4 mmHg (p < 0.01), and that caused by 1 x 10(-9) mol of bradykinin (from 39 +/- 2 to 32 +/- 2 mmHg (p < 0.01). L-NNA had no effect on the vasodilation induced by 1 x 10(-8) mol of bradykinin. Ibuprofen, cyclooxygenase inhibitor, did not affect these vasodilatory responses. These results suggest that the formation of nitric oxide from L-arginine in coronary resistance vessels helps to regulate vascular tone, and that prostaglandins are not related to the vasodilatory responses to acetylcholine or bradykinin.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1993

Cytoprotective action of L-arginine against HCl-induced gastric injury in rats: involvement of nitric oxide?

We examined the cytoprotective effect of L-arginine on gastric damage induced by 0.6 N HCl in rats and investigated whether the mechanism of this action is related to the nitric oxide (NO)-mediated protection. The animals were given 0.6 N HCl by gavage and killed 1 hr later. L-Arginine (100, 300 and 750 mg/kg) given p.o. 30 min before HCl treatment prevented these lesions in a dose-dependent manner, but had no effect when given i.v. (200 mg/kg). Similar effects were observed by D-arginine but not by an equimolar dose of mannitol. This effect of L-arginine (p.o.) was attenuated significantly by prior administration of indomethacin (5 mg/kg, s.c.) but not by NG-nitro-L-arginine methyl ester (L-NAME) (5 mg/kg, i.v.), the NO synthase inhibitor. Both L- and D-arginine produced a reduction in potential difference (PD), inhibition of gastric motility, and increases of luminal pH and mucosal blood flow when they were given intragastrically. Indomethacin significantly mitigated these changes induced by L-arginine except PD reduction, while L-NAME showed significant inhibition only against the increased pH response. We conclude that L-arginine given p.o. exhibits gastric cytoprotection against HCl-induced damage in rats, probably by acting as a mild irritant. The mechanism of this action may appear through "adaptive cytoprotection" mediated by endogenous prostaglandins and does not involve the NO-mediated protective pathway.

Animals↗
PubMed1993

Capsaicin-sensitive sensory nerves in recovery of gastric mucosal integrity after damage by sodium taurocholate in rats.

We compared the recovery process of gastric mucosal integrity after damage by 20 mM sodium taurocholate (TC) in control, sensory deafferented and indomethacin-treated rats. Under anesthetized conditions, the stomach was mounted on a chamber and perfused with saline or 50 mM HCl. Application of TC (30 min) to the saline-perfused stomach produced a marked reduction in the potential difference (PD) (surface epithelial damage), followed by increases of gastric mucosal blood flow (GMBF) and luminal pH (alkalinization), but there was a rapid recovery of PD without development of gross lesions. Chemical ablation of capsaicin-sensitive sensory nerves had no influence on the PD reduction and luminal alkalinization, but significantly inhibited the rise in GMBF and the PD recovery. Indomethacin pretreatment (5 mg/kg, s.c.) significantly inhibited these changes seen after exposure to TC, except for PD reduction. In contrast, TC caused a sizable amount of H+ back-diffusion and a more pronounced and persistent rise in GMBF in the stomach perfused with 50 mM HCl, yet only minimal damage was observed in the control animals. Under these conditions, both sensory deafferentation and indomethacin inhibited such GMBF responses, leading to hemorrhagic damage without affecting the degree of H+ back-diffusion. These results suggest that capsaicin-sensitive sensory nerves contribute to the recovery of gastric mucosal integrity after damage, probably by maintaining GMBF responses associated with H+ back-diffusion and preventing the later extension to gross damage in the presence of acid.

Animals↗
PubMed1993

A case of secondary aldosteronism similar to Bartter's syndrome with no abnormality in renal chloride reabsorption.

We had a 20-year-old male patient of secondary aldosteronism similar to Bartter's syndrome, which had proved to be evident after the remission of nephrotic syndrome. In the patient, hypokalemic alkalosis and hyperreninemic hyperaldosteronemia were observed, although the blood pressure was normal. Hyperplasia of juxtaglomerular cells was observed and no abnormalities indicating either glomerulonephritis or renal artery stenosis were found; the pressor response to intravenously infused angiotensin (ang) II was markedly decreased; urinary prostaglandin (PG) E2, kallikrein and kinin excretion were elevated. The inhibition of PG synthesis with indomethacin decreased renal PG production and partially corrected both hypokalemia and pressor responsiveness to ang II. Thus, this case is considered to be a case of Bartter's syndrome. Contrary to the previously reported observations, the effective fractional chloride reabsorption rate in the renal distal tubules was normal (> 80%) and not changed by PG inhibition. Plasma atrial natriuretic peptide level was normal. An interaction between renin-angiotensin and PG systems appears to play a prior role in this case. To explain the pathophysiology, we have hypothesized an abnormal function of ang II receptor signal transduction which excessively stimulates PLA2, resulting in overproduction of PG synthesis in tissues.

Adult↗
PubMed1993

[Analysis by two-dimensional electrophoresis of the cause of myocardial dysfunction in aging rat hearts].

The severity and frequency of atherosclerosis, diabetes, and ischemic heart disease, which affect cardiac function, increase with aging. Although there are many reports about hemodynamic and histopathological studies about aging hearts, there are very few studies on changes in structural proteins in aging hearts. We investigated the contractile proteins of the left ventricles in rats aged 6, 12 and 125 weeks using two-dimensional electrophoresis. There were no difference in structural proteins in heart between 6-week and 12-week-old rats. The contents of myosin heavy chain, myosin light chain 2, actin, troponin-I in 125-week-old rats decreased compared with those of 12-week-old rats. Myosin heavy chain, which is one component of myosin, interacts with actin and changes chemical energy to mechanical energy. Therefore its decrease leads to a decline in myocardial contractility. These results seem to indicate one of the most important changes in the aging rat heart, as well as impairment in relaxation by the increase of interstitial fibrosis and decline of Ca uptake by sarcoplasmic reticulum.

Aging↗
PubMed1993

Stimulation by nitric oxide synthase inhibitors of gastric and duodenal HCO3- secretion in rats.

The role of nitric oxide (NO) in the regulation of gastroduodenal HCO3- secretion was investigated in anesthetized rats using the NO biosynthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME). HCO3- secretion was measured at pH 7.0 using a pH-stat method in the chambered stomach in the presence of omeprazole or in the proximal duodenum. Intravenous administration of L-NAME (1-5 mg/kg) increased HCO3- secretion in a dose-dependent manner in both the stomach and duodenum, with a concomitant elevation of arterial blood pressure. The stimulatory effect of L-NAME on HCO3- secretion was mimicked by another NO synthase inhibitor, NG-monomethyl-L-arginine (50 mg/kg), but not by the enantiomer NG-nitro-D-arginine methyl ester, and was significantly antagonized by concurrent administration of L-arginine, but not D-arginine, at 200 mg/kg. The exogenous NO donor nitroprusside (4 mg/kg) by itself decreased the rate of HCO3- secretion and significantly antagonized the HCO3- stimulatory action of L-NAME. Furthermore, the increased HCO3- secretion caused by L-NAME was significantly attenuated by prior administration of atropine (1 mg/kg, s.c.) or indomethacin (5 mg/kg, s.c.) and by bilateral vagotomy but was not influenced by sensory deafferentation after capsaicin pretreatment, though none of the treatments had any effect on the changes in blood pressure induced by L-NAME. These results suggest that L-NAME stimulates HCO3- secretion in the gastroduodenal mucosa. This action is associated with the inhibition of NO biosynthesis and may be partly dependent on vagal-cholinergic innervation and mediated by endogenous prostaglandins.

Amino Acid Oxidoreductases↗
PubMed1993

[Relationship between cerebral circulatory arrest and loss of brain functions--analysis of patients in a state of impending brain death].

To clarify the temporal discrepancies between cerebral circulatory arrest and loss of brain functions in relation to neuroradiological differences of brain damage, we analyzed 100 cases of impending brain death evaluated by neurological findings and continuous, simultaneous neuromonitoring of somatosensory and brainstem auditory evoked potentials (SEP, BAEP), compressed spectral arrays (CSA), and transcranial Doppler sonography (TCD). A) Cases of supratentorial lesions: 1) Loss of brain functions after supratentorial circulatory arrest (TCD) were advanced rostrocaudally -(SEP N20 > CSA) > (BAEP III-V > SEP P13/14). 2) All patients demonstrated supratentorial circulatory arrest (TCD) after both neurological and cerebral (CSA) functions had been lost for more than 6 hours or after loss of neurological, cerebral (CSA), and brainstem (BAEP, SEP) functions. B) Cases of diffuse or infratentorial lesions: Supratentorial circulation persisted in a few cases after loss of all brain functions. C) The interval from supratentorial circulatory arrest to brainstem function loss was longer than that to cerebral function loss. Both intervals were less than 24 hours in almost all cases. In applying ancillary studies to the diagnosis of brain death, consideration should be given to the time lag between cerebral circulatory arrest and loss of brain functions caused by pathophysiological differences in brain damage.

Adolescent↗
PubMed1993

[Adequacy of translating health survey questionnaires for cross-cultural surveys--the case of the Todai Health Index].

The adequacy of the language translation of self-administered questionnaire items was examined in a comparative study of adolescent mental health between Japan and the United States. As a screening instrument to be used in both countries, the Todai Health Index (THI) questionnaire had been translated from original Japanese into English. The original version was administered to 570 Japanese adolescents and the translated version was given to 295 middle school students in the United States (aged 12 to 15). The equivalence of the two versions was re-examined based on the results of the surveys by a team of researchers from both countries including a bilingual investigator. For the items which produced a statistically significant different response pattern between the two samples, the investigators attempted to determine whether the observed difference could be attributed to an inadequate translation or to a real cultural difference. For those items judged to suffer from inadequate translation, modifications were made to improve cross-cultural equivalence. The above methodological procedure, though not perfect, proved to be relatively simple but very useful in resolving many practical issues in cross-cultural studies and produced interesting findings. For example, the phrase "worry about" was found to not adequately capture the Japanese meaning of "ki-ni-naru" and instead the phrase "concern about" or "care" was suggested as a more appropriate substitute. Very little is known and insufficient attention has been given to the effect of translation in cross-cultural surveys. These investigations suggest the benefit of more extensive studies and focused discussions of reliability of the translated survey instruments by public health researchers involved in international comparisons.

Adolescent↗
PubMed1993

[Study on platelet satellitism].

The platelet leukocyte adherence phenomenon, so-called 'Platelet Satellitism (PS)', was recognized on peripheral blood smear from ethylenediaminetetraacetic acid (EDTA)-anticoagulated blood in two patients. The present study was undertaken to elucidate both inducing and inhibitory factors for PS by utilizing two patients' blood. Both heparin and sodium citrate could not induce PS in these patients. This phenomenon was inhibited by anti-platelet membrane glycoprotein (GP) IIb/IIIa complex antibody (AP-2), but not by antibodies against platelet membrane glycoprotein (GP) Ib/IX complex, fibrinogen and von Willeb and factor. Patients' sera were subjected to column chromatography of Sephacryl S-300 to obtain immunoglobulin (Ig) G, IgA and IgM fractions. In one patient, IgG fraction, but neither IgA nor IgM fractions could induce PS phenomenon in normal whole blood, while IgA but neither IgG nor IgM could induce PS in another patient. Furthermore, when purified IgG from the first patient was treated with 2U/ml of plasmin to digest Fc portion, PS phenomenon disappeared. The F(ab')2 portion was prepared from whole IgG treated with pepsin, then added to normal whole blood. Purified F(ab')2 fragment by itself could not induce PS phenomenon, whereas the preincubation of F(ab')2 in normal whole blood could inhibit the PS caused by the patient's whole IgG. These results indicate that platelet membrane glycoprotein (GP) IIb/IIIa complex and both Fab and Fc portions of immunoglobulin might be necessary to induce PS phenomenon in EDTA-anticoagulated whole blood.

Adult↗
PubMed1993

[Transvenous pacemaker implantation for sick sinus syndrome with mirror-image dextrocardia].

A case of sick sinus syndrome with mirror-image dextrocardia which was associated with bilateral superior vena cava and an absent inferior vena cava with azygos continuation is reported. A 45-year-old woman was referred to our hospital with the chief complaints of dizziness and palpitation. The electrocardiogram showed a atrial fibrillation with a 4-second period of asystole. A permanent endocardial bipolar demand pacemaker was inserted through the left superior vena cava. Since anomaly of venous system is commonly associated with mirror-image dextrocardia, the angiogram is necessary prior to permanent pacemaker implantation.

Dextrocardia↗
PubMed1993

[Effect of angiotensin-converting enzyme inhibitors in congestive heart failure].

Angiotensin-converting enzyme (ACE) inhibitors, in conjunction with diuretic agents, have an established role in the management of moderate and severe heart failure due to left ventricular dysfunction. ACE inhibitor improves prognosis, symptoms and exercise performance. There have been some promising studies and one of the most widely quoted is the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS I), which demonstrated a 36% reduction in mortality with the ACE inhibitor, enalapril, versus placebo in patients with advanced heart failure. Over the last few years, we have received important information that seems to tell us that ACE inhibitors must be utilized if we hope to reduce mortality. An important topic is study the action of ACE inhibitors in improving prognosis, and the mechanism of the action.

Angiotensin II↗
PubMed1993

[An adult case of secundum atrial septal defect with severe postoperative pulmonary hypertensive crisis].

We reported an adult case of secundum atrial septal defect with severe postoperative pulmonary hypertensive crisis. A 52 year-old female with secundum atrial septal defect and pulmonary hypertension underwent ASD patch closure. After the operation she experienced severe postoperative pulmonary hypertensive crisis. Only administration of PGE1 through the pulmonary artery was effective of hemodynamic improvement and reduction of pulmonary hypertension. Histological diagnosis of lung biopsy showed thromboembolism of small pulmonary artery. Pulmonary hypertension has not been evident during the 3 months since the cardiac catheterization was performed.

Alprostadil↗
PubMed1993

A cloned angiotensin receptor isoform from the turkey adrenal gland is pharmacologically distinct from mammalian angiotensin receptors.

A 2046-base pair cDNA clone, homologous to mammalian angiotensin (AT) AT1 receptors, was isolated from a library prepared from adrenal glands of the domestic turkey (Meleagris gallopavo). Sequence analysis of the cDNA insert in clone pTAT2' reveals a 1077-base pair open reading frame predicting a 359-amino acid protein approximately 75% homologous to mammalian AT1 receptors. Saturation radioligand binding studies performed in membranes of COS-7 cells transfected with pTAT2' show high affinity specific binding of 125I-angiotensin II, with a Kd of 172 pM. The rank order of affinities for a series of ligands determined by competition binding studies is angiotensin II > or = [Sar1,Ile8]-angiotensin II > angiotensin III approximately [Sar1,Ala8]-angiotensin II approximately CGP42112A > angiotensin I > Dup753 > PD123177. This rank order of affinity series differs substantially from that for mammalian AT1 receptors and AT2 binding sites. Angiotensin II (100 nM) can stimulate inositol phosphate production similarly in COS-7 cells transfected with pTAT2' and in COS-7 cells transfected with the AT1a receptor cDNA pCa18b. This response in pTAT2'-transfected cells is not attenuated in the presence of 30 microM Dup753. In contrast, this concentration of antagonist attenuates > 90% of the inositol phosphate response to angiotensin II in COS-7 cells transfected with the rat AT1a receptor cDNA. These results demonstrate an avian structural homologue of mammalian AT1 receptors possessing distinct pharmacological properties with both peptide and nonpeptide AT receptor ligands.

Adrenal Glands↗