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Biomedical subjects

K Takeuchi

Publications and source records attributed to K Takeuchi.

At least 1,009 records · Page 56Linked to original sources
PubMed1989

[Modified Fontan procedure on 106 cases: indication and surgical results].

Since 1974, we have performed modified Fontan procedure on 106 patients, ranging in ages from 1 to 32 years, consisting of 44 cases of tricuspid atresia (TA), 21 with univentricular heart (UVH) of right ventricular type, 18 with UVH of left ventricular type, for which ventricular partition was unfeasible, and 23 with various complex anomalies. Hospital mortality rates for TA and other complex anomalies were 11.4 and 11.3%, respectively. Surgical results have markedly improved recently. Since 1986, 50 cases underwent Fontan procedure with 3 hospital deaths (6.0%). Late death occurred in 4 cases in a mean follow-up period of 49 months. Regarding the indication for operation, majority of patients had 2 to 3 parameters which were out of 10 criteria for Fontan procedure. Regurgitation of atrioventricular valve was repaired by annuloplasty in 19 patients underwent Fontan procedure and 17 survived. Abnormal systemic venous connection was seen in 11 cases and all survived. Association of total anomalous pulmonary venous connection is still a difficult problem and 2 of 5 cases died. Fontan procedure was performed in 8 patients following palliative right ventricular outflow reconstruction for poor development of pulmonary artery and 7 survived. Cumulative mortality rate for the entire series was relatively well at 15.1%.

Adolescent↗
PubMed1988

[Studies on the effects of placental lactogen on calcium metabolism during pregnancy].

In order to clarify the dynamics in maternal calcium metabolism during pregnancy, serum concentrations of ionized calcium, calcium regulating hormones and intestinal calcium absorption were measured in pregnant and hypophysectomized(HX) rats. Serum concentrations of ionized calcium decreased significantly late in pregnancy. Serum levels of 1 alpha,25-(OH)2 vitamin D3 (D3) increased late in pregnancy, however, those of parathyroid hormone (PTH) increased not significantly throughout pregnancy. Serum levels of calcitonin(CT) and intestinal calcium absorption increased as pregnancy progressed. Administration of human placental lactogen(hPL), bovine growth hormone(bGH) and ovine prolactin(oPRL) to the HX-rats remarkably enhanced intestinal calcium absorption. Serum concentrations of 1 alpha,25-(OH)2D3 significantly increased by administration of bGH and hPL to the HX-rats, but they did not increase significantly by oPRL administration. These data suggest that 1) maternal intestinal calcium absorption might be increased by the action of increased serum 1 alpha,25-(OH)2D3 and the maternal bone might be kept at the same density throughout pregnancy because serum CT protects the maternal skeleton by resisting the bone-resorption activities of 1 alpha,25-(OH)2D3; and 2) placental lactogen may play an important role on the increase of intestinal calcium absorption by stimulating the production of 1 alpha,25-(OH)2D3 during pregnancy. From these results, it is considered that these alterations of calcium metabolism in the maternal side are the rational responses to supply Ca to the fetus and newborn for keeping their calcium homeostasis.

Animals↗
PubMed1988

Occurrence of a cobalt-induced and cobalt-containing nitrile hydratase in Rhodococcus rhodochrous J1.

The formation of nitrile hydratase required cobalt ions in Rhodococcus rhodochrous J1. No other transition-metals could replace the cobalt ion. The Rhodococcus nitrile hydratase was purified to homogeneity and found to contain a cobalt atom. The occurrence of a cobalt-induced and cobalt-containing nitrile hydratase, different from the nitrile hydratases in Pseudomonas chlororaphis B23 and Brevibacterium R312 containing a ferric ion in their active center, has been demonstrated here for the first time.

Brevibacterium↗
PubMed1988

The effect of inosine on the post ischemic heart as bio-energy recovering factor in 31P-MRS.

Perfused guinea-pig hearts, which were analyzed by 31P-MRS, were subjected to 30 and 60 minute ischemia and reperfused using two perfusates, one containing 200 microM inosine, and the other without inosine. After 4 hour reperfusion with inosine, ATP levels increased to 95.5% of preischemic value (30 minute ischemia) and 76.2% (60 minute ischemia). However, after 4 hour reperfusion without inosine, ATP levels increased only to 72.2% (30 minute ischemia) and to 48.2% (60 minute ischemia). In 60 minute ischemic hearts reperfused with inosine, left ventricular maximal positive dp/dt (LV dp/dt) was improved significantly to 82.4% after 6 hour reperfusion in contrast to hearts reperfused without inosine (43.1%). Administration of inosine was very useful for increasing myocardial gross energy product and improving cardiac performance.

Adenosine Triphosphate↗
PubMed1988

31P-MRS study of bio-energy recovering phenomenon.

The ATP and creatine phosphate (PCr) contents in isolated guinea-pig hearts were determined by 31P-MRS measurement at 80.75 MHz using the Langendorff technique. Reperfusion of post-ischemic hearts with adenosine for 180 minutes increased ATP to 117.4% and decreased PCr to 59.8% of the preischemic value. Reperfusion without adenosine did not increase ATP and did not decrease PCr. The depressed cardiac function due to ischemia was remarkably improved in post-ischemic hearts by the increase in ATP due to adenosine. We found that the loss of ATP due to ischemia is not necessarily proportional to the extent of myocardial ischemic injury.

Adenosine↗
PubMed1988

Determination of mechanisms of myocardial ischemic injury by 31P-MRS effect of catecholamine on ischemic hearts.

To investigate mechanisms of development in ischemic myocardial injury, intracellular pH and high energy phosphates in perfused guinea-pig hearts were monitored by 31P-MRS. Intracellular ATP content decreased to 1.2% and 26.4% of control during 60 minutes global ischemia, respectively with and without preischemic administration of isoproterenol. Intracellular pH declined to 6.48 and 6.03 respectively. Postischemic cardiac function was severely impaired by isoproterenol. ATP breakdown had little influence on intracellular pH in ischemic hearts. It was verified that inotropic agents can progress ischemic myocardial injury, and that contractile recovery is more correlated with the residual ATP level than intracellular pH.

Adenosine Triphosphate↗
PubMed1988

The effect of an orally administered proteolytic enzyme on the elasticity and viscosity of nasal mucus.

We have evaluated the effect of serratiopeptidase (SER), a proteolytic enzyme, on the elasticity and viscosity of the nasal mucus in adult patients with chronic sinusitis. SER was administered in a dose of 30 mg/day orally for 4 weeks. Nasal mucus was collected from the nasal cavities of each patient before (week 0) and 4 weeks after the start of the medication (week 4). The storage modulus (G') and the dynamic viscosity (eta') of each specimen of nasal mucus were determined by an oscillating sphere magnetic rheometer at frequencies of 0.5, 1, 5, 10 and 20 Hz at a constant temperature of 25 degrees C. The dynamic viscosity (eta') of the mucus at week 4 was significantly lower than that at week 0 (at frequencies of 5, 10 and 20 Hz). No significant differences were observed in the storage modulus (G') between the mucus at week 0 and week 4. SER reduced the viscosity but not the elasticity of the nasal mucus. These findings are discussed in relation to mucociliary clearance.

Administration, Oral↗
PubMed1988

Gastric motility is an important factor in the pathogenesis of indomethacin-induced gastric mucosal lesions in rats.

Effects of atropine, cimetidine, and 16,16-dimethyl prostaglandin E2 (16,16-dmPGE2) on indomethacin-induced gastric lesions were investigated in rats by correlating their effects on gastric acid and HCO3- secretion and motility. Subcutaneously administered indomethacin (25 mg/kg) produced gastric mucosal lesions within 4 hr. In parallel studies, an equivalent dose of indomethacin inhibited gastric HCO3- secretion, and stimulated gastric motor activity measured as intraluminal pressure recordings, whereas acid secretion was unaffected. The lesions induced by indomethacin were significantly prevented by three agents: cimetidine (100 mg/kg), which reduced acid secretion; atropine (1 mg/kg), which reduced acid secretion and gastric motility; and 16,16-dmPGE2 (10 micrograms/kg), which reduced acid secretion and motility and increased gastric HCO3- secretion. If acid (150 mM HCl) was infused into the stomach (1.2 ml/hr) during indomethacin treatment, only the latter two agents significantly prevented the formation of gastric lesions in response to indomethacin. Since only the effect on gastric motility was common to these two agents (atropine and 16,16-dmPGE2), the increased gastric motility may be an important pathogenetic factor in indomethacin-induced gastric lesions. The presence of acid as well as a deficiency of endogenous PGs may be prerequisite for later extension of the lesions but cannot account for the induction of mucosal lesions in rats following administration of indomethacin.

16,16-Dimethylprostaglandin E2↗
PubMed1988

Effects of dopamine on gastric mucosal lesions induced by ethanol in rats. Possible involvement of antigastric motor activity mediated with alpha 2-adrenoceptors.

Acidified ethanol (60% ethanol in 150 mM HCl, per os) induced elongated bands of hemorrhagic lesions along the long axis of the stomach within 1 hr in rats. Pretreatment with dopamine hydrochloride (DA: 1-10 mg/kg, subcutaneously) dose-dependently reduced the severity of these lesions. In parallel study, DA had no effect on acid secretion but inhibited gastric motor activity in a dose-related manner. The inhibitory effects of DA on both acidified ethanol-induced lesions and gastric motor activity were significantly reversed by pretreatment with yohimbine, an inhibitor of alpha 2-adrenoceptors (5 mg/kg, subcutaneously), but not by prazosin, haloperidol, or indomethacin. Similar to DA, both norepinephrine (NE: 1 mg/kg, subcutaneously) and epinephrine (EPI: 1 mg/kg, subcutaneously) showed inhibition of the motor activity and gastroprotection against acidified ethanol, but these effects were also significantly attenuated by yohimbine. A highly significant relationship was found between the inhibitory effects of DA, NE, and EPI on the motor activity and the mucosal lesions (r = 0.8577, P less than 0.05). In addition, administration of gentian violet (0.5% w/v, per os) stained the mucosa deep blue as elongated wide bands in the corpus region, and such localized staining was significantly prevented by DA, suggesting a flattening of the mucosal foldings in the presence of DA. These results suggest that DA (and other catecholamines) protects the rat gastric mucosa against injury caused by acidified ethanol, probably through inhibition of gastric motor activity mediated with stimulation of alpha 2-adrenoceptors.

Animals↗
PubMed1988

Effects of gastric distension and prostaglandin on acid ethanol-induced mucosal lesions in the rat.

The effects of gastric distension on the morphology of acidified ethanol (AE) -induced mucosal lesions and on the protective action of 16,16-dm PGE2 were investigated in rats. AE (50% ethanol in 150 mM HCl) was given by gavage in the intact stomach or through a fistula prepared in the forestomach in the pylorus-ligated stomach. AE produced elongated bands of hemorrhagic necrosis within 1 hr in the former, while in the pylorus-ligated stomach the shape of lesions varied depending upon the volume of irritant. One milliliter produced bandlike lesions, whereas 2 ml or more induced widespread lesions; such volumes were observed to remove the mucosal folds. 16,16-dm PGE2 (0.3-10 micrograms/kg, subcutaneous) dose dependently reduced bandlike lesions in the intact stomach, but had no or little effect on non-band-like lesions in the pylorus-ligated stomach. This agent (10 micrograms/kg) had a slight effect on the reduction of PD caused by 10-min exposure of the stomach to AE (2 ml) in the intact stomach, while such effects were not apparent in the pylorus-ligated stomach. Oral gentian violet (2 ml, 0.3% w/v) produced bandlike staining of the mucosa in intact rats, but the effect was blocked by pyloric ligation. 16,16-dm PGE2 also significantly prevented the localized staining pattern seen in intact rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Importance of pepsin and stomach distension in morphological alterations of stress-induced gastric lesions in pylorus-ligated rats.

Pylorus ligation changed the morphology and location of gastric lesions induced by water-immersion stress (WI stress) in rats; linear lesions in the corpus mucosa disappeared, and punctate lesions appeared in both the corpus and antrum, in association with the loss of H+ and the gain of Na+ in the gastric contents. Oral administration of antipeptic drugs such as amylopectin sulfate and sulfated glyptide or porcine pepsin significantly prevented or aggravated the lesions, respectively, although another type of elongated lesion appeared in response to high doses of antipeptic drugs. These antipeptic drugs or exogenous pepsin significantly reduced or increased pepsin activity, respectively, without effect on the acid output. Similar punctate lesions were produced in the atropinized rats (10 mg/kg) by instillation of acid solution (100 mM HCl plus 54 mM NaCl) with pepsin into the pylorus-ligated stomach and subjecting to WI stress. On the other hand, when the gastric contents were drained through a fistula to prevent accumulation of gastric juice in the pylorus-ligated stomach, WI stress again induced linear lesions only in the corpus mucosa. Acid hypersecretion in these rats induced by intravenous infusion of histamine, tetragastrin, or carbachol significantly aggravated the severity of lesions but did not change their morphology. These results suggest that pepsin in the presence of acid is prerequisite for development of gastric lesions in pylorus-ligated rats induced by WI stress. The morphological alterations may be accounted for by the distensions of the stomach due to accumulation of gastric juice in the lumen caused by pylorus ligation, but not due to acid hypersecretion.

Animals↗
PubMed1988

Effects of hemorrhagic shock on alkaline secretion and mucosal tolerance to acid in rat duodenum. A comparative study with indomethacin.

The effects of hemorrhagic shock (HE) on duodenal HCO3- secretion and mucosal tolerance to acid were investigated in anesthetized rats and compared with those of indomethacin. HE was performed by bleeding from the carotid artery to reduce arterial blood pressure to about 50 mm Hg (3 ml bleeding per 200 g of body weight) with a significant decrease in arterial pH and [HCO3-], and indomethacin was given subcutaneously in a dose of 5 mg/kg. The proximal duodenum (1.7 cm) secreted HCO3- at the rate of 1.5-1.8 mueq/15 min (3.5-4.2 mueq/cm/hr), and responded to luminal acid (10 mM HCl for 10 min) by a significant rise in HCO3- output. Indomethacin had no effect on basal HCO3- output but significantly inhibited the acid-induced HCO3- secretion, while under HE conditions duodenal HCO3- output significantly declined and failed to increase in response to luminal acidification. Subcutaneously administered 16,16-dmPGE2 (30 micrograms/kg) significantly increased HCO3- secretion in the presence of indomethacin but had less effect on the impaired HCO3- output caused by HE. In contrast, intravenous infusion of NaHCO3 (3 mmol/kg/hr) ameliorated the acid-base imbalance caused by HE, and significantly restored the impaired HCO3- responses induced by HE but not by indomethacin. Both HE and indomethacin induced extensive damage in the mucosa when the duodenal loop was perfused with 50 mM HCl for 1.5 hr, and these lesions were significantly reduced by NaHCO3 infusion and 16,16-dmPGE2, respectively. These results suggest that HE impaired duodenal HCO3- secretion and reduced the tolerance of the mucosa to acid.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Pathogenesis of digitoxin-induced duodenal ulcers in pregnant rats. Roles of gastric acid and duodenal alkaline secretion.

Late-stage pregnant rats (day 17) had higher rates of gastric acid secretion (45-55 mu eq/15 min) as compared to nonpregnant and middle-stage pregnant (day 10) rats (20-25 mu eq/15 min). In contrast, basal rates of duodenal alkaline secretion were significantly lower (2-3 mu eq/15 min) in pregnant rats (day 10 and 17) than those in nonpregnant rats (approximately 5 mu eq/15 min), although the duodenal mucosa responded to acid with a significant rise in HCO3- output in these three groups of rats. In pregnant rats (day 17), a single injection of digitoxin, a Na+ K+-ATPase inhibitor (10 mg/kg, subcutaneously), had no effect on basal acid and alkaline secretions, but significantly blocked the acid-induced HCO3- secretion for more than 18 hr from 6 hr after administration. This drug, when given once daily for four days (10 mg/kg, subcutaneously), produced well-defined ulcers in the proximal duodenum with few lesions in the stomach of female rats, and the severity and incidence were significantly higher in late-stage pregnant rats than in the other two groups of rats. Following repeated administration of digitoxin (10 mg/kg) to late-stage pregnant rats (days 17-20), acid secretion significantly declined after two days of treatment, while the acid-induced HCO3- secretion was significantly attenuated after one day of treatment and remained inhibited during the whole period. These results suggest that an impairment of the mechanisms related to acid-induced HCO3- secretion may be associated with the induction of duodenal ulcers caused by digitoxin in female rats, and the high incidence of these ulcers in late-stage pregnant rats may be due to acid hypersecretion.

Animals↗
PubMed1988

Flow cytometric DNA analysis of neuroblastoma: correlation with prognostic variables and survival of patients.

The DNA ploidy of tumor tissues obtained from 41 patients with neuroblastoma, or ganglioneuroblastoma, which is the histologic variant of neuroblastoma, was determined by flow cytometry. The DNA ploidy was diploid in 7 tumors (5 neuroblastomas and 2 ganglioneuroblastomas) and aneuploid in 34 tumors (20 neuroblastomas and 14 ganglioneuroblastomas). The DNA ploidy of tumor cells did not correlate with the survival of patients and there was no correlation between the DNA ploidy of tumor cells and such prognostic variables, histology, primary site, staging of tumors and operative curability.

Cell Separation↗
PubMed1988

Ventricular septal perforation following acute myocardial infarction in a patient with hypothyroidism--a case report.

A 61-year-old woman with profound hypothyroidism underwent surgery for a ventricular septal perforation 15 days following an acute myocardial infarction, with no preoperative thyroid replacement. Her immediate postoperative course was complicated by a low cardiac output, respiratory suppression and high output renal failure, requiring prolonged hemodynamic and respiratory support. Thyroid replacement (50 micrograms of thyronine and 100 micrograms of thyroxine daily) was given in two installments on the 2nd day after the operation. The effect of the inotropic agents increased gradually and the patient was weaned off intra-aortic balloon pumping. A large quantity of diuretics, hydration and hyperalimentation also successfully reduced her elevated BUN and serum creatinine. After full thyroid replacement, she was discharged in good health on the 40th postoperative day.

Female↗
PubMed1988

Influence of exercise on plasma atrial natriuretic factor levels in patients with myocardial infarction.

The influence of dynamic exercise on plasma atrial natriuretic factor (ANF) levels was studied in a group of 10 patients with myocardial infarction (MI) and five patients with atypical chest pain (control group). Exercise protocol consisted of three fixed workloads (25, 50, and 75 watts) every 4 minutes with the use of a supine bicycle ergometer. Plasma ANF levels and hemodynamic indices were measured before, during, and 10 minutes after exercise. In the MI group, plasma ANF levels significantly increased at the 75-watt workload and significantly decreased at 10 minutes after exercise, whereas in the control group, the increase in plasma ANP levels after a 75-watt workload, compared with those at rest, was not significant. Significant correlations of pulmonary artery wedge pressure, right atrial pressure, mean arterial pressure, and heart rate to plasma ANF levels were observed at four points obtained before and during each stage of exercise in the MI group. Furthermore, a significant correlation between maximal creatine kinase levels and plasma ANF levels at a 75-watt workload and a significant inverse correlation between left ventricular ejection fraction and plasma ANF levels at a 75-watt workload were observed. These results suggest that the increase in the circulating ANF level during exercise in MI is associated with elevated atrial pressure resulting from left ventricular dysfunction and that measurement of ANF during exercise may be an indication of the severity of MI and associated left ventricular dysfunction.

Adult↗