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Biomedical subjects

T Enoki

Publications and source records attributed to T Enoki.

At least 37 records · Page 2Linked to original sources
PubMed1997

Surgical stress and the development of complications in relation to polymorphonuclear leukocyte elastase (PMNE) levels.

This study was conducted to examine the effects of surgical stress on changes in polymorphonuclear leukocyte elastase (PMNE) levels, and to evaluate the relationship of these changes to the development of postoperative complication. A total of 69 patients who underwent alimentary surgery were subsequently divided into three groups: a complicated group, comprised of 25 patients; an uncomplicated group with a high blood loss (H) of more than 1000 ml, comprised of 18 patients; and an uncomplicated group with a low blood loss (L) of less than 1000 ml, comprised of 26 patients. The changes in the levels of PMNE, fibronectin (FN), and antithrombin III (AT III) were compared among these three groups. In the uncomplicated H and L groups the PMNE levels rose significantly on postoperative day (POD) 1. On POD 3, high levels of PMNE were still evident in the uncomplicated H group, but a decline was observed in the uncomplicated L group. From POD 7 onwards the levels decreased to the preoperative values in both uncomplicated groups; however, the complicated group continued to show high levels even on POD 14. Significantly decreased FN levels were observed for the first 3 PODs in each group. The uncomplicated H and L groups regained their preoperative levels on PODs 7 and 14, respectively, but no recovery was found in the complicated group. The AT III levels showed similar changes to the FN levels in all groups. These findings indicate that monitoring the PMNE levels could be a useful index for the early detection of postoperative complications following alimentary surgery.

Antithrombin III↗
PubMed1997

The involvement of a novel mechanism distinct from the thrombin receptor in the vasocontraction induced by trypsin.

1. The vasocontracting effect of a serine protease trypsin and its mechanisms were investigated by monitoring the isometric tension in endothelium-denuded rings of rabbit thoracic aortae and its effects on intracellular free Ca2+ concentrations ([Ca2+]i) in dispersed rabbit vascular smooth muscle cells with a Ca2+ indicator fura-2. The actions of trypsin were compared with those of thrombin. 2. Both thrombin and trypsin reversibly contracted aortic rings without endothelium in a concentration-dependent manner. The vasocontraction induced by trypsin was well correlated with the protease activity of trypsin actually added to the tissue baths containing the aortic rings and was completely blocked by soybean trypsin inhibitor and phenylmethylsulphonyl fluoride (PMSF), a serine protease inhibitor. 3. The trypsin-induced contractions of the aortic rings were not the result of irreversible damage to vascular smooth muscle cells, since the contractile responses induced by noradrenaline or 30 mM KCl were unaffected by pretreatment with trypsin. 4. The contractions induced by either thrombin or trypsin were reduced to about 30% of control responses after removal of extracellular Ca2+, indicating that most of the contraction is dependent on extracellular Ca2+. By contrast, the contractions induced by either of the proteases were reduced by an antagonist of L-type voltage-operated Ca2+ channels, nifedipine, to about 70% of control responses, indicating that both nifedipine-sensitive and -resistant Ca2+ channels are involved in these contractions. 5. In the aortic rings precontracted by a maximally effective concentration of thrombin, the second application of thrombin virtually failed to induce contractions but trypsin could still induce contractions amounting to 10% of control values by it's protease activity. 6. After the first application of a maximal concentration of thrombin, the second application of thrombin could not induce an increase in [Ca2+]i, but an application of trypsin could still induce an increase in [Ca2+]i in dispersed rabbit vascular smooth muscle cells. 7. These data suggest that in addition to activation of a thrombin receptor, trypsin can contract rabbit aortae by a proteinase-activated receptor 2 or a novel mechanism.

Animals↗
PubMed1997

Inhibitory effect of nitrovasodilators and cyclic GMP on ET-1-activated Ca(2+)-permeable nonselective cation channel in rat aortic smooth muscle cells.

1. In single vascular smooth muscle cells (VSMCs) isolated from the aortae of male Wistar rats, we examined the effects of nitric oxide (NO) donors such as sodium nitroprusside (SNP) and S-nitroso-N-acetyl-DL-penicillamine (SNAP), and 8-bromo-guanosine-3':5'-cyclic monophosphate (8-bromo-cyclic GMP) on endothelin-1 (ET-1)-activated Ca(2+)-permeable nonselective cation channel by use of whole-cell recordings of patch-clamp technique and monitoring of intracellular free Ca(2+)-concentration ([Ca2+]i) with fura-2 real-time digital microfluorometry. 2. ET-1 evoked an initial transient peak and a subsequent sustained elevation in [Ca2+]i. After removal of extracellular Ca2+. ET-1 evoked only an initial transient peak without a sustained phase. Nifedipine (1 microM), a specific blocker of the L-type voltage-operated Ca2+ channel (VOC), reduced the sustained phase to about 40% of the control level. The remaining part of the sustained phase was abolished by 30 microM SK&F 96365, a blocker of nonselective cation channels. 3. The nifedipine-resistant sustained elevation in [Ca2+]i was abolished by 100 microM SNP, 10 microM SNAP and 300 microM 8-bromo-cyclic GMP. Neither SNP, SNAP nor 8-bromo-cyclic GMP significantly affected the basal level of [Ca2+]i. 4. In a VSMC clamped at a holding potential of -60 mV with K+ in the pipette solution replaced by Cs+, application of 10(-8) M ET-1 induced an inward current with an increase in baseline fluctuation. With fluctuation analysis, unit conductance of the ET-1-induced current was calculated to be about 21 pS. The ET-1-induced current was linearly related to the membrane potentials with its reversal potential of -5.5 mV. 5. The ET-1-induced current was reversibly and completely inhibited by 30 microM SK&F 96365 or 500 microM Cd2+. The current inhibited by SK&F 96365 or Cd2+ was linearly related to membrane potential with a reversal potential of about -5 mV. 6. The ET-1-induced current was reversibly and completely inhibited by 100 microM SNP, 10 microM SNAP and 300 microM 8-bromo-cyclic GMP. The current inhibited by SNP, SNAP or 8-bromo-cyclic GMP showed linear voltage-dependence and reversed at about -5 mV. 7. In a bath solution in which all cations were replaced by 30 mM Ca2+ and 100 mM nonpermeant cation N-methyl-D-glucamine (NMDG), ET-1 evoked a current with a reversal potential of -11 mV, from which PCa2+/Pcs1 was calculated to be 2.1. This Ca2+ current was also abolished by 100 microM SNP, 10 microM SNAP and 300 microM 8-bromo-cyclic GMP. The current inhibited by SNP, SNAP or 8-bromo-cyclic GMP showed linear voltage-dependence and reversed at about -11 mV. 8. These results taken together indicate that NO through a cyclic GMP signalling pathway inhibits ET-1-activated Ca(2+)-permeable nonselective cation channels, thereby suppressing the sustained increase in [Ca2+]i. Thus, the present study indicates that this Ca(2+)-permeable nonselective cation channel is an important target for nitrovasodilators.

Animals↗
PubMed1997

Physiological role of Ca2+-permeable nonselective cation channel in endothelin-1-induced contraction of rabbit aorta.

We previously showed a role for a nonselective cation channel (NSCC) in the ETA-dependent action of endothelin-1 in mouse fibroblast and rabbit aortic smooth-muscle cell. To clarify the physiological significance of NSCCs in endothelin-1 (ET-1)-induced vasocontraction, we examined the effects of NSCC blockers such as mefenamic acid and SK&F 96365 on the contractions of deendothelialized rabbit aortic rings induced by a low (10[-10] M) or high (10[-8] M) concentration of ET-1. Mefenamic acid (< or =10[-3] M) had little effect on the contraction induced by 45 x 10(-3) M K+ or 1 x 10(-6) M Bay K-8644 in combination with 15 x 10(-3) M K+, indicating that it does not affect voltage-operated calcium channels (VOCs) and contractile mechanisms. The contraction by a low concentration of ET-1 was abolished after removal of extracellular Ca2+, but it was reduced only to 50% by a maximally effective concentration (10[-5] M) of nifedipine, an inhibitor of L-type VOCs (L-VOC). Mefenamic acid and SK&F 96365 inhibited the ET-1-induced contraction with 50% inhibitory concentration (IC50) values of 10(-4) M and 2 x 10(-5) M, respectively, and abolished it at 10(-3) M and 10(-4) M. By contrast, nifedipine, mefenamic acid, or SK&F 96365 had little effect on the contraction by a high concentration of ET-1. The contraction induced by a low or high concentration of ET-1 was abolished by an ETA antagonist, BQ-123, but not by an ETB antagonist, BQ-788. These results demonstrate that the contraction induced by ET-1 is totally mediated exclusively by ETA, but that Ca2+ entry through NSCCs in addition to L-VOCs plays an important role in contractions induced by low concentrations of ET-1, whereas it plays only a minor role in contractions induced by high concentrations of ET-1.

Animals↗
PubMed1997

[A case of dermatomyositis with severe retinopathy in a patient who died of acute interstitial pneumonia].

Sight threatening ocular complications are rare in adult patients with dermatomyositis. We encountered a 52-year-old female with dermatomyositis who had severe visual disturbance and rapidly progressive intersitial pneumonia. She was admitted to our hospital because of skin erythema, general fatigue, mild fever, and severe bilateral visual disturbance. Rentinal hemorrhages, cotton wool spots, and macular edema were observed in her fundus at the first ophthalmic examination. A diagnosis of dermatomyositis was made because of the myogenic pattern of her electromyogram, elevation of serum creatine kinase, and skin lesions. Oral prednisolone treatment was started and the retinopathy was improved, but was complicated by acute interstitial pneumonia. The interstitial pneumonia was not respond to steroid pulse therapy with methylprednisolone, and the patient died of respiratory failure on the 47th day after the onset of visual symptoms. In adult dermatomyositis patients, the complication of severe retinopathy should be considered as a risk factor for rapid progress of interstitial pneumonia.

Acute Disease↗
PubMed1996

Cloning and sequencing of the cDNA encoding beta-glucosidase 1 from Aspergillus aculeatus.

A cDNA was isolated from an Aspergillus aculeatus cDNA library using synthetic oligodeoxyribonucleotide mixtures that corresponded to the internal amino acid (aa) sequence of mature beta-glucosidase 1 (BGL1). Analysis of the nucleotide sequence of the cloned cDNA insert revealed a 2580-bp open reading frame (ORF) that encoded a 860-aa protein. The deduced aa sequence of the ORF shared sequence similarity with several BGL from other microorganisms.

Amino Acid Sequence↗
PubMed1995

Long-lasting activation of cation current by low concentration of endothelin-1 in mouse fibroblasts and smooth muscle cells of rabbit aorta.

1. Recombinant human ETA receptors were expressed in a mouse fibroblast cell line (Ltk- cell) and functional coupling of the receptors with Ca2+ permeable channels at low concentrations of endothelin-1 (ET-1) was investigated using whole-cell recordings and monitoring the changes in intracellular free Ca2+ concentrations ([Ca2+]i) with a Ca2+ indicator, fluo-3. A similar type of coupling was investigated in freshly dispersed vascular smooth muscle cells (VSMCs) of rabbit thoracic aorta by use of whole-cell recordings. 2. In Ltk- cells expressing recombinant human ETA receptors, concentrations of ET-1 (10(-8) M, 10(-9) M) evoked an initial transient peak and a subsequent sustained elevation in [Ca2+]i whereas a lower concentration of ET-1 (10(-10) M) evoked only a sustained elevation of [Ca2+]i. After removal of extracellular Ca2+, ET-1 evoked only an initial peak without a sustained elevation of [Ca2+]i. The sustained elevation induced by 10(-10) M ET-1 was blocked by 300 microM mefenamic acid (a cation channel blocker) but not by 10 microM nifedipine (a blocker of voltage-operated Ca2+ channel). 3. In whole-cell recordings with Ltk- cells, a brief (3-5 min) application of ET-1 (10(-10) M) induced a sustained inward current at a holding potential of -60 mV. The current-voltage relationship revealed that the reversal potential of the ET-1-induced current was close to 0 mV (1.9 mV) and was not altered by reducing the concentration of Cl- in the bath solution, indicating that the current is carried by cations. The current was reversibly blocked by 300 microM mefenamic acid, and it persisted after all cations in the bath solution had been replaced by Ca2+ (5 or 30 mM) and nonpermeant cation N-methyl-D glucamine,indicating that the ET-1-activated channel is permeable to Ca2+. Activation of the current was independent of membrane potential and the current was induced even after addition of a high concentration (10 mM) of a Ca2+ chelator, EGTA, to the pipette solution.4. In whole-cell recordings from rabbit aortic VSMCs, ET-l (101-10 M) induced a sustained inward current at a holding potential of -60 mV. The reversal potential was - 12 mV and was not altered when the concentration of Cl- in the pipette solution was decreased, indicating that the current is carried by cations. Again activation of the current was independent of membrane potential and was observed even after addition of a high concentration (10 mM) of a Ca2+ chelator, EGTA to the pipette solution. The current was reversibly blocked by 300 microM mefenamic acid and was permeable to Ca2+,showing marked similarities to ET-1-induced cationic current in Ltk- cells.5. These results indicate that in Ltk- cells transfected with cDNA for recombinant ETA receptors andVSMCs, ETA receptors can functionally couple with a nonselective cation channel permeable to Ca2+.Thus the present data suggest that the cation channel plays an essential role in the sustained elevation of[Ca2+]i at low concentrations of ET-l by causing Ca2+ entry through the channel.

Aniline Compounds↗
PubMed1995

Functional coupling of ETA receptor with Ca(2+)-permeable nonselective cation channel in mouse fibroblasts and rabbit aortic smooth-muscle cells.

Endothelin-1 (ET-1) induces persistent vasoconstriction via a sustained increase in intracellular free Ca2+ concentrations ([Ca2+]i). The mechanisms of the elevation of [Ca2+]i operating at physiologically low concentrations of ET-1 are controversial. Here we report that both native ETA receptors in vascular smooth-muscle cells and recombinant ET(A) receptors expressed in mouse fibroblasts (Ltk cells) are functionally coupled with a non-selective cation channel, which is permeable to Ca2+ and is blocked by mefenamic acid. The channel is persistently activated by a low concentration of ET-1 (10(-10) M) without stimulation of inositol triphosphate (IP3) formation and mediates sustained vasoconstriction.

Animals↗
PubMed1993

Distinct subdomains of human endothelin receptors determine their selectivity to endothelinA-selective antagonist and endothelinB-selective agonists.

The endothelin (ET) family of peptides acts via two subtypes of G-protein-coupled heptahelical receptors termed ETA and ETB, which have distinct rank orders of affinity to endothelin receptor agonists and antagonists. To delineate which portions of the receptor molecules determine ligand selectivity, we have constructed a series of chimeras between human ETA and ETB receptors and characterized the chimeric receptors expressed in heterologous cell lines by competitive radioligand binding analysis and by measuring agonist-induced transients of intracellular Ca2+. We demonstrate that the binding determinant for the ETB-selective agonists ET-3, BQ3020, and IRL1620 residues within the region spanning the putative transmembrane helices IV-VI and the adjacent loop regions. In contrast, the transmembrane helices I, II, III, and VII plus the intervening loop regions specify the selectivity for BQ123, an ETA-selective antagonist. BQ123 exhibited no detectable agonistic activity in all wild-type and chimeric receptors tested. A chimeric receptor that has the transmembrane helices IV-VI (and adjacent loops) from the ETB receptor inserted into the remaining regions from the ETA receptor binds both the ETA- and ETB-selective ligands with high affinities. Moreover, BQ123 competitively inhibits the binding of the amino-terminally truncated ETB agonists, 125I-BQ3020 and 125I-IRL1620, to this chimeric receptor, suggesting that BQ123 is a mimic of the carboxyl-terminal linear portion of endothelins. These findings indicate that there are at least two separable ligand interaction subdomains within the endothelin receptors.

Amino Acid Sequence↗
PubMed1993

The reticuloendothelial system and hepatocyte function in orthotopic liver transplantation.

The reticuloendothelial system function, especially phagocytic activity, and hepatocyte function were investigated in dogs undergoing an orthotopic liver transplantation. The donor's phagocytic index, measured by a lipid emulsion test, was higher in the Survivor group which survived more than 3 days after transplantation (0.063 +/- 0.008 vs 0.024 +/- 0.002; mean +/- standard error of the mean (SEM), P < 0.01). There was a statistically significant difference in the phagocytic index between the survivor and nonsurvivor groups. However, the hepatocyte function at an early phase after transplantation, indicated by the arterial ketone body ratio, hepaplastin test and lecithin cholesterol acyltransferase level, did not distinguish the Survivor group from the Nonsurvivor group at all. In the survivor group, the hepaplastin test and the lecithin cholesterol acyltransferase level were significantly decreased after liver transplantation, namely from 155 +/- 15% to 58 +/- 5% and from 57 +/- 12 unit/ml to 19 +/- 1 unit/ml on the 2nd day after transplantation (P < 0.01, P < 0.05), respectively. On the other hand, the reticuloendothelial system (RES) function, as estimated by the phagocytic index and serum complement activity (CH 50), demonstrated no change throughout the experimental period. The present study therefore demonstrated that the operative results might be affected by the phagocytic activity.

Animals↗
PubMed1992

Attenuation of gastric effects of famotidine by preoperative administration of intravenous fluids.

Effects of preoperative administration of intravenous crystalloids on the gastric effects of famotidine were studied in 89 patients scheduled for elective surgery in the afternoon. Patients were randomly assigned to one of six groups. Groups P1, P2, and P3 received 2.0 mL of intramuscular saline (placebo) and groups F1, F2, and F3 received 20 mg of intramuscular famotidine 1 h before anesthesia. All patients fasted for 14-18 h before surgery. No fluid was administered to groups P1 and F1 preoperatively, whereas 500 mL of intravenous fluid was given to the other groups over a period of 4-5 h before anesthesia: a maintenance fluid with 10% glucose to groups P2 and F2, and lactated Ringer's solution without glucose to groups P3 and F3. After anesthetic induction, the stomach was aspirated using a nasogastric tube and volume and pH of the contents were measured. The gastric volume was significantly less in F2 (4.2 +/- 1.2 mL, mean +/- SEM) than in P1 (30.7 +/- 5.5 mL) (P less than 0.01) and in F3 (12.7 +/- 2.1 mL) than in P3 (26.8 +/- 4.4 mL) (P less than 0.05). There was no significant difference between P2 (23.4 +/- 4.6 mL) and F2 (17.5 +/- 3.5 mL). Mean pH values were significantly higher in F1 (6.82 +/- 0.48) than in P1 (3.21 +/- 0.72) (P less than 0.01). No significance was observed between P2 (3.65 +/- 0.62) and F2 (4.53 +/- 0.77), or P3 (3.17 +/- 0.81) and F3 (5.03 +/- 0.80).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗