Biomedical subjects

Y Taira

Publications and source records attributed to Y Taira.

At least 55 records · Page 3Linked to original sources

PubMed1998

Active collagen synthesis in infantile hypertrophic pyloric stenosis.

M-57 antibody, which is capable of distinguishing newly-synthesized type I procollagen from fully-processed, mature collagen, was used to examine the expression of collagen synthesis in hypertrophic pyloric muscle from patients with infantile hypertrophic pyloric stenosis (IHPS). Seven specimens from IHPS patients were removed at the time of operation; age-matched normal pyloric tissue of 5 post-mortem cases was obtained as controls. Immunohistochemistry was performed using antibody of the amino-terminal end of the procollagen type I propeptide (M-57). Newly-synthesized procollagen (M-57) was strongly detected in both the connective tissue septa between circular muscle bundles, and among the circular-muscle fibers in patients with IHPS. No M-57 staining was observed among the circular-muscle fibers in controls. Our findings show that the hypertrophic circular muscle in IHPS is actively synthesizing collagen, and this may be responsible for the characteristic "firm" nature of the pyloric tumor.

Antibodies, Monoclonal↗

PubMed1998

Upregulated tumor necrosis factor-alpha gene expression in the hypoplastic lung in patients with congenital diaphragmatic hernia.

Recent studies using animal models of congenital diaphragmatic hernia (CDH) have reported a reduction in both surfactant (SF) phospholipids and proteins in CDH lungs compared to controls, resulting in biophysical and physiologic impairment of SF function in the hypoplastic CDH lung. Furthermore, SF replacement has been shown to improve physiological function in CDH lungs. Tumor necrosis factor-alpha (TNF-alpha) is a polypeptide whose overproduction has been implicated in the pathogenesis of a number of pathological conditions, such as neonatal and adult respiratory distress syndrome. TNF-alpha has been shown to selectively inhibit the de-novo synthesis of SF phospholipid components in type II pneumocytes. It has been demonstrated that TNF-alpha is synthesized locally in lung and functions in an autocrine/paracrine mode. The aim of this study was to investigate TNF-alpha messenger RNA (mRNA) expression in hypoplastic CDH lung using in-situ hybridization histochemistry, to determine the molecular basis of the SF deficiency in the hypoplastic CDH lung. Lung-tissue samples were obtained at autopsy from 7 full-term newborns (age range: 1-21 days) with CDH and 4 stillborns with CDH. Normal lung tissue from eight infants with sudden infant death syndrome (age range: 5-30 days) acted as controls. In-situ hybridization was performed using TNF-alpha specific and digoxigenin-labeled oligonucleotide probe and visualized by nitroblue tetrazolium staining. In control lung tissue, mRNA expression of TNF-alpha was absent or weak in type II pneumocytes and alveolar macrophages. In contrast, mRNA expression of TNF-alpha was markedly increased in both type II pneumocytes and alveolar macrophages in hypoplastic CDH lung. Our findings of up-regulated TNF-alpha gene expression in CDH lung suggest that the SF deficiency observed in hypoplastic CDH lung may be the result of increased local production of TNF-alpha.

Case-Control Studies↗

PubMed1998

Comparison of the pulmonary vasculature in newborns and stillborns with congenital diaphragmatic hernia.

The purpose of this study was to compare structural changes in the pulmonary vasculature in newborns with congenital diaphragmatic hernia (CDH) complicated by persistent pulmonary hypertension (PPH) and stillborns with CDH. Victorian blue van Gieson (VVG) staining and immunostaining with anti-alpha smooth-muscle actin (ASMA) was performed on lung tissue obtained at autopsy from 23 newborns with CDH complicated by PPH, 7 stillborns with CDH, and 11 age-matched controls with sudden infant death syndrome (SIDS). The degrees of adventitial and medial thickness and area were measured in pulmonary arteries with an external diameter (ED) of <75 micrometers, 75-100 micrometers, 100-150 micrometers, 150-250 micrometers, 250-500 micrometers, and >500 micrometers by image analyzer and compared statistically. The degrees of adventitial and medial thickness and area were measured in pulmonary veins with an ED of <100 micrometers, 100-200 micrometers, and >200 micrometers by image analyzer and compared statistically. In order to determine whether the characteristic structural changes were size-related, each was related to ED. There was a significant increase in adventitial thickness and area in arteries of all sizes in both newborns and stillborns with CDH compared to SIDS patients (P < 0. 05). The degree of medial thickness in newborns and stillborns with CDH was significantly increased compared to SIDS patients (P < 0.01). The degree of medial area was significantly increased for arteries with ED less than 100 micrometers (P < 0.05) in newborns and stillborns with CDH compared with SIDS patients. There was a significant increase in adventitial thickness and area in veins of all sizes in newborns with CDH compared to stillborns with CDH and SIDS (P < 0. 05). The degree of adventitial thickness and area of pulmonary veins were similar in stillborns with CDH and SIDS. There were no significant differences in medial thickness of veins between the three groups. The presence of abnormally thick-walled pulmonary arteries in stillborns with CDH suggests that the intrapulmonary arteries in CDH may become excessively muscularized during fetal life, becoming unable to adapt normally at birth. The absence of structural changes in pulmonary veins in stillborns with CDH suggests that the pulmonary venous changes observed in newborns with CDH complicated by PPH occur after birth as a result of increases in transvascular pressure or a response to release of peptide growth factors.

Case-Control Studies↗

PubMed1998

Adventitial changes in pulmonary vasculature in congenital diaphragmatic hernia complicated by pulmonary hypertension.

PURPOSE: The purpose of this study was to characterize structural changes in the pulmonary vasculature in congenital diaphragmatic hernia (CDH) complicated by persistent pulmonary hypertension (PPH) with particular emphasis on adventitial thickness. METHODS: Victorian blue Van Gieson (VVG) staining and immunostaining with antialpha smooth muscle actin (ASMA) were performed on lung tissues obtained at autopsy from 23 patients with CDH complicated by PPH and 11 age-matched control tissues of sudden infant death syndrome patients (SIDS). The degree of medial and adventitial thickening was measured in pulmonary arteries with an external diameter (ED) of less than 75 microm, 75 to 100 microm, 100 to 150 microm, 150 to 250 microm, 250 to 500 microm, and greater than 500 microm by IPS-4.01 image analyzer and compared statistically. The degree of medial thickening and adventitial thickening was also measured in pulmonary veins with an ED of less than 100 microm, 100 to 200 microm, and greater than 200 microm. To determine whether the characteristic structural changes were size related, each was related to ED. The area of adventitia and media of the pulmonary arteries and veins was measured using image analyzer. RESULTS: There was a significant increase in medial and adventitial thickness in arteries of all sizes in CDH patients compared with controls (P < .01). The degree of adventitial area was significantly increased for arteries of all sizes (P < .01) and the degree of medial area was significantly increased only for arteries less than 100 microm size (P < .05) in CDH patients compared with controls. Calculation of the areas of the various components in the wall of each artery showed that for small arteries (<100 microm ED), the area of the lumen was smaller, and the areas of the media and adventitia were larger in CDH patients compared with controls (P < .01). There was a significant increase in adventitial thickness and area in veins of all sizes in CDH patients compared with controls (P < .01). The adventitial thickness of pulmonary veins were ED of less than 100 microm: CDH, 13.5 microm +/- 3.5; control, 9.21 microm +/- 2.0; ED 100 to 200 microm: CDH, 21.3 microm +/- 7.5; control, 13.0 microm +/- 4.8; ED greater than 200 microm: CDH, 34.4 microm +/- 12.5; control, 22.3 microm +/- 4.2. CONCLUSIONS: The present study provides the first quantitative demonstration of structural alterations in pulmonary veins in addition to pulmonary arteries in CDH complicated by PPH. The structural remodeling of the pulmonary vein is perhaps as a result of an increase in transvascular pressure in PPH.

Actins↗

PubMed1998

Altered insulin-like growth factor I mRNA expression in human hypoplastic lung in congenital diaphragmatic hernia.

BACKGROUND/PURPOSE: Insulin-like growth factor I (IGF-I) is a peptide growth factor that is synthesized in many organs during human development and plays a role in the growth and differentiation of tissue. IGF-I has been shown to be produced in rat and human fetal lung and to be an important mitogen involved in lung growth and development. The cells responsible for the synthesis of IGF-I in lung in vivo have been demonstrated to be type II pneumocytes, alveolar macrophages, and mesenchymal cells. Recent studies have shown that IGF-I mRNA expression in the lung is predominant during fetal life and decreases before birth, becoming barely detectable in the neonatal lung. The aim of this study was to investigate IGF-I mRNA expression in CDH lung to understand the basis of pulmonary hypoplasia in newborns with CDH. METHODS: Lung tissue samples were obtained during autopsy from 13 patients with CDH. Nine were full-term newborns (mean age, 3.8 days), and four were stillborns. Normal lung tissue from eight sudden infant death syndrome infants (mean age, 15.3 days) acted as controls. In situ hybridization was performed on frozen sections using IGF-I-specific and digoxigenin-labeled oligonucleotide probe and visualized by nitro blue tetrazolium staining. RESULTS: In control lung, IGF-I mRNA expression was absent or weak in type II pneumocytes and alveolar macrophages. In contrast, there was strong IGF-I mRNA expression in type II pneumocytes and alveolar macrophages in hypoplastic CDH lung in newborns as well as stillborns. CONCLUSION: The findings of strong IGF-I mRNA expression in the hypoplastic lung suggest that lung hypoplasia in CDH is a persistence of fetal stage of lung development.

Hernia, Diaphragmatic↗

PubMed1998

Administration of antenatal glucocorticoids prevents pulmonary artery structural changes in nitrofen-induced congenital diaphragmatic hernia in rats.

BACKGROUND/PURPOSE: The aim of this study was to investigate whether maternal administration of dexamethasone has any effect on pulmonary vasculature in nitrofen-induced experimental congenital diaphragmatic hernia (CDH) in a rat model. METHODS: A CDH model was induced in pregnant rats after administration of 100 mg nitrofen on day 9.5 of gestation. Antenatal dexamethasone, 0.25 mg/kg was given intraperitoneally on day 18.5 and 19.5 of gestation. The fetuses were divided into three groups: group I (n = 10), normal controls; group II (n = 10), nitrofen-induced CDH; group III (n = 10), nitrofen-induced CDH with maternal antenatal dexamethasone treatment. The fetuses were killed by cesarean section at term. Victorian blue van Gieson staining and immunostaining with antialpha smooth muscle actin (ASMA) were performed on lung tissue. The degree of adventitial thickness and area, and medial thickness and area were measured in pulmonary arteries by image analyzer and analyzed statistically. RESULTS: There was a significant increase in adventitial thickness and area in group II compared with group I and III (P < .01). There was also a significant increase in medial thickness in group II compared with group I and III (P < .01). The degree of adventitial thickness and area and degree of medial thickness and area were similar in controls and maternal dexamethasone-treated CDH group. CONCLUSION: This study demonstrates that antenatal maternal dexamethasone treatment prevents pulmonary artery structural changes in nitrofen-induced CDH in rats.

Animals↗

PubMed1998

Phosphate and thiophosphate primers for bonding prosthodontic luting materials to titanium.

STATEMENT OF PROBLEM: When resin-bonded prostheses are constructed with titanium, they must be strongly bonded with luting materials for the prostheses to withstand the oral environment over the long term. However, limited information is available about the bond durability between luting materials and titanium. PURPOSE: This study determined whether a phosphate and two thiophosphate primers increase bond strength and durability between a commercially available pure titanium and four luting agents. MATERIAL AND METHODS: Three primers and four luting agents were divided into three groups according to the type of acidic monomers: carboxylic acid derivatives (4-META, 4-AET, and MAC10), a phosphoric acid derivative (MDP), and a thiophosphoric acid derivative (MEPS). Disk specimens were bonded with 16 combinations of 3 primers and 4 luting agents, including 4 controls. Shear bond strengths were determined after 1-day immersion in water and after thermocycling for 100,000 cycles. RESULTS: Bond strengths were influenced by thermocycling, primer, luting agent, and their combinations. After thermocycling, the groups that demonstrated the highest bond strengths were six combinations of two primers (Cesead Opaque Primer and Metal Primer II) and three luting agents (Imperva Dual, Panavia 21, and Super-Bond C&B).

Analysis of Variance↗

PubMed1998

Adhesive bonding to dentin with iron (II) perchlorate primers and a tri-n-butylborane-initiated luting agent.

OBJECTIVES: This study was conducted to measure the tensile bond strength of a resin to dentin when the dentin was primed with iron (II) perchlorate modified aqueous 2-hydroxyethyl methacrylate (HEMA) or an iron (II) perchlorate modified commercial self-etching primer (ED primer, Kuraray Co.). METHODS: Bovine dentin surfaces were ground flat and each specimen underwent one of the following two treatments: (1) priming with 2.0 x 10(-6) to 5.0 x 10(-4) mol/g iron (II) perchlorate in aqueous HEMA solutions after etching with 10 wt% phosphoric acid; (2) priming with self-etching primers containing 4.0 x 10(-7) to 2.0 x 10(-4) mol/g iron (II) perchlorate. Each specimen was then bonded to a stainless-steel rod with a luting agent (MMA-TBB resin) consisting of methyl methacrylate (MMA), poly(methyl methacrylate) (PMMA), and tri-n-butylborane (TBB) initiator. Tensile strengths of the bonded tooth specimens were then determined after 1 day immersion in water. Results were analyzed using ANOVA and Duncan's new multiple range test (p < 0.05). RESULTS: Tensile testing revealed the maximum mean bond strengths (22.5 MPa) when the dentin was primed with 2.0 x 10(-4) mol/g iron (II) perchlorate after etching with 10 wt% phosphoric acid aqueous solution. The highest level of bond strength with self-etching primer (19.6 MPa) was achieved using 1.0 x 10(-4) mol/g iron (II) perchlorate. SIGNIFICANCE: These bonding techniques, combining the use of iron (II) perchlorate modified HEMA primers with MMA-TBB resin, are potentially applicable for seating resin-bonded restorations.

Adhesiveness↗

PubMed1998

Influence of surface oxidation of titanium on adhesion.

OBJECTIVES: The adhesive bonding of titanium was investigated using a methacrylate-phosphate primer and a luting agent. The present study investigates the influence of heat oxidation as well as a suitable durable bonding method for treating the surface of titanium. METHODS: Two groups of disc specimens were fabricated by milling and casting, respectively. Machine-milled specimens were subjected to heat treatment, and three groups of cast metal specimens underwent following respective treatments: (1) as-cast, (2) emery-polishing, (3) alumina-blasting after emery-polishing. The primer contained 10-methacryloyloxydecyl dihydrogen phosphate (MDP); the luting agent was based on methyl methacrylate (MMA), and was initiated with tri-n-butylborane derivative (TBB). Each specimen was primed and bonded to an acrylic rod. Shear bond strengths were determined before and after thermocycling. RESULTS: The mean bond strength of the machine-milled emery-polished group was 32.5 MPa after 5000 thermocycles with only a slight decrease in bond strength. A decrease in the bond strength occurred when the heat-treatment temperature was above 400 degrees C. Although both emery-polishing and alumina-blasting were effective, the minimum decrease in bond strength was obtained with alumina-blasting. CONCLUSIONS: The excess surface oxide layer may be of great concern as a possible cause of decreased bonding durability. Sufficient bonding durability for clinical use was obtained when the titanium was alumina-blasted.

Adhesiveness↗

PubMed1998

Metal chloride primers for bonding dentine with tri-n-butylborane-initiated luting agents.

OBJECTIVES: The bonding of resin to dentine is dependent largely on surface modifications. The purpose of the present study was to test the hypothesis that a role of the metal chlorides used as primers is to initiate polymerization of resin at the resin-dentine interface, thereby affecting bond strength. METHODS: Nine primers were evaluated, comprising aqueous 2-hydroxyethyl methacrylate (HEMA) solutions containing AICl3, CeCl3, CoCl2, CuCl2, FeCl3, NiCl2, MgCl2, SnCl2 or ZnCl2, respectively. One of the two luting agents (Super-Bond resin) consisted of methyl methacrylate (MMA), 4-methacryloyloxyethyl trimellitate anhydride (4-META) and tri-n-butylborane (TBB) initiator. The other luting agent (MMA-TBB resin) consisted of MMA and TBB without 4-META. Extracted bovine teeth were ground to expose the dentine, etched with an aqueous solution of 10% phosphoric acid, primed, and then bonded with stainless-steel rods; tensile bond strengths were determined after 1-day immersion in water. Data were analysed by ANOVA and Duncan's new multiple range test (P < 0.05). RESULTS: Four of the metal chlorides (CuCl2, FeCl3, MgCl2 and ZnCl2) enhanced the bond strengths of MMA-TBB resin to dentine. With Super-Bond resin, maximum bond strengths of 15.6 MPa and 19.0 MPa were recorded with primer containing 2.0 x 10(-5) mol g(-1) FeCl3 and 2.0 x 10(-6) mol g(-1) CuCl2, respectively. CONCLUSIONS: Bonding techniques, combining the use of either cupric primer or ferric primer with 10% phosphoric acid etchant may be suitable for application in seating resin-bonded prostheses with TBB-initiated luting materials.

Acid Etching, Dental↗

PubMed1998

Reduced nicotinamide adenine dinucleotide phosphate diaphorase in the spinal cord of dogs.

The distribution of somatic, fibre-like and punctate, non-somatic reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase activity was examined in dog spinal cord using horizontal, sagittal and transverse sections. The morphological features of NADPH diaphorase exhibiting neurons divided into six different neuronal types (N1-N6) were described and their laminar distribution specified. Major cell groups were identified in the superficial dorsal horn and around the central canal at all spinal levels, and in the intermediolateral cell column at thoracic level. NADPH diaphorase exhibiting neurons of the pericentral region were distributed in a thin subependymal cell column containing longitudinally-arranged small bipolar neurons with processes penetrating deeply into the intermediolateral cell column and/or running rostrocaudally in the subependymal layer. The second pericentral cell column located more laterally in lamina X contains large, intensely-stained NADPH diaphorase exhibiting neurons with long dendrites radiating in the transverse plane. Neurons of the sacral parasympathetic nucleus seen in segments S1-S3 exhibited prominent NADPH diaphorase activity accompanied by heavily-stained fibres extending from Lissauer's tract through lamina I along the lateral edge of the dorsal horn to lamina V. A massive dorsal gray commissure, with high NADPH diaphorase activity, was found in segments S1-S3. At the same segmental level a prominent group of moderately-stained motoneurons was detected in the dorsolateral portion of the anterior horn. Fibre-like NADPH diaphorase activity was found in the superficial dorsal horn and pericentral region in all segments studied. Punctate, non-somatic NADPH diaphorase activity was detected in the superficial dorsal horn, in the pericentral region all along the rostrocaudal axis and in the nucleus phrenicus (segments C4-C5), nucleus dorsalis (segments Th2-L2), nucleus Y (segments S1-S3), and the dorsal part of the dorsal gray commissure (S1-S3). A schematic diagram documenting the segmental and laminar distribution of NADPH diaphorase activity is given.

Animals↗

PubMed1998

Use of 2-isocyanatoethyl methacrylate and iron (II) perchlorate for bonding tri-n-butylborane-initiated luting agents to dentin.

The present study investigated the effect of 2-isocyanatoethyl methacrylate (IEM) and iron (II) perchlorate on dentin adhesion. Four primers were evaluated, consisting of aqueous 2-hydroxyethyl methacrylate (HEMA) solutions containing 5, 10, 20 or 50 micromol/g iron (II) perchlorate. Five luting agents were prepared with methyl methacrylate (MMA), poly(methyl methacrylate) (PMMA), tri-n-butylborane (TBB) initiator and IEM. The concentrations of IEM in the luting agents were 0.2, 0.4, 0.8, 2.0 and 4.0 wt%. Extracted bovine teeth were ground to expose the dentin, etched with an aqueous solution of 10 wt% phosphoric acid, primed, and then bonded with stainless-steel rods; tensile bond strengths were determined after 1 d immersion in water. The highest bond strength (20.7 MPa) was recorded for the group using 10 micromol/g iron (II) perchlorate and 2.0 wt% IEM. The use of IEM was effective in decreasing the optimal concentration of iron (II) perchlorate, and this may contribute to the color stability of iron-containing pretreatment agents.

Acid Etching, Dental↗

PubMed1998

Molecular cloning of cDNA and tissue-specific expression of the gene for SII-K1, a novel transcription elongation factor SII.

BACKGROUND: Transcription elongation factor SII has been shown to promote read-through by RNA polymerase II of pausing sites within various eukaryotic genes in vitro by inducing cleavage of the 3'-end of the nascent transcript in the ternary elongation complex. Recently, we showed that various mouse tissues contain multiple SII-related proteins. Of these, 'general SII' was ubiquitously expressed, whereas the others were expressed in a tissue-specific manner. We have identified testis-specific SII (SII-T1) and shown that it was expressed exclusively in spermatocytes. RESULTS: A new SII cDNA clone (pSII-K1) was isolated from mouse kidney. This clone contained an open reading frame which encoded a protein consisting of 347 amino acid residues (SII-K1). A comparison of the amino acid sequences of SII-K1 with those of general SII and SII-T1 revealed that their amino- and carboxy-terminal regions were very similar, but that the sequence of the 95 internal residues (87/181) was unique to each. The recombinant SII-K1 produced in Escherichia coli stimulated RNA polymerase II as did general S-II. The gene for SII-K1 was found to be expressed strongly in the heart, liver, skeletal muscle and kidney, but not in other tissues examined. Contrary to the expression of the general SII gene, the SII-K1 gene was expressed only in 15- and 17-day-old embryos during mouse embryonic development. CONCLUSIONS: We identified a novel member of SII family transcription elongation factor named SII-K1. This factor was expressed exclusively in the heart, liver, kidney and skeletal muscle. During mouse embryonic development, no significant expression of the SII-K1 gene was detected before the formation of these tissues.

Amino Acid Sequence↗

PubMed1998

Feasibility of the titration method of mild hypothermia in severely head-injured patients with intracranial hypertension.

OBJECTIVE: Clinical strategy to maximize effectiveness and to minimize adverse influences remains to be determined for mild hypothermia therapy for traumatic brain injury. This study was conducted to evaluate the clinical feasibility of the titration method of mild hypothermia in severely head-injured patients in whom a reduction in intracranial pressure was regarded as the target effect. METHODS: Nine consecutive patients with severe head injury were studied. Patient age ranged between 18 and 66 years, Glasgow Coma Scale scores were equal to or less than 8, and intracranial pressures were equal to or greater than 20 mm Hg despite removal of intracranial hematoma and drugs, including glycerol and thiopental. During a maximum of 6 days of hypothermia therapy, jugular venous blood or cerebrospinal fluid temperature was titrated to reduce intracranial pressure to less than 20 mm Hg by means of repeated intragastric cooling with our nasoduodenal tube and surface cooling. The feasibility and the effects on systemic complications of this titration method of mild hypothermia were evaluated. RESULTS: Intracranial pressure variably decreased from before to 3 hours after the beginning of all procedures of cooling. The mean intracranial pressure significantly decreased from 24 to 15 mm Hg with cooling, while temperature reduced an average of 2.0 degrees C. Four patients had systemic infection complications. Increased C-reactive protein and decreased platelet count were observed in all patients during hypothermia. The incidence of good recovery and moderate disability according to the Glasgow Outcome Scale was seven of nine patients. CONCLUSION: The titration method of mild hypothermia to control intracranial hypertension in severely head-injured patients is clinically feasible. However, the method failed to reduce the incidence of infectious and hematological complications.

Adolescent↗

PubMed1998

Effect of beta-Adrenoceptor Antagonists on Phospholipid N-Methylation Activities of Cardiac Sarcolemma.

BACKGROUND: Some beta-adrenoceptor antagonists exert a negative inotropic action by affecting Ca(2+) fluxes in the myocardial cell as a consequence of their interaction with sarcolemmal and sarcoplasmic reticular membranes. This action may be caused by their effects on the chemicophysical properties of membranes phospholipids. Because phosphatidylethanolamine (PE) N-methylation can influence the chemicophysical properties of membranes, these agents may affect PE N-methylation. This study was undertaken to examine the effects of propranolol, acebutolol, and atenolol on PE-N-methylation in rat heart sarcolemma (SL). METHODS AND RESULTS: Sarcolemmal membrane was isolated from rat hearts by the hypotonic shock LiBr method. Incorporation of radiolabeled methyl groups from S-adenosyl-l-methionine was assayed at three catalytic sites involved in the PE N-methylation reaction in the presence and absence of these drugs. A biphasic effect of propranolol at site I was noted; low concentrations (10(-8) M) were inhibitor. Acebutolol (10(-9)-10(-3) M) depressed methyl group incorporation in SL at site II in a dose-dependent manner, whereas atenolol showed no effect. Propranolol also exerted a biphasic effect on sarcoplasmic reticular (SR) methylation at site I, whereas acebutolol depressed the SR enzyme activity at site II and atenolol had no effect. The mitochondrial methyltransferase activities at sites I, II, and III were unaltered by any of these drugs. CONCLUSIONS: It is suggested that propranolol and acebutolol alter SL and SR PE N-methyltransferase activity at site I and site II, respectively, either by affecting the enzyme directly or by changing the physiochemical properties of the membrane.

Journal Article↗

PubMed1998

[Pulmonary artery injury caused by mal-manipulation of a pulmonary artery catheter].

A 71-year-old male was scheduled for aortic valve replacement. After tracheal intubation under high-dose fentanyl anesthesia, a pulmonary artery balloon catheter was inserted via the right internal jugular vein. However, after withdrawing the catheter with the balloon inflated, we found abrupt massive bleeding from the endotracheal tube. Fortunately, hemorrhage stopped with PEEP (20-25 cmH2O). Bronchofiberscopy could not detect the bleeding point. Chest X-ray showed the pulmonary artery balloon catheter in the right pulmonary artery and atelectasis of the middle and lower lobes. Five days later, he was extubated without rehemorrhage. Three weeks after hemorrhage, the patient successfully underwent an aortic valve replacement, and was discharged on the 25th post-operative day.

Aged↗

PubMed1998

[Patient-controlled sedation using propofol for a patient with von Gierke disease].

Patient-controlled sedation (PCS) using propofol under spinal anesthesia in transurethral lithotripsy was carried out in a 44 year old patient with von Gierke disease accompanied with liver dysfunction, chronic renal failure, hypoglycemia and metabolic acidosis. After administering spinal anesthesia PCS was started (0.2 mg.kg-1 intravenous bolus dose of propofol; infusion at 2 mg.kg-1.h-1; a three-minute lockout time interval following an initial doses of 0.4 mg.kg-1). PCS with propofol, throughout the operation, brought about adequate sedation level for this patient with 2 or 3 on Wilson's sedation score, and the sedative effect by propofol diminished quickly within 15 minutes after the end of PCS. In addition, respiratory depression due to this sedation which would be worse in acidotic condition was not seen using PCS during the operation. This patient was much satisfied with this sedation in an interview during the postoperative period. PCS using propofol is a useful method without respiratory depression for a patient with von Gierke disease.

Adjuvants, Anesthesia↗

PubMed1998

[The inhibition of lidocaine metabolism by various barbiturates in rat hepatic microsome].

To evaluate the effects of various barbiturates on lidocaine metabolism by cytochrome P-450 (P-450), enzyme kinetics were analyzed in an in vitro study using rat hepatic microsomes. Phenobarbital, amobarbital, hexobarbital, pentobarbital, and thiamylal showed the mixed type inhibition of lidocaine metabolism with inhibition constants being 4.89, 1.08, 2.76, 0.77 and 0.65 mM, respectively. Same as lidocaine, all barbiturates used in the present study, corresponding to binding with P-450, induced the I type of spectral change of P-450. Since these did not affect cytochrome C reductase activity, it was suggested that this inhibition of lidocaine metabolism in hepatic microsomes may have been caused by the reduction of activity on P-450 by the barbiturates.

Anesthetics, Local↗