Biomedical subjects

Y Sagara

Publications and source records attributed to Y Sagara.

At least 109 records · Page 6Linked to original sources

PubMed1996

Increased antioxidant enzyme activity in amyloid beta protein-resistant cells.

Clones of the rat pheochromocytoma cell line PC12 were selected for their resistance to amyloid beta protein (A beta). These A beta-resistant cells also survive higher concentrations of exogenously applied peroxides than the parent cells. A beta triggers intracellular H2O2 accumulation in the parent PC12 cells but not in the A beta-resistant cells. The absence of H2O2 accumulation in A beta-resistant cells is not attributable to differences in A beta binding to the cell surface. However, the mRNA and protein levels of catalase and glutathione peroxidase, as well as the corresponding enzyme activities, are highly elevated in A beta-resistant clones. These activities correlate well with the increased resistance of cells to A beta or peroxides. Finally, cells transfected with catalase and glutathione peroxidase are also more resistant to A beta toxicity. These results indicate that increased antioxidant enzyme activities in A beta-resistant cells account for at least part of their resistance to A beta and substantiate further the role of H2O2 in A beta toxicity.

Alzheimer Disease↗

PubMed1996

Effect of cystathionine ketimine on the stimulus coupled responses of neutrophils and their modulation by various protein kinase inhibitors.

Human peripheral blood polymorphonuclear leukocytes were perincubated with cystathionine and cystathionine metabolites found in the urine of the patients with cystathioninuria. Among the cystathionine metabolites, cystathionine ketimine significantly enhanced the N-formyl-methionyl-leucyl-phenylalanine-induced superoxide generation, but cystathionine and cyclothionine did not enhance the superoxide generation. Cystathionine ketimine also enhanced superoxide generation induced by opsonized zymosan but not those induced by arachidonic acid and phorbol myristate acetate. Superoxide generation induced by cystathionine ketimine was inhibited by genistein, an inhibitor of tyrosine kinase, and was enhanced by 1-(5-isoquinoline-sulfonyl)-2-methyl-piperazine, an inhibitor of protein kinase C.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1996

Effects of continuous medroxyprogesterone acetate on lipoprotein metabolism in postmenopausal women receiving estrogen.

OBJECTIVE: To investigate the effects of medroxyprogesterone acetate (MPA) on the beneficial effects of estrogen therapy on lipid metabolism in postmenopausal women. METHODS: Postmenopausal women were administered either conjugated equine estrogen (CEE) 0.625 mg daily for 3 months (Group 1) or CEE 0.625 mg in conjunction with MPA 2.5 mg (Group 2) or MPA 5.0 mg (Group 3) daily for 3 months. Plasma levels of cholesterol, triglyceride, lipoprotein lipids, apolipoproteins, sex steroid hormones and lecithin cholesterol acyltransferase activity (LCAT) were determined. Lipoprotein lipase (LPL) and hepatic triglyceride lipase (H-TGL) activities were measured in postheparin plasma. Changes in the lipid concentrations and enzymatic activities were evaluated in each group. RESULTS: Total, low-density lipoprotein (LDL) cholesterol, apolipoprotein B concentrations and LCAT activity were all significantly reduced by treatment in the three groups. The levels of high-density lipoprotein (HDL), HDL2, and HDL3 cholesterol as well as the levels of apolipoprotein AI and AII were significantly elevated in groups 1 and 2. The mean decrease in these parameters was related to the dose of MPA. Levels of triglyceride in the HDL and HDL2 were significantly increased in group 1. The levels of triglyceride in plasma, very low density lipoprotein (VLDL), LDL, HDL3 and VLDL cholesterol and LPL activity were unaffected. H-TGL activity was significantly inhibited only in groups 1 and 2. MPA produced a dose-dependent increase in H-TGL activity. A significant negative correlation was observed between the HDL cholesterol concentration and H-TGL activity (r = 0.58 P < 0.001). CONCLUSIONS: The administration of MPA 2.5 mg and 5.0 mg did not adversely affect the changes in VLDL-LDL metabolism produced by estrogen. However, MPA has dose-dependent negative effects on HDL metabolism by increasing H-TGL activity and the 5.0 mg MPA interferes with the favorable effects on lipids of estrogen in postmenopausal women.

Cholesterol↗

PubMed1996

Identification of cyclic cystathionine sulfoxide and N-acetylcyclic cystathionine in the urine of a patient with cystathioninuria using liquid chromatography-mass spectrometry with an atmospheric pressure chemical ionization interface system.

Perhydro-1,4-thiazepine-4,5-dicarboxylic acid sulfoxide (cyclic cystathionine sulfoxide [cyclic cystaSO]) and N-acetylperhydro-1,4-thiazepine-3,5-dicarboxylic acid (NAc-cyclic cysta) have been identified in the urine of a patient with cystathioninuria as new metabolites of cystathionine for the first time using liquid chromatography-mass spectrometry with an atmospheric pressure chemical ionization interface system (LC/APCI-MS). The concentrations of cyclic cystaSO and NAc-cyclic cysta in the urine of a patient with cystathioninuria have also been determined for the first time using this method: 18.24 +/- 0.79 and 25.23 +/- 0.83 mg/g creatinine, respectively.

Atmospheric Pressure↗

PubMed1996

Identification and mapping of functional domains on human T-cell lymphotropic virus type 1 envelope proteins by using synthetic peptides.

To identify the regions that are important in human T-cell leukemia virus type 1 (HTLV-1) envelope function, we synthesized 23 kinds of peptides covering the envelope proteins and examined the inhibitory effect of each peptide on syncytium formation induced by HTLV-1-bearing cells. Of the 23 synthetic peptides, 2, corresponding to amino acids 197 to 216 on gp46 and 400 to 429 on gp21, inhibited syncytium formation induced by HTLV-1-bearing cells but did not affect syncytium formation induced by human immunodeficiency virus type 1-producing cells. The peptide concentrations giving 50% inhibition of syncytium formation for gp46 197 to 216 and gp21 400 to 429 were 14.9 and 6.0 microM, respectively. A syncytium formation assay with overlapping synthetic peptides containing amino acids 175 to 236 and 391 to 448 of the envelope proteins showed that syncytium formation was inhibited by peptides that contained the amino acid sequences 197 to 205 (Asp-His-Ile-Leu-Glu-Pro-Ser-Ile-Pro) and 397 to 406 (Gln-Glu-Gln-Cys-Arg-Phe- Pro-Asn-Ile-Thr). These observations suggest that the two regions corresponding to amino acids 197 to 216 and 400 to 429 are involved] in HTLV-1 envelope function.

Amino Acid Sequence↗

PubMed1996

Different effects of carboxy-terminal deletion in the adrenodoxin molecule on cytochrome c and acetylated cytochrome c reductions.

In immunoblotting analysis using a rabbit antibody to bovine adrenodoxin, the total proteins of the bovine adrenal cortex gave two bands, suggesting the presence of two forms of adrenodoxin in vivo: full-length and carboxy-terminal deleted adrenodoxins. To examine the effect of the carboxy-terminal deletion of adrenodoxin on its activity, cDNAs for Arg115stop mutant adrenodoxin and for Asp113stop mutant adrenodoxin were constructed. The wild type [Ad(2-128)] and carboxy-terminal deleted [Ad(2-114) and Ad(2-112)] recombinant adrenodoxins expressed in Escherichia coli were purified to give a single band on SDS-PAGE. They showed an A414/A276 value of 0.92. In an NADPH-cytochrome c reduction assay, the Km values for cytochrome c in the reconstituted system with AD(2-128), Ad(2-114) and Ad(2-112) were 39, 235 and 618 mM, respectively. The Vmax values were 638, 700 and 898 mol/min/mol flavin, respectively. In an NADPH-acetylated cytochrome c reduction assay, the maximum activity of Ad(2-128) was obtained at 50 mM NaCl, while the maximum activities of Ad(2-114) and Ad(2-112) were obtained at 100 mM NaCl; the latter values were 4-times higher than that of Ad(2-128). In the presence of 100 mM NaCl, the Km values for acetylated cytochrome c in the system reconstituted with Ad(2-128), Ad(2-114) and Ad(2-112) were 220, 33 and 22 microM, respectively. The Vmax values were 352, 305 and 382 mol/min/mol flavin, respectively. These results indicate that the effects of the carboxy-terminal deletion of adrenodoxin on NADPH-cytochrome c and acetylated cytochrome c reductions are different; the carboxy-terminal region (residues 113-128) of adrenodoxin largely contributes to the binding with cytochrome c but disturbs the binding with acetylated cytochrome c.

Acetylation↗

PubMed1996

Cloning and sequence analysis of a full-length cDNA of rat adrenodoxin.

A cDNA clone which covers the entire coding region for the precursor of adrenodoxin was isolated from a rat adrenal cDNA library. This precursor consists of amino-terminal 64 residues of extrapeptide for transport into mitochondria and the following 124 residues of mature peptide region. The amino acid sequence of rat mature adrenodoxin showed 85-98% homology with mouse, human, chicken, porcine, bovine and sheep counterparts, whereas that of the extrapeptide showed significantly lower values.

Adrenodoxin↗

PubMed1996

Relaxant effect of nitric oxide and prostacyclin on serotonin-induced vasocontraction of human umbilical artery.

BACKGROUND: We investigated the effect of nitric oxide and prostacyclin, which are endothelium-derived vasodilators, on serotonin (5-HT)-induced vasocontraction, and 5-HT1-serotoninergic receptor mediated relaxation in the human umbilical artery. METHODS: Serotonin-stimulated vasocontraction was measured in umbilical artery segments treated with and without 1) L-arginine (10(-4) M approximately 10(-2) M), a precursor of nitric oxide synthesis; 2) methylene blue (10(-5) M) and L-NG-monomethyl arginine (LNMA, 2 X 1O(-4) M), which are specific inhibitors of nitric oxide action and nitric oxide synthesis, respectively; and 3) tranylcypromine (2 X 10(-6) M, 2 X 10(-5) M), an inhibitor of prostacyclin synthesis. 4) Vessels were pretreated with M1, an inhibitor of 5-HT2 serotoninergic receptors, and then prostaglandin F2 alpha (9.O X 1O(-7) M). Finally, we measured the 5-HT1, receptor-mediated relaxation induced by 5-HT. RESULTS: Treatment with L-arginine significantly inhibits 5-HT-induced contraction in a dose-dependent manner. Treatment with methylene blue and LNMA significantly potentiated 5-HT-induced contraction. Tranylcypromine caused no significant changes in 5-HT-induced vasocontraction. 5-HT1 serotoninetic receptor-mediated relaxation was found at higher concentrations of 5-HT (greater than 4.94 X 10(-5) M). CONCLUSIONS: Our results suggest that nitric oxide may exert a strong relaxant effect on 5-HT-induced vasocontraction compared with prostacyclin in human umbilical artery.

Arginine↗

PubMed1996

Potentiating effect of hydrogen peroxide on the serotonin-induced vasocontraction in human umbilical artery.

BACKGROUND: Our objective was to investigate the role of hydrogen peroxide in the vasocontraction induced in the human umbilical artery by serotonin. METHODS: Umbilical arteries collected from healthy women at term were cut helically and suspended in an organ bath to record isometric mechanical activity. In Study I, we measured the concentration-contraction response to serotonin with or without pretreatment with hydrogen peroxide (0.01-10 microM). In Study 2, vessels were pre-incubated with L-arginine (0.1-10mM), or with hydrogen peroxide (10 mM) and L-arginine (1 mM), then serotonin was added cumulatively. In Study 3, vessels were suspended in a calcium-free solution containing potassium chloride 20 mM, and a cumulative concentration-response curve to calcium chloride (10(-5)-10(-3) M) was constructed for vessels pretreated with hydrogen peroxide (10 microM). In Study 4, vessels were pre-treated with M1, an inhibitor of 5-HT2 serotoninergic receptors, and hydrogen peroxide (10 microM), and then prostaglandin F2 alpha (9.0 x 10(-7) M). Finally, we measured the 5-HT1 receptor-mediated relaxation induced by serotonin. RESULTS: Hydrogen peroxide (1 or 10 microM) significantly potentiated the contractile response to serotonin (p < 0.04, p < 0.005). L-arginine (1 or 10 mM) significantly reduced the contractile response to serotonin (p < 0.02, p < 0.0002). Pretreatment with L-arginine significantly suppressed the potentiating effect of hydrogen peroxide on the serotonin-induced contraction. The sensitivity of the arteries to calcium chloride in the presence of hydrogen peroxide did not differ from that in the control group. Pretreatment with hydrogen peroxide significantly reduced the 5-HT1 serotoninergic receptor-mediated relaxation at higher concentrations of serotonin (1.23 x 10(-4) M, 2.47 x 10(-4) M, 2.47 x 10(-4) M). CONCLUSION: Hydrogen peroxide potentiated the umbilical artery contraction induced by serotonin. This action may be mediated by suppression of endogenous nitric oxide activity.

Arginine↗

PubMed1996

[The influence of pregnancy and delivery on the climacteric symptoms].

This study was undertaken to investigate the influence of past pregnancy and delivery on the perimenopausal status in 144 women (48-52 years of age). Individual interviews to ascertain the personal profile, medical history, events at pregnancy, delivery and puerperium, and the kind and severity of climacteric symptoms were held. The subjects were divided into two groups by means of a simplified menopausal index (SMI): group A had climacteric symptoms (SMI > 50) and those in group B had mild symptoms (SMI < or = 50). The analysis of the principal components, and the correlation among the variables revealed that three factors--the impression and events at past pregnancies and deliveries, reproductive functions, and the psycho-character properties--had a significant influence on the status at the perimenopause, but the social-environmental factors appeared to have no significant influence on the severity of climacteric symptoms.

Climacteric↗

PubMed1995

Modulation of endothelium-dependent flow-mediated dilatation of the brachial artery by sex and menstrual cycle.

BACKGROUND: Estrogen has been reported to augment endothelium-dependent vasodilatation. The role of endogenous ovarian hormones in modulating endothelium-dependent vasodilatation, however, remains to be determined. The purpose of the present study was to investigate the effects of sex and menstrual cycle on endothelium-dependent flow-mediated vasodilatation. METHODS AND RESULTS: Seventeen female volunteers 25.1 +/- 0.8 years old and 17 age-matched male volunteers were examined. We measured brachial artery diameters noninvasively using a 7.5-MHz ultrasound machine at rest, during reactive hyperemia, and after sublingual nitroglycerin administration. All female subjects were studied three times each, in three different phases of one menstrual cycle (M, menstrual phase; F, follicular phase; and L, luteal phase). Flow-mediated diameter (D) increase (%FMD; delta D/D x 100) in M, when serum estradiol level was low (121.9 +/- 12.5 pmol/L), was 11.22 +/- 0.58%, and the value was comparable to that in male subjects (10.60 +/- 0.75%). %FMD increased in F (18.20 +/- 0.81%, P < .01 versus M) and L (17.53 +/- 0.74%, P < .01 versus M), when serum estradiol level was high (F, 632.0 +/- 74.5 and L, 533.8 +/- 33.4 pmol/L, P < .01 versus M). Endothelium-independent vasodilatation by nitroglycerin increased in both F and L. However, the increment was smaller than that of %FMD. CONCLUSIONS: Endothelium-dependent vasodilatation varies during the menstrual cycle. The endogenous estradiol may be involved in this menstrual cycle-related vasodilatation.

Adult↗

PubMed1995

Identification of a transcriptional regulatory factor for human aromatase cytochrome P450 gene expression as nuclear factor interleukin-6 (NF-IL6), a member of the CCAAT/enhancer-binding protein family.

Human aromatase cytochrome P450 catalyzes the ultimate reaction in the estrogen biosynthetic pathway by coupling with another enzyme, NADPH-cytochrome P450 reductase, in the endoplasmic reticulum. The expression of the gene encoding the enzyme (CYP19) is regulated, in part, by tissue-specific promoters through the use of alternative-splicing mechanisms. Recently, we have localized a transcriptional activating element at positions -2141 to -2115 relative to the major cap site of the gene, by transient expression analyses in human BeWo choriocarcinoma cells using the bacterial chloramphenicol acetytransferase reporter gene ligated with CYP19 promoter sequences which regulate expression in this tissue. Here, we report the isolation of a cDNA encoding a DNA-binding protein which binds specifically to the regulatory element. The deduced amino-acid sequence of the insert is identical to that corresponding to the DNA-binding domain and the dimerization domain of a transcription factor, nuclear factor interleukin-6 (NF-IL6), a member of the CCAAT/enhancer-binding protein (C/EBP) family. Studies using specific antibodies against members of the C/EBP family demonstrate that NF-IL6 is the major nuclear factor binding to the regulatory element in BeWo cells; nevertheless. C/EBP alpha also seems to be involved. Disruption of the NF-IL6-binding site within the regulatory element resulted in the disappearance of the transcriptional enhancing activity of the element, indicating that NF-IL6 is at least one of the nuclear factor(s) which enhances transcription through binding to the cis-acting element. These results indicate the intrinsic importance of NF-IL6 in the transcriptional regulation of CYP19 expression.

Amino Acid Sequence↗

PubMed1995

A Comparison of Mass Screening for Breast Cancer Using Mammography and Physical Examination Alone in Japan.

To compare the sensivity of breast cancer screening methods by conventional physical examination and film mammography, a trial of mass screening for breast cancer using mammography was principally carried out in asymptomatic women over 50 years of age in Tokushima Prefecture. In this trial craniocaudal and mediolateral oblique imagings of the breast using two-view film mammography and physical examination, using inspection and palpation of the breasts were performed independently. Breast cancer was detected in 8 of a total of 950 examinees by mammography alone, and no cases of breast cancer were detected by physical examination. The detection rate of breast cancer was 0.84%, that is 7 times higher than that(0.12%) obtained by conventional mass screening using physical examination alone. The detection rate of increased especially in the sixth and seventh decades of life. The stage of the detected breast cancer was stage 0 (Tis) in 5 cases and stage T, with a tumor size of 1.0 cm or less, in 3 cases. All 8 cases were in the early stage, and they underwent breast conservation therapy. Based on these results, it is recommended to employ mammography in breast cancer screening for asymptomatic women aged over 50 years. We consider mammography alone may be sufficient for mass screening for breast cancer in these subjects.

Journal Article↗

PubMed1995

Amyloid peptides are toxic via a common oxidative mechanism.

beta-Amyloid protein (A beta) is a member of a small group of proteins that accumulate as amyloid deposits in various tissues. It has recently been demonstrated that the toxicity of A beta toward some neural cells is caused by oxidative damage. Since all of the amyloid diseases are characterized by protein deposited in the antiparallel beta-sheet conformation, it was asked whether there is a common toxic mechanism. It is shown here that the protein components of other human amyloidoses, including amylin, calcitonin, and atrial natriuretic peptide, are all toxic to clonal and primary cells. The toxicity is mediated via a free radical pathway indistinguishable from that of A beta. Experiments with synthetic peptides suggest that it is the amphiphilic nature of the peptides generated by their beta structure rather than their beta structure per se that causes toxicity. These results tend to rule out the alternative that amyloid toxicity is exclusively mediated via specific cell surface receptors.

Amino Acid Sequence↗

PubMed1995

Amplifying effect of endothelin-1 on serotonin-induced vasoconstriction of human umbilical artery.

OBJECTIVE: The purpose of this study was to evaluate the role of endothelin-1 in serotonin-induced vasoconstriction in human umbilical artery. STUDY DESIGN: Umbilical arteries collected from 41 normal subjects at term were cut helically and suspended in an organ bath for recording isometric mechanical activity. In study 1 we measured the concentration-contraction response to serotonin or endothelin-1 according to a cumulative concentration schedule. In study 2 vessels were preincubated with a subthreshold concentration of endothelin-1 (100, 250, or 500 pg/ml), and then serotonin was added cumulatively. In study 3 vessels were preincubated with H-7 (3 x 10(-6) mol/L), an inhibitor of protein kinase C, or with 12-tetradecanoylphorbol-13 acetate (10(-9) to 10(-7) mol/L), an activator of protein kinase C; then serotonin was added cumulatively. In study 4 vessels were suspended in a calcium-free solution containing 2 mmol/L ethylene glycol-bis(beta-aminoethyl ether) N,N,N',N'-tetraacetic acid and 60 mmol/L potassium chloride, and then a cumulative concentration-response curve to calcium chloride (10(-7) to 10(-3) mol/L) was constructed for vessels pretreated with endothelin-1, 500 pg/ml or 5 ng/ml. RESULTS: The threshold concentrations of serotonin and endothelin-1 were 5 and 1 ng/ml, respectively. A subthreshold concentration of endothelin-1 (250 or 500 pg/ml) potentiated significantly the concentration response to serotonin (p < 0.084, p < 0.009, by analysis of variance). Pretreatment with H-7 significantly suppressed the amplifying effect of endothelin-1 on serotonin-induced contraction. Treatment with 12-tetradecanoylphorbol-13 acetate (10(-7) or 10(-8) mol/L) significantly potentiated the contractile response to serotonin (p < 0.0003, p < 0.015). The sensitivity of the arterial segments to calcium chloride in the presence of a subthreshold concentration of endothelin-1 did not differ from that in the control group. CONCLUSION: Endothelin-1 at a subthreshold concentration amplified the smooth muscle contraction induced by serotonin. The mechanism of action may be mediated by activation of intracellular protein kinase C.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1995

Lipoprotein metabolism in postmenopausal and oophorectomized women.

OBJECTIVE: To investigate the mechanisms of accumulating cholesterol, and to analyze the metabolism of excess tissue cholesterol in women with low plasma levels of sex steroid hormones. METHODS: We measured plasma concentrations of cholesterol, triglyceride, apolipoproteins, sex steroid hormones, and lecithin cholesterol acyltransferase activity in 20 premenopausal, ten postmenopausal, and ten bilaterally oophorectomized women. Lipoprotein lipase and hepatic triglyceride lipase activities were measured in postheparin plasma. We compared the three groups and evaluated a correlation between lipid metabolism and sex steroid hormone concentrations. RESULTS: The mean plasma low-density lipoprotein (LDL) cholesterol level, lecithin cholesterol acyltransferase activity, and postheparin plasma lipoprotein lipase activity were higher in the postmenopausal and surgically menopausal groups. The mean plasma high-density lipoprotein (HDL) cholesterol concentration and postheparin plasma hepatic triglyceride lipase activity did not differ significantly among the three groups. The plasma LDL cholesterol level and postheparin plasma lipoprotein lipase activity showed a significantly negative correlation with plasma concentration of estrone (LDL: r = 0.64, P < .001; lipoprotein lipase: r = 0.54, P < .005) and estradiol (LDL: r = 0.65, P < .001; lipoprotein lipase: r = 0.47, P < .01), but not with that of testosterone. There was no significant relationship between postheparin plasma hepatic triglyceride lipase activity and plasma sex steroid hormones. Plasma lecithin cholesterol acyltransferase activity correlated significantly with plasma LDL cholesterol concentration, but not with levels of sex steroid hormones. CONCLUSION: Because of low endogenous estrogens, enhanced postheparin plasma lipoprotein lipase activity may lead to an elevated plasma LDL cholesterol concentration in postmenopausal and bilaterally oophorectomized women. We demonstrated an accelerated cholesterol esterification in HDL cholesterol that may have been induced by LDL cholesterol accumulation, although the HDL cholesterol concentration remained unchanged.

Adult↗

PubMed1995

Purification and characterization of rat adrenodoxin.

Adrenodoxin was purified from the rat adrenal gland. The A414/A280 value of the purified rat adrenodoxin was 0.90 and the oxidized spectrum showed absorption maxima at 320, 414 and 455 nm, similar to those of bovine adrenodoxin. On SDS-PAGE, the rat adrenodoxin showed a single band with a molecular mass of 11.2 kDa, while the apparent molecular mass by gel filtration through Sephadex G-75 equilibrated with 10 mM K-phosphate (pH 7.5) was 27 kDa. In the reconstituted system, Vmax of NADPH-cytochrome c reduction activity and the Km for the rat adrenodoxin were much the same as those for recombinant bovine adrenodoxin. In the case of cholesterol side-chain cleavage activity, however, these values of the rat adrenodoxin were about half of those of the bovine adrenodoxin. The CD spectrum of the rat adrenodoxin was similar to that of the bovine adrenodoxin but showed a significantly lower ellipticity value in the 195-205 nm region than that of the bovine adrenodoxin. The structural differences may possibly explain differences in the enzymic properties between rat and bovine adrenodoxins.

Adrenal Glands↗

PubMed1995

Ephedrine-induced increases in arterial blood pressure accelerate regression of epidural block.

We investigated the hypothesis that ephedrine-induced increases in blood pressure accelerate the regression of epidural block. In patients undergoing minor gynecologic surgery, we performed lumbar epidural blockade using 2% lidocaine containing 1:200,000 epinephrine to which was added 0.1 mg of fentanyl. Eighty minutes after the epidural injection, we started an ephedrine infusion to increase the systolic blood pressure by 20% in 10 min and maintained the value for the following 20 min. Then we compared the proximal extent of sensory analgesia at 80 min with that at 140 min. Ephedrine significantly (P = 0.001) hastened the regression of sensory analgesia. We conclude that an ephedrine-induced blood pressure increase accelerates regression of epidural blockade.

Adjuvants, Anesthesia↗