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Biomedical subjects

M Endoh

Publications and source records attributed to M Endoh.

At least 199 records · Page 11Linked to original sources
PubMed1994

[Is extensive usage of arterial grafts in revascularization of the circumflex appropriate?: comparative study with the saphenous vein].

From September 1975 to March 1992, 584 patients underwent coronary artery bypass grafting (CABG) including revascularization of the circumflex artery (LCX) with either saphenous vein (Group S, n = 496) or arterial grafts (Group A, n = 88). Group S was divided into two subgroups. Group S I is the patients who underwent CABG before April 1988, when the first case of arterial revascularization of the LCX, and Group S II is the patients who underwent CABG after April 1988. No significant differences were noted in early mortality, late mortality, or event free curve among three groups. Although graft flow was significantly less in Group A (27.8 +/- 12.8 ml/min) than Group S (60.0 +/- 35.7 ml/min), the patency rate was better in Group A (94.3%) than Group S I (88.6%) or Group S II (87.7%). The proportion of usage of arterial grafts in revascularization of the left anterior descending artery (LAD) was smaller in Group A (65.5%) than Group S II (80.3%), but the patency rate was acceptably good in both groups (Group A: 98.8%, Group S II: 99.5%). These findings justify extensive usage of arterial grafts to the LCX area under proper assignment of grafts to obtain good patency rate and long-term results with keeping quality of revascularization of the LAD area.

Abdominal Muscles↗
PubMed1994

[Massive intraventricular hemorrhage from prolactinoma during bromocriptine therapy: case report].

We are reporting herein a case with massive intraventricular hemorrhage secondary to prolactinoma, which initially extended into the suprasellar cistern but reduced in size after one year of bromocriptine therapy, resulting in intrasellar herniation. This is the 6th reported case of intraventricular hemorrhage from a pituitary adenoma. Neuroradiographic features are described in detail and the pertinent literature is reviewed.

Administration, Oral↗
PubMed1994

[Emergency coronary artery bypass grafting for left main trunk stenosis in a patient with systemic lupus erythematosus].

A 57-year-old female who had been treated for SLE with prednisolone for 11 years was transferred to our hospital due to unstable angina caused by stenoses of the left main trunk (LMT) and the left anterior descending artery (LAD). She underwent emergency coronary artery bypass grafting of the LAD and the left circumflex artery (LCX) using saphenous vein grafts (SVGs). Since we were afraid the internal thoracic arteries (ITAs) and right gastroepiproic artery were less usable because preoperative angiography showed too small (1.2 mm) ITAs and she had undergone Miles' operation for anal canal cancer, SVG usage seemed more advantageous as an emergency procedure. Pre- and postoperatively, leukocytopenia was treated with granulocyte colony stimulating factor and she was free from infection. She had no chest pain postoperatively. However, postoperative angiography confirmed an occluded SVG to the LCX and a patent SVG to the LAD which supplied blood flow to the LCX area.

Aged↗
PubMed1994

Dissociation of the positive inotropic effect of methoxamine from the hydrolysis of phosphoinositide in rabbit ventricular myocardium: a comparison with the effects of phenylephrine and the subtype of the alpha-1 adrenoceptor involved.

The effects of methoxamine on the contractile force and the hydrolysis of phosphoinositide (PI) were examined and compared with those of phenylephrine in the rabbit ventricular myocardium. Methoxamine, as well as phenylephrine, caused the concentration-dependent accumulation of [3H]inositol monophosphate in rabbit ventricular slices. The maximal responses of the two drugs were equivalent, but methoxamine was approximately 10 times less potent than phenylephrine. The extents and time courses of accumulation of [3H]inositol phosphates induced by 10(-4) M methoxamine and 10(-5) M phenylephrine were very similar, whereas the positive inotropic effect (PIE) of methoxamine developed much more slowly and its extent was much smaller than that of phenylephrine. The maximal inotropic response achieved with 10(-4) M methoxamine was one third of that achieved with phenylephrine. The PIE of methoxamine induced by a single administration was markedly attenuated when the same dose was given by cumulative administration. The concentration-response curve for the PIE of phenylephrine was shifted to the right and downward in the presence of methoxamine in a concentration-dependent manner. These results indicate that methoxamine accelerates the hydrolysis of PI as effectively as does phenylephrine, but it has a smaller PIE because of its depressant effect on the process subsequent to acceleration of the hydrolysis of PI induced by alpha-1 adrenoceptors. The accumulation of [3H]inositol 1,4,5-trisphosphate induced either by methoxamine or by phenylephrine was abolished by 10(-5) M chlorethylclonidine, whereas the maximal inhibition induced by WB 4101 was 60%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Myocardial alpha 1A-adrenoceptor subtypes in rabbit: differentiation by a selective antagonist, HV723.

The influence of a newly developed alpha 1-adrenoceptor antagonist, HV723 (alpha-ethyl-3,4,5-trimethoxy-alpha-(3-((2-(2-methoxy-phenoxy)ethyl)-ami no)- propyl) benzeneacetonitrile fumarate), on the positive inotropic effect and acceleration of phosphoinositide hydrolysis induced by phenylephrine via alpha 1-adrenoceptors in the presence of bupranolol (0.3 microM) was studied in the rabbit ventricular muscle: (1) HV723 at low concentrations (1-100 pM) attenuated the maximal inotropic response by 15-20% without altering the pD2 value for and [3H]inositol monophosphate accumulation induced by phenylephrine. The inhibitory action of HV723 (1-100 pM) showed a close resemblance to that of a selective alpha 1A antagonist, (+)-niguldipine. (2) HV723 (> or = 1 nM) shifted the concentration-response curve for phenylephrine to the right and downwards in association with a partial inhibition (42.5%) of [3H]inositol monophosphate accumulation. The IC50 values of HV723 for the inhibition of the inotropic response and phosphoinositide hydrolysis were approximately equal to the Kilow value determined by displacement of [3H]prazosin-specific binding. The mode of the inhibitory action of HV723 (> or = 1 nM) resembled that of another alpha 1A antagonist, WB 4101. These results indicate that HV723 shows a differential antagonistic action on the alpha 1A-mediated responses depending on the concentration: HV723 (1-100 pM) selectively inhibits the (+)-niguldipine-sensitive subclass to lead to a decrease in the maximal inotropic response with no change in phosphoinositide hydrolysis; HV723 (> or = 1 nM) may antagonize the WB 4101-sensitive subtype coupled to acceleration of phosphoinositide hydrolysis.

Acetonitriles↗
PubMed1993

Selective inhibition by phorbol 12,13-dibutyrate of the alpha 1-receptor-mediated positive inotropic effect.

Influence of the protein kinase C activator phorbol 12,13-dibutyrate on the alpha 1- and beta-adrenoceptor-mediated positive inotropic effect was studied in the rabbit ventricular myocardium. Phorbol 12,13-dibutyrate (10(-8)-10(-6) M) inhibited the positive inotropic effect mediated by alpha 1-adrenoceptors in a concentration-dependent manner, while the positive inotropy mediated by beta-adrenoceptors was not affected by phorbol 12,13-dibutyrate up to 3 x 10(-7) M. Phorbol 12,13-dibutyrate at 10(-6) M decreased the beta-mediated effect, but the extent of inhibition was less than that of alpha 1-mediated effect produced by 10(-8) M phorbol 12,13-dibutyrate. Thus, the inhibition induced by phorbol 12,13-dibutyrate was 100-fold more selective for alpha 1- than for beta-mediated inotropy. Phorbol 12,13-dibutyrate at 10(-7) M increased the basal force of contraction in some preparations, but decreased it at 3 x 10(-7) M and higher in a concentration-dependent manner. In membrane fractions derived from the rabbit ventricular muscle, phorbol 12,13-dibutyrate did not affect the specific binding of [3H]prazosin. A nonhydrolyzable GTP analogue GTP gamma S shifted the epinephrine-induced displacement curve of [3H]prazosin to the right, but phorbol 12,13-dibutyrate did not affect the curve. Accumulation of [3H]inositol monophosphate induced by alpha 1 stimulation was inhibited by phorbol 12,13-dibutyrate. These findings indicate that phorbol 12,13-dibutyrate may induce the selective uncoupling of the myocardial alpha 1-receptor stimulation to activation of phospholipase C, and inhibit selectively the alpha 1-mediated positive inotropy.

Animals↗
PubMed1993

Reactive astrocytes express NADPH diaphorase in vivo after transient ischemia.

In the hippocampus, ten minutes of transient global ischemia results in the death of CA1 pyramidal cells after a period of one to three days. The neurons in the CA1 region constitutively express NADPH-D (NADPH diaphorase activity). In contrast, astrocytes in the hippocampus do not normally express NADPH-D; but a population of reactive astrocytes (GFAP+ cells) begin to express of NADPH-D one day after transient global ischemia. NADPH-D is thought to be a histological marker for Nitric Oxide Synthase (NOS), the enzyme that is responsible for the synthesis of NO, a potent neurotoxin. We suggest that this increase in NADPH-D/NOS expression is an important element in the sequence of changes that occurs after ischemia, and that NO derived from reactive astrocytes or from neurons may play a causal role in neural cell death after ischemia in the hippocampus.

Amino Acid Oxidoreductases↗
PubMed1993

Cyclic AMP metabolism in intact rat ventricular cardiac myocytes: interaction of carbachol with isoproterenol and 3-isobutyl-1-methylxanthine.

Experiments were carried out to elucidate the characteristics of regulation of cyclic AMP levels in intact myocardial cells. For this purpose, the influence of isoproterenol, a nonselective cyclic nucleotide phosphodiesterase (PDE) inhibitor 3-isobutyl-1-methylxanthine (IBMX) and carbachol on cyclic AMP levels was investigated in isolated rat cardiac myocytes. The extent of cyclic AMP accumulation induced by isoproterenol was much less than that produced by IBMX: submaximal concentrations of isoproterenol and IBMX elevated the cyclic AMP level 2.4- and 4.8-fold of the control level, respectively. Both agents in combination increased the cyclic AMP level markedly 48-fold. Carbachol inhibited the cyclic AMP accumulation induced by isoproterenol, IBMX and their combination by 30%, 60% and 80% of the respective response. The extent of inhibition produced by carbachol of the cyclic AMP accumulation induced by IBMX + isoproterenol was smaller than that caused by propranolol, and carbachol produced only a marginal additional inhibitory action to that of propranolol, implying that carbachol does not affect the process of cyclic AMP degradation. The present findings indicate that in intact cardiac myocytes the rate of cyclic AMP degradation catalyzed by PDE may be a crucial process of cyclic AMP turnover. This view is supported by the observations that the inhibitory action of carbachol on the effect of isoproterenol was less than that on the effect of IBMX, and that the inhibitory action of carbachol was markedly enhanced by the simultaneous presence of IBMX.

1-Methyl-3-isobutylxanthine↗
PubMed1993

Modulation by aging of the coronary vascular response to endothelin-1 in the rat isolated perfused heart.

Changes with age in the coronary vascular response to endothelin-1 were investigated in perfused hearts isolated from 2-, 6- and 24-month-old (mo) male Fisher-344 rats. Endothelin-1 injected as a single bolus (0.3, 3 and 30 nmol) into the coronary artery supply caused dose-dependent vasoconstriction in all three age groups. While there was no age-related change in the vasoconstriction induced by the lower doses (0.3 and 3 nmol), the higher dose (30 nmol) elicited a more pronounced vasoconstriction in 6- and 24-mo rats than that in 2-mo rats. NG-nitro-L-arginine (L-NNA), an inhibitor of nitric oxide formation, markedly enhanced the vasoconstriction induced by 30 nmol endothelin-1 in 2- and 6-mo rats but only slightly and non-significantly enhanced that vasoconstriction in 24-mo rats. Haemoglobin, which inhibits activation of guanylate cyclase by nitric oxide, enhanced the endothelin-1-induced vasoconstriction in 2-mo rats, but not in 6- and 24-mo rats. The acetylcholine-induced coronary vasodilation was more pronounced in 2- and 6-mo rats than in 24-mo rats and was attenuated by L-NNA in 2- and 6-mo rats. The coronary vasodilation induced by nitroprusside (0.1 mmol), a pharmacological precursor of nitric oxide, did not change with age. Endothelin-1 (30 nmol) markedly increased the release of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in all three age groups. The prostaglandin synthesis inhibitor indomethacin enhanced the endothelin-1-induced vasoconstriction in 2- and 6-mo rats to a similar extent.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1993

Pronounced direct inhibitory action mediated by adenosine A1 receptor and pertussis toxin-sensitive G protein on the ferret ventricular contraction.

An adenosine A1 receptor agonist R-N6-phenylisopropyladenosine (R-PIA) elicited a pronounced negative inotropic effect with the EC50 value of 0.69 mumol/l in the presence of a beta-adrenoceptor blocking agent bupranolol (0.3 mumol/l) in the isolated ferret papillary muscle. The negative inotropic effect of R-PIA was not associated with changes in cyclic AMP level. Adenosine and other A1 receptor agonists also elicited a negative inotropic effect. DPCPX (1,3-dipropyl-8-cyclopentyl xanthine) antagonized the negative inotropic effect of R-PIA in a competitive manner (pA2 value = 8.4). The inhibitory action of R-PIA was markedly attenuated in the ventricular muscle preparation isolated from ferrets pretreated with pertussis toxin that caused ADP-ribosylation of 39 kDa proteins in the membrane fraction. In the membrane fraction derived from the ferret ventricle, [3H]-DPCPX bound to a single binding site in a saturable and reversible manner with high affinity (Kd value = 1.21 +/- 0.41 nmol/l; Bmax = 12.8 +/- 3.02 fmol/mg protein; n = 7). The binding characteristics of [3H]-DPCPX in the rat ventricle (Kd value = 1.51 +/- 0.09 nmol/l; Bmax = 12.7 +/- 1.47 fmol/mg protein; n = 5) were similar to those in the ferret. On the other hand, the content of G(o), a major pertussis toxin-sensitive G protein in the ferret heart, was much higher in the ferret than in the rat ventricle. The present results indicate that adenosine receptors may play an important role in the inhibitory regulation of ventricular contractility in the ferret in contrast to other mammalian species. The signal transduction process subsequent to agonist binding to A1 receptors including the pertussis toxin-sensitive G protein and ion channels may be responsible for the unique inhibitory action of adenosine in this species.

Adenosine Diphosphate Ribose↗
PubMed1993

Survival and recurrence after low anterior resection and abdominoperineal resection for rectal cancer: the results of a long-term study with a review of the literature.

Morbidity, survival, and recurrence in 203 patients treated with curative low anterior resection (LAR) were compared with those in 100 patients treated with curative abdominoperineal resection (APR). The overall 5-year survival figures for the total number of, LAR and APR patients were 75.6 +/- 5.7%, 79.8 +/- 6.4% and 67.7 +/- 9.6%, respectively. The prognosis for cancers situated low enough in the rectum to involve the anal canal was poor even when managed by APR, as evidenced by a low survival at 5 years of 59.0 +/- 9.6% and a high pelvic recurrence rate of 34%. For all except these tumors, LAR proved at least equal to, or better than APR as a curative surgical method for middle and low rectal cancers, on the basis of 5-year survival being 79.8 +/- 6.4% vs 78.7 +/- 5.2%, operative mortality being 1.5% vs 1.0%, morbidity being 39.4% vs 59.0%, and the incidence of pelvic recurrence being 8.9% vs 13.5%. When deciding upon the most appropriate surgical procedure for rectal cancer, especially for middle or low rectal lesions, the patient should not simply be condemned to a permanent colostomy. Thus, we first attempt LAR for every lesion except those which are very advanced or those with anal canal involvement, if technically feasible and suitable for the individual patient.

Adult↗
PubMed1993

Immunohistochemical demonstration of membrane cofactor protein (MCP) of complement in normal and diseased kidney tissues.

The immunohistochemically stained membrane cofactor protein of complement (MCP/CD46), one of the complement regulatory proteins, was up-regulated in some diseased kidney tissues. MCP in diseased kidneys was strongly concentrated along the glomerular capillary walls as well as in the mesangial regions, while MCP in normal kidneys was weakly detected in all glomerular structural cells and in the epithelial cells of tubules. Since the enhanced staining was noted in those areas where depositions of C3b/C3c occurred, ongoing complement reaction might be responsible for the up-regulation of MCP expression. MCP expression may be up-regulated by complement fragments generated during complement activation in glomerulonephritis. Furthermore, anti-MCP staining was stronger in intensity in patients with moderate to massive proteinuria, indicating that up-regulation of MCP expression could be directly correlated to the kidney damage.

Antigens, CD↗
PubMed1993

Pharmacological characteristics of the positive inotropic effect of angiotensin II in the rabbit ventricular myocardium.

1. In order to elucidate the mechanism underlying the positive inotropic effect (PIE) of angiotensin II (AII), we measured changes in phosphoinositide hydrolysis and contractile force induced by AII in the rabbit ventricular myocardium. 2. AII (1.0 nM-3 microM) produced a PIE in a concentration-dependent manner in the presence of bupranolol (0.3 microM) and prazosin (0.1 microM), the maximal response being about 40% of that to isoprenaline and the EC50 30 nM. 3. The PIE of AII was associated with a concentration-dependent increase in the total duration of contraction; the time to peak force and the relaxation time were prolonged. 4. AII (10 nM-30 microM) elicited an accumulation of [3H]-inositol monophosphate in a concentration-dependent manner in rabbit ventricular slices prelabelled with myo-[3H]-inositol. 5. The PIE and the accumulation of [3H]-inositol monophosphate induced by AII were inhibited by a non-selective AII receptor antagonist, saralasin (10 nM-1 microM) and by a selective AT1 receptor antagonist, losartan (10 nM-1 microM), but not a selective AT2 receptor antagonist, PD 123319 (1 microM). 6. A tumour-promoting phorbol ester, phorbol 12,13-dibutyrate (PDBu, 10-100 nM), inhibited the AII-induced PIE and [3H]-inositol monophosphate accumulation in a concentration-dependent manner. 7. These results suggest that AII exerts a PIE through activation of AT1 receptors and subsequent acceleration of phosphoinositide hydrolysis. Activation of protein kinase C by PDBu may inhibit the AII-induced stimulation of phosphoinositide hydrolysis and thereby the PIE of AII in the rabbit ventricular myocardium.

Angiotensin II↗
PubMed1993

Effects of the positive inotropic agent Org 30029 on developed force and aequorin light transients in intact canine ventricular myocardium.

The action of a novel cardiotonic agent N-hydroxy-5,6-dimethoxy-benzo[b]thiophene-2-carboximide hydrochloride (Org 30029) on intracellular aequorin light transients and isometric contractions was investigated in isolated canine ventricular trabeculae. The positive inotropic effect of Org 30029 (30 microM-3 mM) was consistently associated with prolongation of the duration of contraction and an increase in the amplitude of the intracellular Ca2+ transients. The maximum inotropic response to Org 30029 was approximately 150% of the maximum response to isoproterenol, whereas the maximum increase in the amplitude of Ca2+ transients produced by Org 30029 was only 20% of the isoproterenol-induced maximum. The duration of isometric contractions was prolonged by Org 30029, with no change in the duration of the light transients. The concentration-response curve for the positive inotropic effect of Org 30029 was shifted by carbamylcholine chloride (carbachol, 3 microM) to the right and downward, but the maximum response to Org 30029 was greater than that to isoproterenol even in the presence of carbachol. Carbachol abolished the increase in light transients and cAMP accumulation induced by Org 30029 (1 mM), whereas it only partially attenuated the positive inotropic effect of Org 30029. In the presence of carbachol (3 microM), Org 30029 increased the force of contraction in a concentration-dependent manner without augmenting the aequorin light transients. These results are compatible with the hypothesis that Org 30029 increases cardiac contractility by increasing myofilament Ca2+ responsiveness.

Actin Cytoskeleton↗
PubMed1993

Nerve growth factor induces transcription of NGFIA through complex regulatory elements that are also sensitive to serum and phorbol 12-myristate 13-acetate.

The expression of NGFIA (also known as egr1, zif268, TIS8, krox24, and d2) is rapidly and transiently increased by nerve growth factor (NGF) in PC12 cells. The 5'-region of this gene includes four serum response elements (SREs), a cAMP-like response element, an AP1-like response element, and an SP1-binding site. From deletion analysis of chloramphenicol acetyltransferase reporter constructs, we have established that the first 106 basepairs 5' of the transcriptional start site are sufficient for induction of NGFIA by NGF in PC12 cells; deletion beyond this point results in dramatically reduced induction of the gene. Using defined mutations in the NGFIA promoter and NGFIA-thymidine kinase hybrid promoters, we have defined three elements (SRE1, SRE2, and AP1-like) in the first 106 basepairs of upstream DNA, each of which contributes to induction of NGFIA by NGF. Cooperation by two of these elements (i.e. the two SREs or one SRE and the AP1-like element) is sufficient to confer transcriptional induction by NGF, but the combination of all three elements increased induction by NGF more effectively than a pair of elements. This suggests that the response of NGFIA to NGF is mediated by a cis-acting sequence that is composed of at least three distinct elements. An oligonucleotide composed of SRE1 and SRE2 that can confer the ability for NGF induction to heterologous promoter constructs complexes with proteins in PC12 cell nuclear extracts, but the protein-DNA complexes do not appear to be altered by NGF treatment, as measured by DNA mobility shift assays. We have also established that the regulatory region of NGFIA that mediates NGF induction also mediates the induction by serum and phorbol 12-myristate 13-acetate, suggesting that multiple signal transduction pathways must converge on these sequences to regulate the expression of this gene.

Animals↗