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Biomedical subjects

A Iguchi

Publications and source records attributed to A Iguchi.

At least 181 records · Page 10Linked to original sources
PubMed1994

Adrenocorticotropin and growth hormone secretions after intracerebroventricular administration of neostigmine in rats: their relationships to hypothalamic monoaminergic neuronal activities.

Serum adrenocorticotropic hormone (ACTH) and growth hormone (GH) concentrations were assessed simultaneously with hypothalamic neuronal activities of norepinephrine (NE), dopamine (DA), and serotonin (5-HT) 60 min after the third cerebroventricular administration of neostigmine (a cholinesterase inhibitor) in awake rats. Serum ACTH and GH concentrations were significantly increased and decreased, respectively. Neostigmine caused significant increases in hypothalamic NE and DA activities and a significant decrease in hypothalamic 5-HT activity. The reciprocal changes of serum ACTH and GH concentrations were similar to those of hypothalamic NE and 5-HT activities. Multiple regression analyses with stepwise procedure revealed that hypothalamic NE and 5-HT activities were respectively significant determinants of serum ACTH and GH concentrations. Apart from the direct influence of neostigmine on ACTH and GH secretions, it is suggested that the changes in hypothalamic monoaminergic activities play an important role in modulating ACTH and GH secretions following the administration of neostigmine.

Adrenocorticotropic Hormone↗
PubMed1994

Biphasic effect of estrogen on neuronal constitutive nitric oxide synthase via Ca(2+)-calmodulin dependent mechanism.

Estrogen is known to retard the development of atherosclerosis and to work in the brain, but the mechanism of hormonal action is completely unknown. We investigated the effect of estrogen on the activity of neuronal constitutive nitric oxide synthase (NNOS). A low concentration of estrogen (10(-10)(-7) M) enhanced the activity of homogenates of the cytosol fraction of rabbit cerebellums and also that of partially purified NNOS, and high dose (10(-6)(-5) M) attenuated them. The study using estrogen receptor antagonists, tamoxifen, clomiphene, and ICI182780 suggested that estrogen receptor did not relate significantly to those effects of 17 beta-estradiol. 17 alpha-estradiol or progesterone did not change significantly it in low doses, although moderately inhibited it in high doses. Estrogen enhanced the fluorescence of dansyl-calmodulin in low doses and attenuated it in high doses, suggesting that estrogen affects Ca(2+)-calmodulin directly. This study demonstrated that estrogen has a biphasic effect on the activity of NNOS through a Ca(2+)-calmodulin.

Amino Acid Oxidoreductases↗
PubMed1994

Effects of adrenoceptor antagonists on the hyperthermia and hyperglycemia induced by prostaglandin F2 alpha in rats.

We investigated the effects of intraperitoneal administration of adrenoceptor antagonists to the hyperthermia and hyperglycemia induced by prostaglandin F2 alpha (50 micrograms) injected into the third cerebral ventricle in anesthetized rats. Phentolamine inhibited the hyperthermia and hyperglycemia induced by prostaglandin F2 alpha. Prazosin inhibited the hyperthermia induced by prostaglandin F2 alpha, while enhancing the hyperglycemia. Yohimbine inhibited the prostaglandin F2 alpha-induced hyperglycemia without an effect on the hyperthermia. Propranolol had no effect on either prostaglandin F2 alpha-induced hyperglycemia or hyperthermia. These observations suggest that the hyperglycemia induced by prostaglandin F2 alpha is regulated by alpha 2-adrenoceptor systems while the hyperthermia is regulated by alpha 1-adrenoceptor systems in rats.

Adrenergic alpha-Antagonists↗
PubMed1994

Prophylactic intravesical chemotherapy with adriamycin plus verapamil for primary superficial bladder cancer: preliminary results. The Kyushu University Urological Oncology Group.

A prospective randomized trial was conducted to compare the prophylactic effect of intravesical installation of Adriamycin (ADM) plus verapamil (VR) with that of ADM alone for recurrence of superficial bladder cancer. A total of 226 patients were enrolled and randomized into 2 groups. Group A received intravesical instillation of ADM (30 mg/30 ml physiological saline) on 19 occasions during a 1-year period after transurethral resection, whereas group B received intravesical instillation of ADM (30 mg/24 ml physiological saline) plus VR (15 mg/6 ml saline) according to the same schedule used for group A. Evaluation was possible in 157 of the 226 registered patients (group A, 76; group B, 81). There was no significant difference in the patients' characteristics between the two groups, and there was no significant difference in the overall nonrecurrence rate determined over a 24-month follow-up period. However, group B showed a significantly higher nonrecurrence rate than did group A for tumors measuring less than 1 cm in diameter (P < 0.05) and for histological grade 2 tumors (P < 0.01) in spite of there being no significant difference in the other characteristics of each subgroup of patients. The incidence and severity of side effects were similar in both groups, and VR caused no significant systemic toxicity. Although further follow-up is necessary, these results suggest that intravesical instillation of ADM plus VR is clinically safe and may be more effective than instillation of ADM alone in preventing the postoperative recurrence of superficial bladder cancer (less than 1 cm in diameter, histological grade 2).

Administration, Intravesical↗
PubMed1994

Chelation of copper reduces inhibition by oxidized lipoproteins of endothelium-dependent relaxation in porcine coronary arteries.

We examined the effect of dialyzing oxidized low-density lipoprotein (oLDL) against Krebs-Ringer solution, in the absence (yielding d-oLDL) or presence (yielding EDTA-oLDL) of ethylenediamine tetraacetic acid (EDTA), to investigate the mechanism that underlies the inhibition of endothelium-dependent relaxation (EDR) by o-LDL. Oxidation of LDL by exposure to Cu2+ resulted in the formation of a thiobarbituric acid-reacting substance (TBARS) and lipid hydroperoxide (LPO). At a concentration of 5 mg/dl, d-oLDL markedly attenuated EDR in the porcine coronary artery. Analysis of d-oLDL by gel filtration revealed that TBARS was ditributed in both the lipoprotein and the aqueous phases, whereas LPO was present only in the lipoprotein particles. Lysophosphatidylcholine (LPC), which has been suggested to be responsible for the impairment of EDR by oLDL, was present not only in the lipoprotein but also in the aqueous phase. However, EDR inhibitory activity was observed only in the oLDL particles, not in the aqueous phase. Almost all Cu2+ associated with the oLDL particles was removed by dialysis of oLDL against Krebs-Ringer solution containing EDTA. EDTA-oLDL or native LDL, at concentrations as high as 75 mg/dl, exerted only a moderate inhibitory action on EDR, Both TBARS and LPO in EDTA-oLDL were distributed only in the lipoprotein particles, not in the aqueous phase. These results demonstrate that the impairment of EDR by oLDL is related both to LPO and to transition metal ions such as Cu2+ associated with the lipoprotein particles, not to the amount of the TBARS or negative charge, and that factors other than LPC may affect EDR.

Animals↗
PubMed1994

Comparative toxicity of oxidatively modified low-density lipoprotein and lysophosphatidylcholine in cultured vascular endothelial cells.

Oxidative modification of low-density lipoprotein (LDL) may play an important role in the initiation and progression of atherosclerosis. We previously showed that the cytotoxicity of oxidized LDL (oxLDL) depended on the level of lipid hydroperoxides. Meanwhile, it has been shown that during LDL oxidation, a significant part of the LDL phosphatidylcholine (PC) is degraded to lysophosphatidylcholine (LPC) by an intrinsic phospholipase A2-like activity, and that LPC is toxic to various cells. In the present study, we compared the toxicity of oxLDL with that of LPC in cultured bovine aortic endothelial cells. Cytotoxicity induced by LPC, assessed by the release of lactate dehydrogenase (LDH), reached a plateau within 1 h. LDH release induced by oxLDL occurred much later, at about 3 h, and increased linearly until nearly all the LDH was released at 10 h. The addition of deferoxamine, a Fe3+ chelator, to the reaction medium prevented the toxic effects of oxLDL, but not of LPC. Native LDL and oxLDL inhibited the toxicity of LPC, while native LDL promoted the toxicity of oxLDL. Albumin inhibited the toxicity of LPC but not of oxLDL. Preincubation of endothelial cells with an antioxidant, probucol, protected against oxLDL toxicity, but not against LPC toxicity. These results suggest that lipid hydroperoxides associated with the oxLDL particle, not LPC, constitute the toxic moiety of oxLDL. These substances may generate lipid peroxyl and alkoxyl radicals in the presence of ionic iron, probably from intracellular iron stores in endothelial cells, and produce cytotoxicity.

Animals↗
PubMed1994

Activation of central GABAA receptors suppresses the alteration of plasma catecholamine levels induced by neostigmine or histamine in rats.

We investigated the effects of intraventricular injection of muscimol, the GABAA receptor agonist, on the alteration of plasma epinephrine (E) and norepinephrine (NE) levels induced by neostigmine or histamine in anesthetized rats. Injection of neostigmine (10 nmol) into the third cerebral ventricle increased plasma levels of E more than NE, while histamine (500 nmol) increased plasma levels of NE more than E. Concomitant injection of muscimol (2.5 nmol) with neostigmine or histamine significantly suppressed the alteration of E and NE levels induced by neostigmine or histamine. These findings suggest that activation of central cholinergic neuron stimulates the adrenal medullary response more than the sympathetic nervous system, while activation of central histaminergic neuron stimulates the sympathetic nervous system more than the adrenal medullary response in anesthetized rats. Activation of GABAA receptors in the CNS suppresses these effects.

Animals↗
PubMed1994

Effects of central GABA receptors activation on catecholamine secretion in rats.

We investigated the effects of muscimol, the GABAA receptor agonist, and baclofen, the GABAB receptor agonist, injected into the third cerebral ventricle on plasma epinephrine (E) and norepinephrine (NE) levels in anesthetized rats. Baclofen (0.4-5 nmol) increased plasma NE levels in a dose dependent manner but did not affect plasma E levels. Muscimol (2.5 nmol) affected neither plasma E nor NE levels. Concomitant injection of muscimol (2.5 nmol) with baclofen (5 nmol) attenuated the baclofen (5 nmol)-induced NE secretion. These findings suggest that activation of GABAB receptors in the central nervous system (CNS) stimulates the sympathetic nervous system but not the adrenal medullary response. In contrast, activation of GABAA receptors in the CNS affects neither the sympathetic nervous system nor the adrenal medullary response, but inhibits the sympathetic neural activity induced by activation of GABAB receptors in anesthetized rats.

Animals↗
PubMed1994

CNS regulation of blood lactate concentration in anesthetized rats.

This study evaluated the effect of stimulating the central nervous system (CNS) with neostigmine, an inhibitor of acetylcholinesterase, on the blood lactate concentration in fed rats and in rats fasted for 48 hours. After the rat was anesthetized with pentobarbital, neostigmine was stereotaxically injected into the third cerebral ventricle. In fed rats, the central injection of neostigmine significantly increased the blood lactate level, while concomitantly increasing plasma glucagon, epinephrine and norepinephrine concentrations. Constant infusion of somatostatin throughout the experiments, to inhibit glucagon secretion from the pancreas, did not affect alterations in blood lactate by central injection of neostigmine. In adreno-medullated rats, CNS-stimulation by neostigmine still increased plasma norepinephrine significantly, however, the alteration in blood lactate was only one-third of that in intact rats. Intraperitoneal propranolol, but not phentolamine, prevented the rise in lactate. Neostigmine increased lactate in fasted rats as well as in fed rats. We conclude that in anesthetized rats, stimulation of the CNS by neostigmine increases blood lactate mainly through circulating epinephrine and partially through circulating norepinephrine or direct sympathetic nervous stimulation; glucagon does not appear to be involved in the increase in blood lactate.

Anesthesia, General↗
PubMed1994

Protein C response to induction of warfarin treatment after coronary bypass operation.

To investigate the effect of warfarin on the anticoagulant pathway, protein C antigen and activity levels were compared in two groups of patients treated with different regimens of sodium warfarin during the initial stage of anticoagulant therapy following heart surgery. Group I received 6 mg of warfarin per day for 3 days. Group II received 8 mg twice a day for 2 or 3 days. Preoperative levels of Protein C antigen and activity averaged 108 +/- 16% and 102 +/- 18% (mean +/- SD), respectively, and by one hour after the operation, levels had fallen significantly (protein C antigen to 76 +/- 14%; protein C activity to 70 +/- 16%). After the initiation of warfarin treatment, the levels of protein C activity in group II were significantly lower than those of group I. In contrast, the reductions in factor X were much slower and were similar in the two groups. As the factor X level reflects the antithrombotic effect of warfarin, this result suggests that the rapid reduction of protein C activity may have given rise to a transient hypercoagulable state in the patients of group II.

Aged↗
PubMed1994

Bicuculline methiodide influences the central nervous system to produce hyperglycemia in rats.

The influence of bicuculline methiodide (BMI), a gamma-aminobutyric acid (GABA) receptor antagonist, on central nervous system regulation of blood glucose homeostasis was studied in fed rats. Injection of BMI (1-10 nmol) into the third ventricle was found to produce hepatic venous hyperglycemia in a dose-dependent manner. This change was associated with increased secretion of epinephrine and glucagon. The role of epinephrine in hyperglycemia was then studied in bilaterally adrenalectomized (ADX) rats injected with BMI. Plasma glucose concentration was found to increase in ADX rats although the level was approximately half that for intact rats and significantly higher than for controls. The increase in epinephrine and glucagon secretion seen in intact rats, but not in ADX rats, suggests BMI induced epinephrine release is responsible for the glucagon secretion. Three possible mechanisms are suggested to account for the rise in plasma glucose in the hepatic vein after injection of BMI: 1) that epinephrine is secreted by the adrenal medulla, 2) that epinephrine secretion stimulates glucagon secretion or 3) that there may be some direct innervation of the liver in rats.

Adrenal Medulla↗
PubMed1994

Japanese family with a deficiency of lecithin:cholesterol acyltransferase (LCAT).

We present findings in the ninth known Japanese family with lecithin:cholesterol acyltransferase (LCAT) deficiency. A 54-year-old man (proband) and his 58-year-old brother presented with corneal opacity. Both subjects showed a marked decrease in serum high density lipoprotein (HDL)-cholesterol and in the cholesteryl ester ratio. Although apo A-I and A-II were low, apo E tended to be high. Serum LCAT activity and mass were not detectable. Urinary examination showed microhematuria or proteinuria. Renal function was normal and no anemia was demonstrated, but blood smears showed poikilocytosis with target cells. The serum LCAT activity of the proband's three sons, obligate heterozygotes of LCAT deficiency, was about one-half the normal level, and HDL-cholesterol and apo A-I levels were low normal.

Adult↗
PubMed1994

[The prognostic value of mean nuclear area and mean nuclear volume in bladder cancer].

To evaluate the prognostic value of mean nuclear area (MNA) and mean nuclear volume (MNV) in bladder cancer, a retrospective study was performed comprising 67 bladder cancer patients who could be followed up for more than 3 years. Cosmozone 1SA, a Nikon image analyzing system was used for the morphometric study. The specimen of initially biopsied tumor tissue was set in an Olympus microscope at 400-fold magnification, and the image was superimposed on the monitor picture through a video camera attached to the microscope. MNA and MNV were measured by tracing the contour of the nucleus which were selected by the point-sampled intercept methods. The time required for measurement of the area and volume was about 15 minutes per case. MNA in cases with histological grade 1, 2 and 3 were 35 +/- 3 microns2 (mean +/- SD), 42 +/- 10 microns2 and 62 +/- 12 microns2 respectively. MNV with grade 1, 2 and 3 were 282 +/- 46 microns3, 371 +/- 148 microns3 and 644 +/- 182 microns3 respectively. The morphometric results were significantly related to histological grade. In cases with a value of MNA of 40 microns2 or more and/or a value of MNV of 370 microns3 or more, the proportion of cases who underwent cystectomy or died of cancer was significantly high and demonstrated poor survival. In contrast, those who showed MNA and MNV less than the above value had better prognosis. These results suggest that the measurements of MNV seems to be useful for objectively evaluating the malignant potential of bladder cancer.

Adult↗
PubMed1994

[Occult CSF flow disturbance of patients with Alzheimer type dementia and vascular dementia--results from iotrolan CT-cisternography].

We report results of Iotrolan CT-cisternography on 41 demented patients (13 males and 28 females) to find "occult normal pressure hydrocephalus". These patients were suspected to have CSF flow disturbance from clinical symptoms and simple brain CT scan findings. Their average age, duration of dementia, and score of Hasegawa's dementia scale (HDS) were 76.2 years, 5.9 years, 9.5/32.5, respectively. Before performing CT-cisternography, clinical diagnosis for their dementia were vascular dementia in 18 patients, Alzheimer type dementia in 12, suspect of NPH in 5, and other diagnoses in 6. From the results of cisternography, we found 13 patients with CSF flow disturbance (contrast material remained in the ventricle more than 48 hours after injection), and 17 patients with normal CSF flow. The former showed lower scores of HDS, higher urinary incontinence scores and smaller areas of the interhemispheric fissure on CT scan than the latter. But the former showed no significant difference from the latter in the average age, duration of dementia and width of the ventricles.

Aged↗
PubMed1994

[Plasma fibrinogen as a cardiovascular risk factor].

Recent prospective epidemiological studies have shown that plasma fibrinogen is a powerful, independent risk factor of arteriosclerotic diseases such as ischemic heart disease, stroke and peripheral vascular disease. Cross-sectional studies have shown correlation of fibrinogen with various factors, including age, gender, race and smoking. Plasma fibrinogen strongly affects blood coagulation, blood rheology and platelet aggregation. In addition, fibrinogen, fibrin and their degradation products have direct effects on the vascular wall. The migration of vascular smooth muscle cells from the media into the intima and their proliferation play an important role in the pathogenesis of atherosclerosis and in the organization of thrombi. Smooth muscle cells adhere to substrate-bound fibrinogen/fibrin. The cells migrate to a gradient of soluble fibrinogen (chemotaxis). The cells also migrate in a dose-dependent manner to a gradient of substrate-bound fibrinogen and fibrin (haptotaxis). The relation among hyperfibrinogenemia, atherosclerosis and thrombosis is highly complicated. There is no prospective study on fibrinogen and cardiovascular disorders among Japanese. Studying plasma fibrinogen to predict cardiovascular disorders may provide some new insight into their pathophysiological mechanisms.

Aged↗
PubMed1993

Presence and possible involvement of Ca/calmodulin-dependent protein kinases in insulin release from the rat pancreatic beta cell.

Roles of Ca/calmodulin-dependent protein kinase II (Ca/CaM kinase II) and myosin light chain kinase (MLCK) in insulin release from rat pancreatic islets were investigated. Western blotting using polyclonal antibody to Ca/CaM kinase II suggested the presence of this kinase in the pancreatic islets. Extracts of pancreatic islets phosphorylated exogenous myosin light chain, which was inhibited by ML-9, an inhibitor of MLCK. KN-62 and KN-93, inhibitors of Ca/CaM kinase II, and ML-9 at microM concentrations inhibited insulin release stimulated by glucose or high K+. KN-62 and KN-93, but not ML-9, inhibited insulin release increased by glucose and forskolin, an activator of adenylate cyclase. These inhibitors had no effect on insulin release evoked by 12-O-tetradecanoyl phorbol-13-acetate, an activator of Ca(2+)-sensitive, diacylglycerol-dependent protein kinase. These results suggest that Ca/CaM kinase II and MLCK may participate in the control of insulin release.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1993

Replacement of the transverse aortic arch for type A acute aortic dissection.

Surgical treatment of acute aortic dissection involving the segment of transverse aortic arch is difficult and often associated with a high mortality and morbidity. The high mortality and morbidity are primarily related to anatomic features and techniques of cerebral protection employed during the period of aortic branch occlusion needed for reconstruction. This study reports our experience of 20 consecutive cases of acute type A aortic dissection treated by repair or replacement of the transverse aortic arch during emergency operation. Ages of the patients ranged from 56 to 76 years. All patients were referred to us within 2 weeks of onset (mean time, 58 hours). Selective cerebral perfusion or deep hypothermia with complete circulatory arrest was employed during the period of aortic branch occlusion. Duration of cerebral perfusion, circulatory arrest, myocardial ischemia, and cardiopulmonary bypass averaged 106 minutes, 32 minutes, 127 minutes, and 248 minutes, respectively. There were three operative deaths. All three dissections were ruptured ones, and the patients died of hemorrhage, deep coma, or multiple organ failure. One patient died of infection 3 months after operation. The remaining patients are alive and well without any detectable neurological deficit 1 month to 4 years postoperatively. This experience emphasizes that repair or replacement of acute type A aortic dissection involving the aortic arch can be performed safely by adequate selection of patients, supportive measures, and operative methods.

Acute Disease↗