International forum: Japan report on informed consent in blood transfusions.
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Adolescent↗
Biomedical subjects
K Kamata
Publications and source records attributed to K Kamata.
Elevated plasma endothelin-1 level in streptozotocin-induced diabetic rats and responsiveness of the mesenteric arterial bed to endothelin-1.
1. Both the plasma endothelin-1 (ET-1) levels and the plasma glucose levels were markedly elevated in streptozotocin (STZ)-induced diabetic rats. 2. The maximum contractile response of the mesenteric arterial bed to ET-1 was significantly reduced, and the vasodilatation induced by the ET(B)-receptor agonist IRL-1620 in the mesenteric arterial bed was significantly reduced in STZ-induced diabetic rats. 3. ET-1 (10(-8) M) caused a transient vasodilatation followed by a marked vasoconstriction in methoxamine-preconstricted mesenteric arterial beds. The ET-1-induced vasodilatation was significantly larger in beds from diabetic rats than in those from age-matched controls. By contrast, the ET-1-induced vasoconstriction was significantly smaller in STZ-induced diabetic rats than in the controls. 4. Both removal of the endothelium with Triton X-100 and preincubation with BQ-788 (10(-6) M) (ET(B)-receptor antagonist) abolished the ET-1-induced vasodilatation. Preincubation with BQ-485 (10(-6) M) or BQ-123 (3 x 10(-6)) (ET(A)-receptor antagonist) significantly augmented the ET-1-induced vasodilatation in control mesenteric arterial beds, but not that in beds from diabetic rats. 5. These results demonstrate that marked increases not only in plasma glucose, but also in plasma ET-1 occur in STZ-induced diabetic rats. We suggest that the decreased contractile response and the increased vasodilator response of the mesenteric arterial bed to ET-1 may both be due to desensitization of ET(A) receptors, though ET(B) receptors may also be desensitized. This desensitization may result from the elevation of the plasma ET-1 levels seen in STZ-induced diabetic rats.
Animals↗
Ca2+ mobilization in the aortic endothelium in streptozotocin-induced diabetic and cholesterol-fed mice.
1. Experiments were performed to compare Ca2+ mobilization in the aortic endothelium in streptozotocin (STZ)-induced diabetic and cholesterol-fed mice with that in age-matched controls. 2. The intracellular free Ca2+ ([Ca2+]i) in the fura PE-3 loaded endothelium of aortic rings was dose-dependently increased by cumulative administration of acetylcholine (ACh). ACh caused a transient rise in [Ca2+]i in Ca2+-free medium. The ACh-induced increase in [Ca2+]i in normal or Ca2+-free medium was significantly weaker in both STZ-induced diabetic and cholesterol-fed mice. 3. The weaker [Ca2+]i response in Ca2+-containing medium in STZ-induced diabetic and cholesterol-fed mice was normalized by chronic administration of cholestyramine. 4. The increased low density lipoprotein (LDL) levels seen in both STZ-induced diabetic and cholesterol-fed mice were normalized by the same chronic administration of cholestyramine (300 mg kg(-1), p.o. daily for 10 weeks). Chronic administration of cholestyramine had no effect on the plasma glucose level. 5. Lysophosphatidylcholine (LPC) decreased the [Ca2+]i responses to ACh in the aortic endothelium from normal mice. 6. These results suggest that ACh increases both Ca2+ influx and Ca2+ release from storage in the aortic endothelium. The weaker [Ca2+]i influx seen in the endothelium of aortae from both STZ-induced diabetic and cholesterol-fed mice was improved by the chronic administration of cholestyramine, and we suggest that this improvement is due, at least in part, to a lowering of the plasma LDL level. It is further suggested that LPC may have an important influence over Ca2+ mobilization in the endothelium.
Animals↗
Effect of probucol on serum lipoprotein and apoprotein profiles in renal transplant patients.
The therapeutic effect of probucol on hypercholesterolemia in cyclosporine A (CyA)-treated renal transplant patients was prospectively studied. Twelve posttransplantation patients aged 34.2+/-2.5 years with serum total cholesterol (t-CHL) of 250 mg/dL or greater, whose serum creatinine was 2.9 mg/dL or less, and who had no diabetes mellitus or hypoproteinemia, were treated with probucol, 250 mg twice daily for 3 months. Seventeen age-matched (36.8+/-1.6 years) normal volunteers served as control. Blood was drawn after at least a 12-hour fast to measure lipids in serum and lipoprotein fractions, apoproteins (apo), lipoprotein fractions, lethicin cholesterol acyl transferase (LCAT), free fatty acids (FFA), and CHL-ester. Serum t-CHL, triglycerides (TG), and phospholipids (PL) in posttransplantation patients before treatment were significantly higher compared with normal control subjects. Very-low-density lipoprotein (VLDL) and low-density lipoprotein (LDL) fractions in these patients were significantly expanded. The pretreatment levels of serum apo AII, B, CII, and CIII were significantly increased compared with those of normal controls. After treatment with probucol, serum t-CHL, LDL-CHL, high-density lipoprotein (HDL)-CHL, PL, LDL-PL, and apo AI were significantly decreased, and CHL-ester significantly increased compared with the pretreatment levels. These data suggest that although probucol causes a decrease in HDL-CHL, it may act anti-atherogenically by modulating HDL metabolism and stimulating reverse transfer of CHL from peripheral tissue.
Adult↗
Prevalence of hepatitis G virus RNA and anti-E2 in a Japanese haemodialysis population.
BACKGROUND: Patients on maintenance haemodialysis (HD) are at greater risk of parenterally transmitted infection with not only A-E hepatitis virus but also with hepatitis G virus (HGV) that has been recovered from patients with non A-E hepatitis. The prevalence of HGV infection in HD patients, which is based on the detection of HGV RNA using reverse transcription-polymerase chain reaction techniques, differs widely between countries. Recently, a new assay has been developed that detects an antibody to the envelope protein (E2) of HGV (anti-E2) that appears to be associated with the loss of HGV RNA from the serum and which may be a useful marker for previous HGV infection. METHODS: To determine the actual prevalence of HGV infection in maintenance HD patients, we examined both HGV RNA and anti-E2 antibody in sera from 200 patients undergoing maintenance HD. RESULTS: Thirty patients (15%) tested positive for HGV RNA, and 14 (7%) tested positive for E2 antibody. Of these, two individuals tested positive for both markers. Overall, 21% of these HD patients had been exposed to HGV. A logistic regression analysis failed to show any clinical feature associated with the detection of HGV RNA. The duration of HD and the presence of HCV RNA were associated with anti-E2. Male gender and HCV RNA were risk factors for the elevation of serum ALT activities. HGV RNA sequences of the patients were not identical to each other. CONCLUSIONS: Our data indicate that HGV infection is prevalent in patients undergoing HD but that liver abnormalities are rare. The nosocomial transmission of HGV in the HD unit was not confirmed.
Aged↗
Tolosa-Hunt syndrome in uraemic patients undergoing maintenance haemodialysis.
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Abducens Nerve↗
Delayed aseptic swelling after fixation of talar neck fracture with a biodegradable poly-L-lactide rod: case reports.
A 63-year-old woman complained of acute swelling and pain in her ankle at 15 months, after fixation of a talar neck fracture with poly-L-lactide rods. Roentgenographic and laboratory data revealed no abnormalities, but T1-weighted magnetic resonance imaging showed a diffuse area of low intensity in the talus. After nonweightbearing for 1 month, local findings had disappeared and the area of low intensity shown by magnetic resonance imaging had decreased without surgical treatment. Although there have been some reports of aseptic swelling or synovitis after fixation of a fracture with polyglycolide rods or screws, there has been no report of such cases with poly-L-lactide rods or screws.
Acute Disease↗
[A surgical case of cervical canal stenosis caused by atlas hypoplasia in an elderly patient].
We report an 81-year-old man with hypoplastic atlas resulting in a severe stiff feeling in the bilateral shoulders, spastic tetraparesis, and hypesthesia below the C2 segment level of the spinal cord. These symptoms are compatible with compression of the high cervical cord. Neuroimaging studies revealed a narrowing of the spinal cord by compression of the hypoplastic atlas. Laminoplasty of the atlas was performed under general anesthesia, and the patient's symptoms were resolved. Operated cases of older patient's with atlas hypoplasia have been rarely reported. Laminoplasty of the atlas is a safe and useful procedure for high cervical compression due to hypoplastic atlas.
Aged↗
Toxocara cati-induced ocular Toxocariasis.
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Adult↗
Vitrectomy for caterpillar seta-induced endophthalmitis.
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Animals↗
A comparative study on the rat aorta and mesenteric arterial bed of the possible role of nitric oxide in the desensitization of the vasoconstrictor response to an alpha 1-adrenoceptor agonist.
1. In thoracic aortic strips with intact endothelium, the first and second (1 h later) dose-response curves obtained with methoxamine were almost the same. 2. Methoxamine caused a dose-dependent increase in perfusion pressure in the rat isolated mesenteric arterial bed, but the second (1 h later) dose-response curve for methoxamine showed a significant attenuation of the response in comparison with the first. 3. The attenuation shown by the second dose-response curve for methoxamine was significantly reduced, but not abolished, in mesenteric arterial beds without endothelium. Incubating endothelium-intact mesenteric arterial beds with NG-nitro-L-arginine (L-NOARG) caused a significant, but not complete, reversal of the attenuation shown in the second dose-response curve. 4. Incubating the mesenteric arterial bed with capsaicin, tetrodotoxin, indomethacin or with isotonic high k+ (60 mM) plus nicardipine did not affect the above attenuation seen in the second dose-response curve. 5. The guanosine 3':5'-cyclic monophosphate (cyclic GMP) level in the effluent from the perfused mesenteric arterial bed was significantly increased after the second exposure to methoxamine. This effect was significantly smaller after removal of the endothelium or pretreatment with L-NOARG. 6. These results suggest that a desensitization to methoxamine develops rapidly in the mesenteric arterial bed, but not in the aorta, and that release of nitric oxide from the endothelium plays a major role in this desensitization.
Adrenergic alpha-1 Receptor Agonists↗
Effect of VA-045, a novel apovincaminic acid derivative, on closed head injury-induced neurological dysfunction in aged rats.
Effects of VA-045, a novel apovincaminic acid derivative, on behavioral outcome following closed head injury (CHI) were examined in aged (21-28 months) rats. CHI was induced by dropping a 400 g weight through a tube from 150 cm above a steel helmet placed on the vertex. Beam balancing latency, neurological deficits and body weight were recorded before CHI and for up to 14 days after CHI. When compared with the sham group, all measurements of parameters of behavioral outcome in the CHI group were significantly worsened after CHI. Intraperitoneal administration of VA-045 (1 and 3 mg kg-1) or thyrotropin-releasing hormone (TRH, 10 mg kg-1) and vehicle was started 24 h after CHI, and continued once daily for 13 days. VA-045 but not TRH significantly overcame the CHI-induced neurological deficits, shortened the latency of beam balancing and decreased body weight loss. VA-045 may prove useful for treating aged patients with disturbances of consciousness or motor deficits after CHI.
Age Factors↗
Persistence of cyclopiazonic acid-induced endothelium-dependent vasodilatation in spontaneously hypertensive and streptozotocin-induced diabetic rats.
We recently reported that cyclopiazonic acid (CPA) releases a novel endothelium-derived relaxing factor that is not prostacyclin, nitric oxide or endothelium-derived hyperpolarizing factor in rat mesenteric arterial bed. The acetylcholine-induced vasodilatation of the isolated mesenteric bed in spontaneously hypertensive rats (SHR) was not different from that in Wistar Kyoto rats (WKY), but it was significantly smaller in streptozotocin (STZ)-induced diabetic rats than in age-matched controls. The CPA-induced vasodilatation was not affected in SHR or in STZ-induced diabetic rats. These results suggest that the CPA-induced endothelium-dependent vasodilatation is resistant to the effects of diabetes.
Acetylcholine↗
Further studies concerning possible transmitters from NANC nerves in the circular muscle of the rat stomach fundus.
We examined the characteristics of the non-adrenergic, non-cholinergic (NANC) inhibitory response of the circular muscle of the rat stomach fundus to transmural nerve stimulation or high K+. Treatments with isotonic high K+ (20 mM), nitric oxide (NO) and sodium nitroprusside (SNP) all elevated cyclic GMP levels in the rat stomach fundus in the presence of atropine and guanethidine. Isotonic high K+-induced formation of cyclic GMP was completely inhibited by tetrodotoxin (TTX) or NG-nitro-L-arginine (L NNA). The K+ also increased cyclic AMP levels and this response was completely inhibited by TTX. Dose-dependent relaxation of the fundus in response to SNP was shifted to the right by a prior incubation with high concentration of SNP (10(-4) M) for 2 hrs. Incubating the fundus with SNP for 2 hrs significantly inhibited NO induced cyclic GMP formation. Relaxation responses to transmural stimulation (1 Hz or 30 Hz), isotonic high K+ and NO were significantly reduced by a prior incubation with SNP. Isotonic high K+ (20 mM)-induced relaxation of circular muscle strips was not completely inhibited by combined treatment with 10(-5)M L-NNA, 5 x 10(-5)M oxyhemoglobin and anti VIP (1:200). These results suggest that NO as well as VIP is possible transmitter from NANC nerves in the circular muscle of the rat stomach fundus and there should be one or more inhibitory mediators other than VIP and NO.
Animals↗
Endothelial dysfunction in the perfused kidney from the streptozotocin-induced diabetic rat.
The vasodilator effects of acetylcholine were examined in methoxamine-preconstricted perfused kidneys taken from rats with streptozotocin (STZ)-induced diabetes. Acetylcholine-dependent vasodilatation was significantly weaker in STZ-induced diabetic rats than in age-matched controls, and it was completely abolished by treatment with 60 mM K+ plus NG-nitro-L-arginine (L-NNA) plus methylene blue in the control rats and was significantly but not completely inhibited by these treatment in the diabetic rats. Although acetylcholine-induced vasodilation was not affected by indomethacin in control rats, it was attenuated by indomethacin in the diabetic rats. Arachidonic acid-induced vasoconstriction was slightly but significantly increased in the diabetic rats. Acetylcholine increased significantly the level of 6-keto-prostaglandin F1 alpha in the effluent from perfused kidneys from diabetic rats. These results suggest that the endothelium-dependent vasodilatation induced by acetylcholine in the renal vascular bed of age-matched control rats is due to the release of nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF), whereas the vasodilatation induced by acetylcholine in the STZ-diabetic kidney also involves prostaglandin I2 as well as NO and EDHF.
6-Ketoprostaglandin F1 alpha↗
Characteristics of vasodilatation induced by cyclopiazonic acid in the rat perfused kidney.
We examined the possible existence of a novel endothelium-derived relaxing factor in the endothelium of the perfused rat kidney. Acetylcholine-induced vasodilatation was abolished by treatment with NG-nitro-L-arginine (L-NNA) and methylene blue in isotonic high K+ (60 mM) medium, whereas cyclopiazonic acid (CPA)-induced vasodilatation of the perfused kidney was slightly increased by this treatment. When the kidney was perfused with 0.47% CHAPS solution for 1 min, acetylcholine- or cyclopiazonic acid-induced vasodilatation was almost abolished. Acetylcholine- or cyclopiazonic acid-induced vasodilatation was not affected by indomethacin. These results suggest that CPA may release a novel endothelium-derived relaxing factor, which is not prostanoids, nitric oxide nor endothelium-derived hyperpolarizing factor in the endothelium of the renal vascular bed.
Acetylcholine↗
Characteristics of contractile responses of aorta to norepinephrine in db/db mice.
In the isolated mouse aorta with endothelium, although norepinephrine (NE) showed only a slight increase in tension in control mice, the NE-induced dose-dependent contraction was markedly increased in spontaneously diabetic mice. NE-induced contractile responses were significantly enhanced by pretreatment with 10(-4) NG-monomethyl-L-arginine (L-NMMA), 5 micrograms/ml lysophosphatidylcholine (LPC), and the combined treatment with L-NMMA and LPC. When the aortic ring was precontracted with 3 x 10(-6) M PGF2 alpha, NE (10(-8) to 3 x 10(-5) M) caused dose-dependent relaxation. The NE-induced relaxation was significantly inhibited by 10(-4) L-NMMA or 5 micrograms/ml LPC in the normal mice. These results suggest that insensitivity of the mouse aorta to NE is due to the release of nitric oxide from the endothelium, and that an increased contraction induced by NE in spontaneously diabetic mice is due to an impairment of the endothelium.
Acetylcholine↗
Changes in electrophysiological and mechanical responses of the rat papillary muscle to alpha- and beta-agonist in streptozotocin-induced diabetes.
To clarify the changes occurring in diabetic animals in the responsiveness of the myocardium to alpha 1- and beta-adrenoceptor agonists, we examined both alpha- and beta-adrenoceptor-mediated electrophysiological and mechanical responses in the depolarized right ventricular papillary muscle of streptozotocin (STZ) induced diabetic rats and age-matched controls. Both methoxamine (10(-7)-10(-4) M) and isoproterenol (10(-9)-10(-6) M) enhanced the slow response action potential in a concentration-department manner. The amplitude and the APD50 (time required for 50% repolarization) of the methoxamine-induced slow response action potential were both markedly increased in STZ-induced diabetic rats in comparison with control rats, whereas those of the isoproterenol-induced slow response were significantly decreased. The methoxamine-induced contraction in depolarized muscle was slightly but not significantly increased in STZ-induced diabetic rats, whereas the isoproterenol-induced contractile response was significantly attenuated. The maximum number of binding sites (Bmax) for [3H]dihydroalprenolol and for [3H]prazosin were both significantly decreased in diabetic rats, compared with age-matched control rats, without any change in the affinity constants. The slow response action potential induced by methoxamine but not isoproterenol was attenuated by IAP (islet-activating factor) treatment (50 micrograms/kg, i.v. for 3 days). These results suggest that an alpha-adrenoceptor-mediated electrophysiological response is unmasked when the beta-adrenoceptor-mediated response is desensitized in the papillary muscle of STZ-induced diabetic rats.
Action Potentials↗