Biomedical subjects

T Funakoshi

Publications and source records attributed to T Funakoshi.

At least 91 records · Page 5Linked to original sources

PubMed1994

Effect of terbium on protease activity in pancreas of mice.

The effect of terbium (Tb) on the protease activity in pancreas of mice was studied. Administration of Tb at doses of 20 and 200 mumol/kg increased the activities of trypsin and carboxypeptidase A, but did not affect the activities of chymotrypsin and carboxypeptidase B. High Tb concentrations were found in the liver and spleen compared to the kidney and pancreas. Increases in Ca concentrations in the pancreas, kidney, and spleen after Tb administration were observed. The pancreatic slice experiments showed the increase in trypsin activity after Tb treatment and increases in trypsin and carboxypeptidase A after Ca treatment. Tb inhibited strongly the activities of authentic chymotrypsin and carboxypeptidase A. These results suggest that the increase in trypsin activity in the pancreas after Tb administration results from the activation of trypsinogen by Tb and Ca ions and that the increase in carboxypeptidase A activity is due to the activation of procarboxypeptidase A by trypsin and Ca ion, which increased after Tb administration.

Amino Acid Sequence↗

PubMed1994

[Qualitative evaluation of 123I-IMP SPECT using a rotating gamma camera in atherosclerotic large-artery disease].

PURPOSE Quantitative measurement of regional cerebral blood flow (rCBF) needs special equipment or invasive blood sampling. Therefore, with a popularly used rotating gamma camera, we tried to establish a convenient modality of qualitative evaluation of hemodynamics in patients with atherosclerotic large-artery disease, according to the distribution pattern of isotope-uptake on SPECT image. PATIENTS AND METHODS Forty-one patients with atherosclerotic large-artery disease [9 internal carotid artery (ICA) stenosis, 17 ICA occlusion, 8 middle cerebral artery (MCA) stenosis, and 7 MCA occlusion] and 32 control patients documented as having small cerebral infarction without atherosclerotic large-artery disease were investigated. Using the rotating gamma camera, they underwent 123I-IMP SPECT at baseline and after acetazolamide loading. According to the distribution pattern of low isotope-uptake, early images were classified into four types: Type I: no low uptake, Type II: low uptake in a single watershed, Type III: low uptake in two watersheds with or without a partial MCA territory, Type IV: low uptake in a whole MCA territory. RESULT In patients with large-artery disease, baseline images presented Type I in 12 cases, Type II in 16, Type III in 9, Type IV in 4, and loading images Type I in 3, Type II in 2, Type III in 8, Type IV in 28. Of 37 patients except for 4 belonging to Type IV at baseline, 32 (86.5%) had a more extensive low isotope-uptake area after acetazolamide loading than at baseline. In control patients, baseline images presented Type I in 25, Type II in 7, and the Type III & IV in 0, and the Type after loading was the same as the Type at baseline. CONCLUSION We established the qualitative evaluation of 123I-IMP SPECT image by detecting the "extent" of the ischemic region, taking notice of watershed. The pathognomonic findings on SPECT image of atherosclerotic large-artery disease showed that low isotope-uptake area at baseline extended into two watersheds or MCA territory by acetazolamide loading. The modality of qualitative evaluation based on these pathognomic findings of SPECT image may be useful for easily assessing patients with atherosclerotic large-artery disease using a rotating gamma camera.

Adult↗

PubMed1993

Further study of effects of chelating agents on excretion of inorganic mercury in rats.

The effects of three chelating agents, N-benzyl-D-glucamine dithiocarbamate (BGD), 2,3-dimercaptopropanol (BAL) and D-penicillamine (D-PEN), on the excretion of mercury in rats exposed to mercuric chloride (HgCl2), the chemical forms of mercury compounds excreted in the bile and urine and the intestinal reabsorption of mercury compounds in the bile were studied. Rats were injected intraperitoneally with 203HgCl2 (300 micrograms Hg and 74 kBq of 203Hg/kg) and 24 h later, they were injected intraperitoneally with a chelating agent (a quarter of an LD50). The injection of the chelating agents significantly enhanced the biliary and urinary excretions of mercury. The enhancing effect of BGD on the excretions of mercury was almost the same as that of BAL and much larger than that of D-PEN. The major chemical form of mercury in the bile and urine of rats injected with BGD after HgCl2 treatment was Hg-BGD compounds. The chemical form of mercury in the bile and urine of rats injected with BAL after HgCl2 treatment was mainly Hg-GSH compound. The mercury after HgCl2 and D-PEN treatment was excreted mainly via the urine in the form of Hg-D-PEN compound. The intestinal reabsorption of mercury from the bile of rats injected with BGD or D-PEN was only 0.18% or 0.38% of the dose, respectively. The intestinal reabsorption of mercury from the bile of rats injected with BAL was 27.38% of the dose. It was suggested that the Hg-GSH compound excreted in the bile after HgCl2 and BAL treatment is partly degraded to Hg-cysteine (Cys) by the intestinal membranous enzymes and that the ligand of Hg-Cys is replaced by BAL in the bile, resulting in the effective reabsorption of Hg-BAL compound from the intestine.

Animals↗

PubMed1993

Primary osteosarcoma of the skull--a case report and review of the literature.

Primary osteosarcoma of the skull (POS) in a young man with intracranial involvement is reported. After an initial transient remission by surgical intervention and chemotherapy, he began to deteriorate due to tumor recurrence and intracranial hemorrhage, and died 15 months following the time of diagnosis. The rarity and poor prognosis of POS are emphasized together with the review of the clinical and therapeutic aspects in the previously reported 98 cases in the literature.

Adult↗

PubMed1993

Prediction of cerebral infarction due to vasospasm following aneurysmal subarachnoid haemorrhage using acetazolamide-activated 123I-IMP SPECT.

Prediction of cerebral infarction due to vasospasm (VS) following aneurysmal subarachnoid haemorrhage (SAH) was investigated using acetazolamide-activated (A-A) N-isopropyl-p-[123I]iodoamphetamine (123I-IMP) single photon emission computed tomography (SPECT) in 79 SAH patients. A-A SPECT was undertaken twice or more for one each patient by Day 18. Fifty-six (71%) of the 79 patients presented with reduction of cerebral vasodilatory capacity (CVC) on SPECT due to VS by Day 18. Of the 56 patients, 29 showed CVC by Day 8 (Group A), while the other 27 first showed CVC reduction between Day 9 and 18 (Group B). Cerebral infarction on CT was revealed by Day 18 in 15 patients (52%) of Group A and 3 (11%) of Group B. Of the 56 patients, 20 showed reduced CVC in watershed[s] (Type 1), 12 in a sole territory of the intracranial major arterial trunk (Type 2), and 24 in several territories or in a sole territory with distant watershed[s] (Type 3). Cerebral infarction on CT by Day 18 was revealed in one patient (5%) in Type 1, 3 (25%) in Type 2, and 14 (58%) in Type 3. Twelve (71%) of 17 patients belonging to both Group A and Type 3 resulted in cerebral infarction. These results suggest that early and extensive CVC reduction are significant factors responsible for cerebral infarction due to VS following SAH. Cerebral infarction can be reasonably predicted using A-A SPECT in SAH patients.

Acetazolamide↗

PubMed1993

Prevention of renal toxicity of cis-diamminedichloroplatinum by dithiocarbamates in rats.

Animals↗

PubMed1993

N-benzyl-D-glucamine dithiocarbamate and N-p-isopropylbenzyl-D-glucamine dithiocarbamate improve the protective effect of diethyldithiocarbamate against cadmium-induced testicular toxicity in rats.

The protective effects of combined treatment with diethyldithiocarbamate (DED) plus N-benzyl-D-glucamine dithiocarbamate (BGD) or DED plus N-p-isopropylbenzyl-D-glucamine dithiocarbamate (PBGD) against the testicular toxicity caused by acute exposure to cadmium (Cd) in rats were studied. Rats were injected subcutaneously with 109CdCl2 (3 mg Cd and 74 kBq of 109Cd/kg) and 30 min later, they were injected intraperitoneally with the chelating agents (1 mmol/kg each). Cd injection increased lipid peroxidation and concentrations of hemoglobin, Ca and Fe in the testes, decreased the testicular weight and nonprotein SH (NP-SH), and caused sterility. The coadministration of DED with BGD or PBGD significantly prevented the increase in the lipid peroxidation, hemoglobin, Ca and Fe in the testes, the decrease in the testicular weight and NP-SH, and the sterility caused by Cd injection. DED plus BGD or DED plus PBGD significantly decreased the Cd concentration in the testes without the redistribution of Cd to the brain and kidney, which is observed following treatment with DED alone. The coadministration of DED plus BGD or DED plus PBGD significantly increased the blood Cd concentration and the Cd distribution in the red blood cells compared to Cd alone. These results indicate that the coadministration of BGD or PBGD with DED prevents the accumulation of Cd in the testes on the basis of greater blood distribution of Cd, which results from the uptake of Cd by the red blood cells, without the redistribution of Cd to the brain, resulting in an improvement of the protective effect of DED against the Cd-induced testicular toxicity.

Animals↗

PubMed1993

Protective effects of dithiocarbamates against toxicity of cis-diamminedichloroplatinum in mice.

The protective effects of various dithiocarbamates such as N-benzyl-D-glucamine dithiocarbamate (BGD), N-p-hydroxymethylbenzyl-D-glucamine dithiocarbamate (HBGD), N-p-carboxybenzyl-D-glucamine dithiocarbamate (CBGD), and diethyldithiocarbamate (DDTC) on cis-diamminedichloroplatinum (DDP)-induced toxicity in mice were studied. The mice were injected i.v. with a chelating agent (1 mmol/kg) immediately or 5 min after i.v. injection of DDP (15 or 20 mg/kg). The lethal toxicity of DDP (20 mg/kg) was completely prevented by treatment with HBGD or CBGD immediately after DDP. The survival time of mice treated with HBGD or CBGD 5 min after DDP tended to be longer than that treated with BGD or DDTC. Significant increases in blood urea nitrogen (BUN) level and plasma aspartate aminotransferase (AST) activity were observed 3d after DDP injection. The increase in BUN level was completely prevented only by HBGD and CBGD among these chelating agents, while increase in AST activity was significantly prevented by treatment with these two agents. Treatment with HBGD or CBGD immediately after DDP (20 mg/kg) completely protected against DDP-induced diarrhea. These chelating agents significantly decreased the platinum (Pt) contents in the kidney and liver after DDP administration. Treatment with HBGD or CBGD was the most effective in decreasing the renal Pt content, resulting in maximum protection against DDP-induced renal damage. The antitumor efficacy of DDP (15 mg/kg) in the colon 26 carcinoma-bearing mice was not affected by HBGD administration.

Animals↗

PubMed1993

Increased plasma endothelin concentrations in patients with acute heart failure after myocardial infarction.

We have investigated the relationship between plasma endothelin (ET) concentrations and several clinical characteristics in 31 patients with acute myocardial infarction (MI). ET levels were also measured in 10 age-matched healthy subjects, 9 patients with unstable angina, and 20 patients with chronic heart disease. In patients with MI, although no significant relationship was observed between plasma ET concentrations and measured hemodynamic parameters, plasma levels were higher in patients with pulmonary congestion than in those without this complication (1.61 +/- 0.29 vs 1.21 +/- 0.33 fmol/ml; p < 0.01). No significant difference in plasma ET levels was found between cardiac and peripheral sampling sites (pulmonary artery; 1.07 +/- 0.28, right atrium; 1.02 +/- 0.28, peripheral artery; 1.12 +/- 0.23, peripheral vein; 1.14 +/- 0.38 fmol/ml: N.S.), or among patients with uncomplicated MI, unstable angina (1.00 +/- 0.32 fmol/ml), and healthy subjects (1.01 +/- 0.29 fmol/ml). Increased level were observed in patients with decompensated heart failure due to chronic heart disease, but were not found in patients without pulmonary congestion (1.62 +/- 0.60 vs 1.11 +/- fmol/ml; p < 0.01). These observations suggest that plasma ET concentrations are elevated in the presence of congestive heart failure or severe ventricular depression, but are not persistently increased by myocardial ischemia per se.

Acute Disease↗

PubMed1993

Effects of long-term infusion of synthetic atrial natriuretic factor on hemodynamics and water input-output balance in patients with acute myocardial infarction.

The administration of atrial natriuretic factor (ANF) increases coronary blood flow and decreases coronary vascular resistance. However, little is known about the feasibility and reliability of intravenous long-term infusion of ANF in patients with coronary heart disease. We therefore examined the effects on hemodynamic parameters and water input-output balance of 24-hour administration of synthetic ANF (ANF-[99-126]: 20-50 ng/kg/min) in 8 patients with acute myocardial infarction (6 men and 2 women; mean age 55 years). The ANF infusion significantly decreased pulmonary capillary wedge pressure to a maximum of greater than 50% 4 hours after infusion (from 16 +/- 2 to 7 +/- 2 mmHg; p < 0.01), and the effect was sustained throughout the 24-hour infusion without diuresis (mean water balance, + 25 +/- 12 ml/hr). This reduction was significantly correlated with the baseline value before infusion (r = -0.85, p < 0.01). The effect on pulmonary capillary wedge pressure was accompanied by small reductions (approximately 20%) in systemic blood pressure and cardiac index, without significant changes in systemic vascular resistance and heart rate. These results indicate that prolonged administration of low to medium doses of synthetic ANF causes potent and sustained left ventricular unloading without reflex, tachycardia and volume depletion, and may thus be safe and have potential benefits for patients with coronary heart disease.

Adult↗

PubMed1993

Prognostic implications of plasma levels of atrial natriuretic factor in patients with acute myocardial infarction.

Several neurohormonal factors have been proposed as markers of the severity of acute myocardial infarction (MI). To determine whether plasma concentrations of atrial natriuretic factor (ANF) might predict post-MI prognosis, we studied 130 patients with acute MI (97 males and 33 females, mean age 62 years). Within one-half to one day after admission, a blood sample was taken for estimation of circulating ANF. The mean follow-up period was 37 months, and the follow-up rate was 97%. Of the 130 patients, 28 died from cardiac causes during the follow-up period. Patients were classified into three groups according to plasma ANF levels (group 1, < 99 pg/ml; group 2, 100-199 pg/ml; group 3; > 200 pg/ml). The survival curves were constructed by the Kaplan-Meier method. There were significant differences in the cumulative survival rate among the three groups (group 1 > group 2 > group 3; p < 0.001). The baseline characteristics (age, atrial pressure, and cardiac index) were different among the groups, therefore these variables were analyzed by a Cox multiple regression model. Significant predictors of cardiac mortality were plasma ANF class (p < 0.002) and pulmonary capillary wedge pressure (p < 0.007). In conclusion, these observations demonstrated that stratification of acute MI patients by plasma ANF level is a useful non-invasive method for predicting prognosis and for identifying individuals at high risk of cardiac death.

Analysis of Variance↗

PubMed1992

Relationship between plasma atrial and brain natriuretic peptide concentration and hemodynamic parameters during percutaneous transvenous mitral valvulotomy in patients with mitral stenosis.

Brain natriuretic peptide (BNP), a family of peptides with structural and biologic homologies to previously identified atrial natriuretic peptide (ANP), has been found in human cardiac tissue and plasma. To examine the secretion mechanism of these peptides, we have studied the relationship between their plasma concentrations and hemodynamic parameters before and at 0.5 and 24 hours after percutaneous transvenous mitral commissurotomy (PTMC) in 14 patients with mitral stenosis. We have also investigated the validity of measuring plasma natriuretic peptides as a means for estimating changes in hemodynamic parameters after PTMC. The procedure decreased left atrial pressure (p < 0.01) with an elevation in left ventricular end-diastolic pressure (p < 0.05). Plasma ANP levels decreased significantly after PTMC (before, 64.1 +/- 33.7 fmol/ml; at 0.5 hour, 58.9 +/- 27.7 fmol/ml; at 24 hours, 45.7 +/- 18.3 fmol/ml; p < 0.01), whereas plasma BNP levels remained unchanged after the procedure (before, 5.3 +/- 1.5 fmol/ml; at 0.5 hour, 5.6 +/- 1.9 fmol/ml; at 24 hours, 5.0 +/- 1.9 fmol/ml; p = NS). There was a significant relationship between basal plasma ANP and left atrial pressure (r = 0.88; p < 0.001), and changes in plasma ANP were correlated with those in left atrial pressure (r = 0.69; p < 0.01). Basal plasma BNP was significantly correlated with basal left ventricular end-diastolic pressure (r = 0.65; p < 0.05) but not with the other measured hemodynamic parameters or with plasma volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

Effects of dithiocarbamates on testicular toxicity in rats caused by acute exposure to cadmium.

N-Benzyl-D-glucamine dithiocarbamate (BGD), N-p-isopropylbenzyl-D-glucamine dithiocarbamate (PBGD), and diethyl-dithiocarbamate (DED) were compared for their protective effects against the testicular toxicity in rats induced by acute exposure to cadmium. Rats were injected subcutaneously with 109CdCl2 (3 mg Cd and 74 kBq of 109Cd/kg) and 30 min later, they were injected intraperitoneally with the chelating agents (0.4 or 3 mmol/kg). Cadmium injection increased lipid peroxidation and concentrations of hemoglobin and Ca in the testes, decreased the testicular weight, and caused sterility. The treatment with BGD (0.4 mmol/kg) did not satisfactorily protect against the testicular toxicity of cadmium. The administration of PBGD or DED at a dose of 3 mmol/kg significantly prevented the increase in the lipid peroxidation and hemoglobin concentration in the testes, the decrease in the testicular weight, and the sterility caused by cadmium. PBGD and DED significantly decreased the cadmium concentration in the testes, but DED increased the cadmium concentration in the kidney and brain. Only DED significantly prevented the increase in the testicular Ca concentration after cadmium. These results indicate that PBGD and DED protect against the sterility caused by cadmium in rats and that the effect of DED to increase the brain level of cadmium is more dangerous than the lack of effect of PBGD to prevent the increase in the testicular Ca level. The protective effects of PBGD and DED against the cadmium-induced testicular toxicity presumably result from a decrease in the cadmium concentration in the testes.

Animals↗

PubMed1992

Characterization of gold in urine and bile following administration of gold sodium thiomalate with chelating agents to rats.

Gold was characterized in the urine and bile of rats treated with D-penicillamine (D-PEN), 2,3-dimercaptosuccinic acid (DMSA), 2,3-dimercaptopropane sulphonate (DMPS), or N-(2-mercapto-2-methylpropanoyl)-L-cysteine (bucillamine) immediately after gold sodium thiomalate (AuTM) injection by both gel chromatographic and electrophoretic methods. It is suggested that the gold in the urine and bile after AuTM administration was predominantly bound to high molecular weight compounds. The characterization of gold in the urine after administration of AuTM with D-PEN, DMSA, or DMPS showed that most of the gold was bound to the chelating agents. In the treatment with the chelating agents such as D-PEN and DMPS, the gold was mainly excreted as a gold-chelating agent compound in the bile and a minor portion of the gold was present in the form of a gold-L-cysteine compound and high molecular weight compounds. DMSA treatment showed that a major portion of the gold was bound to high molecular weight compounds in the bile and a minor portion of the gold was present in the forms of gold-DMSA and gold-L-cysteine compounds. The administration of AuTM and bucillamine indicated that the gold was mainly present as a gold-Me-bucillamine compound in the urine and a gold-bucillamine compound in the bile.

Animals↗

PubMed1992

Effect of L-cystine on toxicity of paraquat in mice.

The protective effect of L-cystine on the toxicity of paraquat (PQ) in mice was studied. Lipid peroxidation in the lung significantly increased after oral administration of PQ (200 mg/kg) and the increase in lipid peroxidation was prevented by L-cystine treatment (300 mg/kg). PQ administration produced an increase in superoxide dismutase (SOD) activity and a decrease in glutathione peroxidase (GSH-Px) activity in the lung at 24 h after PQ. L-Cystine treatment significantly prevented the changes in SOD and GSH-Px activity in the lung after PQ. L-Cystine treatment prevented the decrease in non-protein sulfhydryl (NP-SH) content in the lung after PQ administration. The tissue distribution and excretion of PQ after PQ administration were not changed by L-cystine treatment. Plasma aspartate aminotransferase activity did not change after PQ administration. These results suggest that L-cystine protects against the toxicity of PQ by maintaining reduced glutathione levels in the cells.

Animals↗

PubMed1992

Renal, haemodynamic and hormonal interactions between atrial natriuretic factor and arginine vasopressin in patients with congestive heart failure.

1. Nine patients with compensated heart failure were infused with synthetic arginine vasopressin at a rate of 0.1 m-units min-1 kg-1 for 60 min to increase their plasma arginine vasopressin concentration. Synthetic human atrial natriuretic factor (3 pmol min-1 kg-1) or placebo was co-infused with the arginine vasopressin in random order in a single-blind cross-over design. 2. The resultant plasma concentrations of arginine vasopressin and atrial natriuretic factor fell to within the upper range observed in congestive heart failure. Compared with the infusion of arginine vasopressin alone, atrial natriuretic factor co-infusion enhanced both the urine flow rate and the sodium excretion rate (both P less than 0.05) without significant haemodynamic and hormonal effects. 3. Systematic blood pressure was elevated by arginine vasopressin infusion (P less than 0.05) without any change in heart rate. Co-infusion of atrial natriuretic factor did not affect these haemodynamic parameters. 4. These results suggest that an increased release of atrial natriuretic factor maintains water and sodium excretion in the presence of arginine vasopressin-induced renal modulations, and that the pressor effect of arginine vasopressin is not antagonized by the increased plasma level of atrial natriuretic factor in patients with congestive heart failure.

Aged↗

PubMed1992

Endothelium-dependent vasodilation is augmented by angiotensin converting enzyme inhibitors in healthy volunteers.

We have examined the effects of local intra-arterial infusion of enalaprilat (an angiotensin converting enzyme inhibitor) on responses initiated by concomitantly infused acetylcholine (an endothelium-dependent vasodilator) and sodium nitroprusside (a direct dilator of smooth muscle) in the forearm arterial beds of healthy volunteers. Although the angiotensin converting enzyme inhibitor alone did not affect basal forearm blood flow or vascular resistance, it significantly augmented the increase in blood flow and reduction in vascular resistance induced by acetylcholine (both p < 0.05). Coinfusion of enalaprilat did not enhance sodium nitroprusside-induced vasodilation. Pretreatment with NG-monomethyl-L-arginine blocked the augmentation of blood flow induced by the angiotensin converting enzyme inhibitor. The effect of enalaprilat was still observed after the administration of acetylsalicylic acid (p < 0.05). These results suggest that angiotensin converting enzyme inhibitors potentiate nonprostanoid endothelium-derived relaxing factor in normal human forearm vasculature.

Acetylcholine↗

PubMed1992

Clinical analysis of a series of vertebral aneurysm cases.

We reviewed 38 cases of aneurysms of the vertebral artery treated over the last 10 years: 26 (68%) located at the junction of the vertebral and posterior inferior cerebellar arteries, 10 (26%) at the vertebral artery, and 2 (5%) at the vertebrobasilar union. There were three distinct forms of aneurysms: 20 saccular (53%), 10 fusiform (26%), and 8 dissecting (21%). Among these 38 aneurysms, 33 (87%) had ruptured: 18 of the saccular aneurysms (90%), all 10 of the fusiform aneurysms (100%), and 5 of the dissecting aneurysms (63%). Computed tomography of the 28 ruptured aneurysms revealed diffuse subarachnoid hemorrhage in the basal cistern combined with intraventricular hemorrhage in 24 cases (86%). Magnetic resonance imaging was useful for differentiating between fusiform and dissecting aneurysms. Abnormalities such as a double lumen of the vertebral artery were demonstrated in four of the dissecting aneurysms. The overall surgical results were good for 22 of the 27 surgically treated cases (81%). New bleeding was observed in 8 (24%) of the 33 ruptured aneurysms. The rate of new bleeding was high (60%) in the patients with dissecting aneurysms, and occurred mostly in the acute stage. The incidence of vasospasm was 27%, and only two patients suffered permanent neurological deficits. These findings indicate that the rate of new bleeding tends to be high in patients with saccular and dissecting aneurysms, and thus, they should be treated as early as possible. A preoperative balloon occlusion test should be conducted if proximal occlusion of the vertebral artery is necessary, since proximal occlusion is not always safe, despite angiographic evidence of sufficient contralateral arterial flow.

Aortic Dissection↗