Biomedical subjects

T Funakoshi

Publications and source records attributed to T Funakoshi.

At least 19 recordsLinked to original sources

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↗

PubMed1992

Anticoagulant action of vanadate.

Sodium orthovanadate (vanadate) prolonged the clotting time of normal human plasma in a dose-dependent manner. The prolongation of clotting time by vanadate linearly decreased with an increase in the concentration of amiloride. Vanadate also was completely additive to prolongation by heparin. When factor Xa or thrombin was incubated with vanadate, the amidolytic activity of each decreased in a dose-dependent manner with vanadate. Amiloride protected the decrease of amidolytic activity of both factor Xa and thrombin by vanadate. The amidolytic activity of trypsin also was inhibited by vanadate, but that of alpha-chymotrypsin was not inhibited, suggesting that vanadate preferentially inhibits the amidolytic activity of trypsin and trypsin-like enzymes. These results show that vanadate prolongs the clotting time of plasma through mechanisms involving in part the inhibition of the activity of both factor Xa and thrombin.

Amino Acid Sequence↗

PubMed1992

Brain tumors manifesting as intracranial hemorrhage.

The clinical course and computed tomographic (CT) findings of 23 patients with brain tumors manifesting as tumoral hemorrhage were reviewed. The most common symptoms were headache and clouding of consciousness. A CT finding of a lesion located next to a solid or irregular clot indicated intratumoral hemorrhage. Precontrast CT demonstrating an indent on the hematoma surface was a valuable indicator of tumoral hemorrhage. A CT finding of accumulated levels of blood/fluid or a hyperdense mass containing small hematoma indicated intratumoral hemorrhage, and obscure hyperdensity indicated intratumoral hemorrhagic infarction. Such findings were often difficult to distinguish from spontaneous intracerebral hemorrhage due to other factors. The incidence of rebleeding from residual tumors was high, carrying a very poor prognosis, so radical removal of brain tumors with hemorrhage is very important.

Adolescent↗

PubMed1992

Anticoagulant action of rare earth metals.

Some of the lanthanides, the rare earth metals, lanthanum (La), cerium (Ce), neodymium (Nd), samarium (Sm), terbium (Tb), dysprosium (Dy), erbium (Er) and ytterbium (Yb) prolonged the clotting time of normal human plasma in a dose-dependent manner when clotting was induced either by thromboplastin or by kaolin in the presence of cephalin and Ca2+. They also prolonged the activated factor X induced clotting time of platelet-rich plasma. The amidolytic activities of activated factor X and thrombin progressively decreased with increasing amount of rare earth metals. These results suggested that the rare earth metals appear to show their anticoagulant effect with mechanisms in part the inhibition of the enzymatic activities of both activated factor X and thrombin.

Anticoagulants↗

PubMed1992

Effect of repeated administration of chelating agents on distribution, excretion, and renal toxicity of gold sodium thiomalate in rats.

The effects of the repeated administration of D-penicillamine, 2,3-dimercaptosuccinic acid, 2,3-dimercaptopropane sulphonate, and N-(2-mercapto-2-methylpropanoyl)-L-cysteine 24 h after gold sodium thiomalate (AuTM) injection on the distribution, excretion, and renal toxicity of gold in rats were investigated. Three i.p. injections of these chelating agents (1.2 mmol/kg) at 1, 3, and 5 days after AuTM injection (0.026 mmol/kg) removed gold from kidney and liver through urinary and fecal excretion, and protected against the renal damage induced by AuTM. These findings indicate that these compounds are useful antidotes for gold toxicity.

Animals↗

PubMed1991

Acetazolamide reactivity on cerebral blood flow in patients with subarachnoid haemorrhage.

Cerebral vasodilatory capacity was evaluated by acetazolamide-activated N-isopropyl-p-[123I]iodoamphetamine (123I-IMP) single photon emission computed tomography (SPECT) in 42 patients with subarachnoid haemorrhage (SAH). A low perfusion area was present in the corresponding region of haematoma seen on the CT and continued to be noted throughout the time courses. Deteriorated acetazolamide reactivity affected by surgical intervention was seen in 100% of the patients who underwent aneurysm repair in the 1st postoperative week, 92% in the second week, 73% in the third week, and 47% in the fourth week. Three patients with acute diffuse brain swelling seen on CT showed intracranial non-filling of 123I-IMP on SPECTs performed on Day 6, and all three died by Day 10. Some low perfusion areas, due to probable vasospasm, were present in 77% of Hunt and Hess grades I and II patients and in 100% of grades III, IV, and V patients throughout their time courses. Overall, low perfusion areas, due to probable vasospasm, were seen in 10 patients (31%) of 32 who underwent SPECT between Day 4 and 8,23 (77%) of 30 between Day 9 and 14, 21 (72%) of 29 between Day 15 and 21, and 11 (48%) of 23 between Day 22 and 28. The results suggest acetazolamide-activated 123I-IMP study is of value in evaluating changes in vasodilatory capacity in SAH patients in the acute and subacute stages.

Acetazolamide↗

PubMed1991

Comparative effects of N,N-disubstituted dithiocarbamates on excretion and distribution of cadmium in mice.

Sodium N-benzyl-D-glucamine dithiocarbamate (BGD), sodium N-p-hydroxymethylbenzyl-D-glucamine dithiocarbamate (HBGD), sodium N-p-carboxybenzyl-D-glucamine dithiocarbamate (CBGD) and sodium N-p-methoxybenzyl-D-glucamine dithiocarbamate (MeOBGD) were evaluated for their efficacy in the distribution and excretion of cadmium in mice exposed to cadmium. Mice were injected i.p. with 109CdCl2 (1 mg Cd/kg and 74 kBq of 109Cd/animal) and 30 min or 24 h later, they were injected with chelating agents (400 mumol/kg). At 30 min after treatment with cadmium, these chelating agents all significantly enhanced the biliary excretion of cadmium, and HBGD and CBGD significantly increased the urinary excretion of the metal. At 24 h after cadmium injection, BGD, HBGD, and MeOBGD significantly increased the biliary excretion of cadmium and HBGD was the most effective on the biliary excretion of the metal. These chelating agents were effective in mobilizing cadmium from the liver at 30 min after cadmium treatment. At 24 h after cadmium treatment, HBGD and MeOBGD effectively depressed cadmium content in the liver and only HBGD among these chelating agents significantly reduced the cadmium content in the kidney. In another experiment, mice were injected i.p. with 109CdCl2 and three days later, they were injected with chelating agents every other day for 2 weeks. HBGD was the most effective on the fecal and urinary excretions of cadmium. The hepatic cadmium content was decreased after HBGD or MeOBGD injection. The injection of HBGD caused a much greater decrease in renal cadmium content than did BGD, CBGD, or MeOBGD. The results of this study indicated that the injection of HBGD to mice pretreated with cadmium can remove cadmium from the body, mainly through fecal excretion, without redistribution of cadmium to other tissues such as the brain, testes, and heart, more effectively than that of BGD, CBGD, or MeOBGD.

Animals↗

PubMed1991

Protective effects of dextran sulfate and polyvinyl sulfate against acute toxicity of paraquat in mice.

The protective effects of sodium dextran sulfate (SDS) and potassium polyvinyl sulfate (PPS) against the acute toxicity of paraquat (PQ) in mice were studied. The survival rates of mice treated with SDS (2000 mg/kg) or PPS (2000 mg/kg) immediately after PQ ingestion (200 mg/kg) were 100% or 100%, respectively. When treated with SDS (2000 mg/kg) or PPS (2000 mg/kg) 15 or 30 min after PQ ingestion (200 mg/kg), the survival rates were 83% or 67% for SDS-treated groups and 67% or 33% for PPS-treated groups, respectively. Treatment with SDS (2000 mg/kg) or PPS (2000 mg/kg) immediately after oral administration of PQ (200 mg/kg) increased the fecal excretion of PQ, decreased the urinary excretion of PQ and decreased the contents of PQ in the lung, liver and kidney. Such effects of SDS and PPS were reduced in the treatment with these drugs at 15 min after PQ. The in situ small intestinal absorption of PQ was significantly reduced in the presence of SDS or PPS. The binding of PQ to SDS or PPS was determined by an ultrafiltration method. These results indicate that SDS and PPS inhibit the gastrointestinal absorption of PQ on the basis of the increased intestinal transit of PQ and the binding of PQ to the drugs resulting in the protective effectiveness of SDS and PPS on the acute toxicity of PQ.

Animals↗

PubMed1991

Correlation between magnetic resonance imaging and histopathology of intracranial glioma.

Postmortem histopathology of eight gliomas was studied in correlation with magnetic resonance imaging (MRI) and computed tomography (CT) findings. MRI demonstrated the lesions more clearly and widely than CT. Also, T2-weighted images (T2WI) had a greater ability to depict the lesion than T1-weighted images (T1WI). The areas in which neoplastic cells had invaded corresponded to the high intensity areas on T2WI in four cases of glioblastoma multiforme. In the case of a grade II astrocytoma, neoplastic cells were scattered beyond the region corresponding to the high intensity area on T2WI. In the case of a grade III astrocytoma, neoplastic cells did not come up to the line corresponding to the margin of the high intensity area on T2WI. In the remaining two cases, although the high intensity areas on T2WI were depicted as being larger than the areas in which neoplastic cells were seen histopathologically, the high intensity regions corresponding to the outside zones of the tumour-infiltrated area were thought to be a radiation necrosis in one case and a 'periventricular high intensity' in the other. The high cellularity of the glioma was seen mainly as a low intensity area on T1WI and as an isointensity or a slightly high intensity area on T2WI. However, the signal intensities of glioma on MRI, reflecting T1 or T2 values of the tumour tissues, did not correlate with the malignancy of the tumour.

Adult↗

PubMed1991

Mobilization of renal and hepatic cadmium by dithiocarbamates in rats.

Sodium N-benzyl-D-glucamine dithiocarbamate (BGD), sodium N-p-hydroxymethylbenzyl-D-glucamine dithiocarbamate (HBGD), sodium N-p-carboxybenzyl-D-glucamine dithiocarbamate (CBGD), and sodium N-p-methoxybenzyl-D-glucamine dithiocarbamate (MeOBGD) were evaluated for their efficacy in the distribution and excretion of cadmium in rats exposed to cadmium. Rats were injected intraperitoneally with 109CdCl2 (1 mg Cd/kg and 74 kBq of 109Cd/one animal) and 30 min or 24 h later, they were injected with chelating agents (400 mumol/kg). At both 30 min and 24 h after treatment with cadmium, these chelating agents all significantly enhanced the biliary excretion of cadmium. At 24 h after cadmium injection, BGD and MeOBGD were the most effective on the biliary excretion of the metal. These chelating agents were effective in mobilizing cadmium from the liver at 30 min after cadmium treatment. At 24 h after cadmium treatment, BGD and MeOBGD significantly depressed cadmium content in the liver. In another experiment, rats were injected intraperitoneally with 109CdCl2 and 3 d later, they were injected with BGD, HBGD, or MeOBGD every other day for 2 weeks. The fecal excretion of cadmium was significantly increased by these chelating agents and MeOBGD was the most effective. The hepatic and renal cadmium contents were significantly decreased after BGD, HBGD or MeOBGD injection. The injection of MeOBGD to rats pretreated with cadmium was more effective than that of BGD, HBGD, or CBGD in removing cadmium from the liver. HBGD injection was more effective in decreasing the cadmium content in the kidney. The treatment with these chelating agents did not cause the redistribution of cadmium to brain, testes, and heart.

Animals↗

PubMed1991

N-fatty acyl compounds inhibit myristoyl acylation of pp60v-src and reduce tumorigenicity of Rous sarcoma virus-infected cells.

Prevention of NH2-terminal myristoylation of pp60v-src was determined with N-fatty acyl glycinal derivatives. Of all the compounds tested, N-myristoyl and N-lauroyl glycinal diethylacetal, N-myristoyl glycyl glycinal diethylacetal, and N-myristoyl-4-aminobutyl aldehyde diethylacetal strongly inhibited myristoylation of pp60v-src; but N-myristoyl diglycyl, N-myristoyl triglycyl, N-decanoyl glycinal diethylacetal, and N-palmitoyl glycinal diethylacetal did not. N-Myristoyl glycinal diethylacetal (25 or 50 microM) suppressed both morphological transformation and colony formation of Rous sarcoma virus-infected chick embryo fibroblasts.

Acylation↗

PubMed1991

[Intracranial accumulation of 99mTc-phosphorous compound on bone scintigraphy].

Bone scintigrams of 99mTc-phosphorous compound in 4,579 cases were reviewed concerning the intracranial accumulation. Intracranial accumulations were demonstrated in 8 cases (0.17%). The lesions with intracranial accumulation were two cases of primary brain tumor (1 meningioma and 1 astrocytoma), five cases of metastatic brain tumor (1 rectal cancer, 1 gastric cancer, 1 uterine cervical cancer and 2 lung cancers) and one case of cerebral infarction. Calcification was detected in one of eight cases on CT scans. It is important to pay attention to the intracranial accumulation on routine bone scintigram because brain tumor or infarction may be detected.

Aged↗