Biomedical subjects
Publications and source records attributed to T Fukuyama.
A 19-year-old male consulted our department, complaining of a painful scrotal mass. On palpation, the mass was discriminated from testis, epididymis, and spermatic cord in the left scrotum. He underwent total excision of the mass. Pathologic examination revealed cavernous hemangioma. Scrotal hemangioma is a relatively rare lesion and this is the 37th case reported in Japan.
We examined HPA genotypes derived from polymorphisms of platelet membrane receptors in 88 Japanese patients with early-onset myocardial infarction and in 100 control subjects. The results indicated that HPA genotypes 1 through 6 are not associated with early-onset myocardial infarction.
Atherosclerotic lesions of the thoracic aorta were induced in exogenously hypercholesterolemic (ExHC) rats by treating initially with hypervitamin D2 and subsequently feeding on hypercholesterolemic diets for 180 days. Dietary soybean protein, in comparison with casein, substantially decreased the degree of atherosclerotic lesions, which was evaluated by intimal thickening, although with a similar topographical distribution. The casein-fed rats tended to maintain a high concentration of serum cholesterol, particularly in triacylglycerol-rich lipoproteins. The concentrations of apo A-I and TBARS in the serum was comparable between the dietary protein groups. The data suggest that dietary soybean protein, compared to casein, produced lipoproteins which were less atherosclerotic by partitioning cholesterol in the triacylglycerol-poor lipoproteins.
We report a case of uretero-aortic fistula. A 69-year-old man with rectal cancer underwent a pelvic exenteration and a double--barreled cutaneous ureterostomy in the right lower abdomen. Stomal stenosis necessitated continuous indwelling of double J stents in the two ureters. Two years postoperatively, massive bleeding occurred during exchange of double J catheters. Occlusive ureterogram demonstrated a uretero-aortic fistula at the crosspoint between the left ureter and the aorta. The surgical repair consisted of closure of the aortic fistula, ligation of the left ureter proximal to the fistula and percutaneous left nephrostomy.
Iodine-123-metaiodobenzylguanidine (MIBG) imaging was used to assess myocardial adrenergic nerve activity in patients with heart failure MIBG planar images were obtained in 94 patients. The uptake of MIBG, calculated as the heart-to-mediastinum activity ratio in the immediate image (15 min), showed a significant decrease only in patients with severe heart failure due to cardiomyopathy, but was not changed in those with valvular diseases. Storage and release of MIBG, calculated as the percentage myocardial MIBG washout from 15 min to 4 hours after isotope injection, was substantially accelerated in both patients with cardiomyopathy and valvular diseases in proportion to the severity of heart failure. These data suggest that, in severe heart failure associated with cardiomyopathy, norepinephrine uptake is reduced. Also, myocardial adrenergic nerve activity is accelerated in proportion to the severity of heart failure independent of the underlying cause. MIBG images were analyzed in 20 patients with mitral stenosis with the same methods to clarify whether myocardial adrenergic nerve activity is different in patients with heart failure without left ventricular volume or pressure overload. Myocardial uptake of MIBG did not show any significant difference. The percentage myocardial MIBG washout was increased in patients with severe heart failure. The closest correlation was between myocardial washout and cardiac output. In heart failure due to mitral stenosis, myocardial adrenergic nerve activity is intensified. Decrease in cardiac output associated with mitral stenosis acts as a potent stimulus for this intensification.
OBJECTIVES: To clarify whether myocardial adrenergic activity is different in patients with heart failure without left ventricular volume or pressure overload, we used iodine-123 metaiodobenzylguanidine (MIBG) imaging to study patients with mitral stenosis. BACKGROUND: In patients with heart failure due to cardiomyopathy or to valve diseases with volume or pressure overload, or both, myocardial adrenergic nerve activity is accelerated independent of underlying cause. However, it is not clear whether this change in myocardial adrenergic nerve activity is present in patients without left ventricular volume or pressure overload. METHODS: The study patients were 20 men and women with normal left ventricular function and heart failure due to mitral stenosis. Planar MIBG images obtained from these patients were compared with images from nine age-matched healthy subjects (control group). Myocardial uptake of MIBG was calculated as the heart/mediastinal activity ratio. Storage and release of MIBG were calculated as percent myocardial MIBG washout from 15 min to 4 h after isotope injection. All 20 study patients underwent echocardiography, and 16 underwent right heart catheterization. RESULTS: The heart/mediastinal activity ratio in the immediate images (15 min) did not show any significant difference between the patient and control groups. Myocardial washout was increased in patients with severe heart failure. The level of myocardial washout correlated with left atrial diameter (r = 0.51, p = 0.02) and mitral valve area calculated with Doppler echocardiography (r = -0.61, p < 0.01) and mitral valve area calculated with cardiac catheterization (r = -0.62, p = 0.02). The closest correlation existed between myocardial washout and cardiac output (r = -0.80, p < 0.01). CONCLUSIONS: In heart failure due to mitral stenosis, myocardial adrenergic nerve activity is intensified. A decrease in cardiac output associated with mitral stenosis acts as a potent stimulus for this intensification.
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Mucin-producing tumours of the pancreas have been recently reported with increasing frequency and most cases have occurred in middle-aged and elderly people. In the present report, a case of a 21-year-old man with mucinous cystadenoma of the pancreas is reported. He had a long history of recurrent pancreatitis from the age of 8. When he was aged 10, the first branch of the main pancreatic duct was shown to be enlarged on endoscopic retrograde pancreaticography (ERP). A series of ERP studies and computed tomography scans performed over a period of 11 years demonstrated continuing growth of this enlargement of the pancreatic duct. Pancreaticoduodenectomy was performed and the patient has been well without further episodes of acute pancreatitis and has been free of recurrent tumour for 1 year.
The effect of pentobarbital on the biliary excretion of diclofenac was investigated in a rat liver perfusion system following a pulse input of the drug. Without albumin in the perfusate, a trace amount of diclofenac was detected in the outflow from the liver (< 0.1%). The total biliary excretion of diclofenac (intact diclofenac plus its glucuronide) decreased from 23.8% (diclofenac 6.01, glucuronide 17.8%) to 16.3% (diclofenac 5.09, glucuronide 11.2%) with an increase in the perfusate concentration of pentobarbital from 0 to 2.5 micrograms mL-1. At pentobarbital concentrations exceeding 2.5 micrograms mL-1, the biliary excretion of diclofenac and its glucuronide (14% total diclofenac) was not reduced further. The mean local excretion times of both diclofenac and its glucuronide were approximately 17 min and were unchanged at all pentobarbital concentrations tested. The ratios of biliary excreted diclofenac and its glucuronide to total diclofenac were 22 and 78%, respectively, and these values were virtually constant at all concentrations of pentobarbital in the perfusate. These results suggest that the glucuronidation of diclofenac and the biliary excretion of its glucuronide are rapid processes and that pentobarbital blocks a step before glucuronidation.
Because the liver is the main organ eliminating many drugs from the body and because pentobarbitone and other analogues can inhibit biliary secretion, the influence of pentobarbitone on hepatic local disposition of diclofenac has been investigated. Diclofenac was infused into the portal and femoral veins of non-anaesthetized rats (group A) and rats anaesthetized with pentobarbitone (group B) and the plasma concentration of diclofenac and the total amount of diclofenac excreted in the bile (in both cases intact diclofenac plus its glucuronide) were simultaneously monitored by HPLC at appropriate time intervals. The time-courses of plasma concentration and amount excreted in the bile were evaluated by moment analysis with trapezoidal integration. The hepatic recovery ratio (FH) was calculated by comparing the area under the curve (AUC) of plasma concentration after intravenous infusion with that after intraportal infusion. The mean biliary transit time (tb) was estimated by subtracting the mean residence time (MRT) of the plasma data from the mean biliary residence time (MRTb) of the biliary excretion data. The FH values of diclofenac were 0.664 in group A and 0.643 in group B. The biliary excretion ratio (Fb) of total diclofenac after intravenous administration was 27.0% in group A and 14.1% in group B. The tb values for total diclofenac were estimated to be 0.192 h (intravenous) and 0.159 h (intraportal) in group A, and 0.174 h and 0.238 in group B. Analysis of variance showed that differences among these four tb values were insignificant at the 5% level. The differences in the mean residence time (MRT), total clearance (CL) and distribution volume at steady state (Vss) were insignificant between groups A and B. Whereas total and the hepatic clearance of diclofenac were not affected by pentobarbitone, biliary clearance was extensively reduced. It took a relatively long time for diclofenac to move from the sinusoid into the bile and the time was not affected by pentobarbitone.
The local absorption kinetics from the intestinal tract into the portal system was evaluated using the portal-venous concentration difference (P-V difference) after oral administration of diclofenac in conscious rats. The local absorption ratio (Fa), mean local absorption time (ta), and relative variance (sigma 2/ta2) from the intestinal tract into the portal system were estimated by simultaneously measuring the portal and venous concentrations, using diclofenac as a model drug. The effect of bile on diclofenac intestinal absorption was also investigated. The awakening rats simultaneously cannulated into the jugular and portal veins were divided into group A with intact enterohepatic circulation (EHC) and into another group with bile-duct cannulation to block EHC. The rats in the latter group were further divided into group B without the bile supply to the intestinal tract and into group C with the bile supply from the other rat. After oral administration of diclofenac to rats in groups A, B, and C, the portal and venous concentrations of diclofenac in each rat were simultaneously monitored by HPLC method at proper time intervals. The absorption time profile of diclofenac into the portal system was directly predicted from P-V difference. Plasma concentrations of diclofenac in the portal vein were constantly higher than those in the jugular vein after the oral administration. It was demonstrated that P-V difference was caused by absorption from the intestinal tract into the portal system. Fa in groups A, B, and C were estimated to be 91.5% for 8 hr, 33.8% for 3 hr, and 57.8% for 3 hr, respectively. ta in groups A, B, and C were estimated to be 2.26 hr, 0.65 hr, and 0.96 hr, respectively. sigma 2/ta2 in groups A, B, and C were 1.31, 0.48, and 0.55, respectively. Fa and ta of diclofenac extensively increased in the presence of the bile in the intestinal tract, whereas sigma 2/ta2 was unaffected by the bile. The mean absorption time (MAT) almost agreed with ta, which demonstrates that the mean transit time through the liver (tH) is negligible in MAT(= ta+tH).
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UNLABELLED: Simultaneously acquired dual-isotope imaging is a unique and useful approach in SPECT. Photon spillover, however, is a potential limitation of this technique. METHODS: To investigate the degree of 99mTc downscatter into the 201Tl window in patients, simultaneously acquired dual-isotope 201Tl/99mTc-pyrophosphate imaging was performed in 17 patients with acute myocardial infarction (MI). Thallium-201 SPECT imaging was performed first, with a 201Tl photopeak window after the 201Tl injection (early 201Tl images), followed by 99mTc injection and SPECT acquisition using dual-isotope windows (dual 201Tl images). Twenty-four hours after the 99mTc injection, a third set of 201Tl images was obtained (24-hr 201Tl images). Thallium defect size (extent score) and defect severity (severity score) were calculated from these three sets of 201Tl images to quantify the MI. RESULTS: Technetium-99m accumulation of varying intensity was recognized in all patients. Extent scores and severity scores were identical in early 201Tl images and 24-hr 201Tl images. Both scores, however, in the dual 201Tl images were decreased by 36% and 53%, respectively. CONCLUSION: There in a considerable 99mTc downscatter into the 201Tl window, which prevents precise quantification of MI in simultaneously acquired dual-isotope 201Tl/99mTc-pyrophosphate imaging.
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OBJECTIVES: This study was undertaken to assess myocardial adrenergic activity using iodine-123 metaiodobenzylguanidine (MIBG) imaging in patients with heart failure. BACKGROUND: In patients with congestive heart failure, adrenergic nerve activity is accelerated. However, whether myocardial adrenergic nerve activity reflects the severity of heart failure and its relation to the underlying cause have not yet been elucidated. METHODS: Planar MIBG images were obtained from 96 patients with heart failure and compared with images from 9 age-matched healthy subjects. Groups 1 and 2 included 65 patients with heart failure related to impaired myocardial function and whose left ventricular ejection fraction was < 40% (group 1 = 40 patients with dilated cardiomyopathy; group 2 = 25 patients with ischemic cardiomyopathy). Group 3 included 31 patients with heart failure related to a mechanical abnormality and whose left ventricular ejection fraction was > 40% (mitral regurgitation in 16, aortic regurgitation in 9, aortic and mitral regurgitation in 4, ruptured aneurysm of Valsalva in 2). Myocardial uptake of MIBG was calculated as the heart/mediastinal activity ratio. Storage and release of MIBG were calculated as percent myocardial MIBG washout from 15 min to 4 h after isotope injection. RESULTS: The heart/mediastinal activity ratio in the immediate images (15 min) showed a significant decrease only in patients with severe heart failure (groups 1 and 2). The myocardial washout was accelerated in all three heart failure groups. The level of myocardial washout was related to severity of heart failure and correlated well with New York Heart Association functional classification. CONCLUSIONS: In severe heart failure associated with cardiomyopathy, norepinephrine uptake is reduced. In addition, myocardial adrenergic nerve activity is accelerated in proportion to severity of heart failure, independent of the underlying cause.
PURPOSE: We evaluated the first-pass effects in vivo by the intestine and liver during enterophepatic circulation (EHC) by simultaneously measuring the portal and venous plasma concentrations of the rat. METHODS: The venous and upper portal blood vessels were cannulated through the jugular and the pyloric veins, respectively, to obtain simultaneously blood samples from both sites. After diclofenac was injected as a bolus through the jugular vein, the concentrations of diclofenac in the portal and jugular veins were measured at time intervals. The absorption rate from the intestinal tract into the portal system was determined using the portal-venous difference in plasma concentrations of diclofenac, considering 40% partitioning of diclofenac into erythrocytes. RESULTS: After one hour, the plasma concentration in the portal vein was always higher than that in the jugular vein in awakening rats with intact EHC (portal-venous blood concentration difference). No portal-venous difference was observed in awakening rats with bile-duct cannulation. Therefore, it was concluded that this portal-venous concentration difference was not due to the hepatic clearance but to diclofenac reabsorption from the intestinal tract. CONCLUSIONS: Approximately 40% of the dose of diclofenac was reabsorbed over 8 hours from the intestinal tract into the portal system. By comparing the reabsorbed amounts in the portal system and in the systemic circulation, the hepatic extraction ratio in vivo (FH) of diclofenac was estimated to be 63%.
The effect of the acute hepatic failure induced by CCl4 on the pharmacokinetics of diclofenac, which is definitely subject to enterohepatic circulation (EHC) in normal rats, was evaluated. This hepatic failure extinguished the secondary peak on the plasma time course which is usually observed in normal rats due to EHC. In the group without EHC by means of bile cannulation, the total clearance (CL) markedly decreased by CCl4-intoxication from 0.7 l/h/kg down to 0.1 l/h/kg, and mean residence time (MRT) increased from 0.29 h up to 2.8 h. The plasma time curves of the rats with laparotomy and with bile duct-cannulation were almost the same in the CCl4-intoxicated group. The bile excretion ratio of diclofenac markedly decreased by CCl4-intoxication from 43% down to 13%. In both groups, 92% of the total diclofenac excreted into the bile was glucuronide. While EHC made area under the curve (AUC) and MRT obviously increase in the CCl4-free rats, the effect of EHC on these moments was negligible in the CCl4-intoxicated rats. In the CCl4-intoxicated condition, the elimination of diclofenac in the rats with laparotomy was considerably slower than that in the rats without laparotomy. The plasma time courses were obviously monoexponential in the former group, while those were almost biexponential in the latter group.