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Biomedical subjects

A Iguchi

Publications and source records attributed to A Iguchi.

At least 253 records · Page 14Linked to original sources
PubMed1988

[High resolution ultrasound examination in the diagnosis of the undescended testis in the inguinal region].

Twenty-six undescended testes in 22 patients between 1 and 31 years old were evaluated with ultrasonographic examination between October, 1981 and December, 1985. All 22 patients were operated on, and the accuracy of the ultrasonic diagnosis was evaluated in comparison to that of palpation diagnosis. Fourteen of 26 testes could be palpated preoperatively and these were all identified ultrasonographically and surgically. Twelve testes could not be palpated. On these 12 testes, surgical exploration revealed 9 testes in the inguinal region and absence of 3 testes. Ultrasound examination predicted its presence in 5 of 9 testes and its absence in all 3 testes. Both sonography and palpation failed to identify their presence in 4 tests. Thus, sensitivity of ultrasound examination was 82.6%, specificity 100% and accuracy 84.6% retrospectively. We conclude that ultrasound examination is useful in diagnosis of impalpable undescended testes in inguinal region.

Adolescent↗
PubMed1987

Early intravesical instillation of adriamycin with oral administration of 5-fluorouracil after transurethral resection for superficial bladder cancer: preliminary results.

In all, 199 patients were entered in this study by 21 collaborating hospitals. Patients with superficial transitional cell carcinoma of the bladder were randomized postoperatively into four groups. Group A received early (immediately and 2 days after transurethral resection) instillation of adriamycin (30 mg/30 mg); group B received early instillation of adriamycin with oral administration of 5-fluorouracil (200 mg/day); group C received delayed (7 days after transurethral resection) instillation of adriamycin (30 mg/30 ml); and group D received delayed instillation of adriamycin with oral administration of 5-fluorouracil (200 mg/day). All patients subsequently received instillations weekly for 2 more weeks, and then every 2 weeks for a further 14 weeks. After 4 months, they received one instillation per month for 8 months. 5-Fluorouracil was administered p.o. for 1 year. The postoperative follow-up period was 12 months. After 3 and 6 months there were significant differences in the non-recurrence rates between groups B and C. After 12 months the overall non-recurrence rates were 87.9% in group A, 83.5% in group B, 89.2% in group C, and 82.8% in group D, and there were no significant differences among the four groups. The number of patients entered and the follow-up period are not adequate for firm conclusions, and further studies are necessary. The main side effect was bladder irritation, which was observed in 38.8% of patients in the early instillation groups and in 26.3% of those in the delayed instillation groups. No severe systemic side effects were observed in this study.

Administration, Intravesical↗
PubMed1987

Prostaglandins affect the central nervous system to produce hyperglycemia in rats.

The influence of prostaglandins (PG) on central nervous system regulation of blood sugar homeostasis was studied in rats. Substances were injected into the third cerebral ventricle of anesthetized rats while rectal temperature and hepatic venous plasma glucose concentration were recorded. Stereotaxic microinjection of PGD2, E1, E2, and F2 alpha produced hyperglycemia and hyperthermia. The relative order of potency in hyperglycemia, PGF2 alpha greater than D2 greater than E1 greater than E2, was not consistent with that of hyperthermia, PGE2 greater than F2 alpha greater than E1 greater than D2, which suggests that hyperglycemia was a primary, not secondary, response to hyperthermia. Injection of PGF2 alpha caused a dose dependent (5-200 micrograms) increase in the hepatic venous plasma glucose level. Neither the injection of PGF2 alpha (50 micrograms) into the cortex nor into the systemic vein caused hyperglycemia. The injection of PGF2 alpha into the ventricle resulted in the increase of not only glucose, but also glucagon, epinephrine, and norephinephrine in the hepatic venous plasma. However, constant infusion of somatostatin through the femoral vein completely prevented the increase of glucagon after administration of PGF2 alpha, although the increase of plasma glucose level was still observed. PGF2 alpha-induced hyperglycemia did not occur in adrenodemedullated rats. Intravenous injection of naloxone or propranolol did not affect the hyperglycemia, but phentolamine significantly prevented the hyperglycemic effect of PGF2 alpha. These results suggest that intraventricular PGF2 alpha affects the central nervous system to produce hyperglycemia by increasing epinephrine secretion from the adrenal medulla.

Alprostadil↗
PubMed1987

Biochemical and hemodynamic changes in the hypertrophied dog heart subjected to chronic protein-calorie malnutrition.

Biochemical and hemodynamic changes were assessed in 13 dogs subjected to sub-coronary valvular aortic stenosis and chronic protein-calorie malnutrition (PCM). Red blood cell, hemoglobin, serum albumin, free fatty acids, blood glucose, cholinesterase and blood amino acid levels were measured. The dynamic geometry of the left ventricle (LV) was assessed with chronically implanted sonomicrometric piezoelectric crystals. Cardiac function was evaluated by mean velocity of circumferential fiber shortening (mean VcF) and the relationship between LV end-systolic pressure (LVESP) or LV wall stress (LVWst) and LV end-systolic diameter (LVESD). The following results were obtained: A decrease in body weight and increases in free fatty acids and 3-Methylhistidine were observed following long-term PCM. Mean VcF was not depressed in dogs subjected to PCM. The relationship between LVESP or LVWst and LVESD shifted downward and to the right after PCM, indicating reduced myocardial contractility. These findings suggest that the left ventricle in hypertrophied dog hearts subjected to PCM retains normal pump function, despite a low state in the myocardium.

Animals↗
PubMed1987

Useful antiglobulin crossmatch test for DST-sensitized patients.

The AG-CDC tests were performed in parallel with C-CDC tests for studying sensitization of DST patients. Fourteen of 56 DST patients were positive by the AG-CDC tests after DST. Ten of 14 were also positive by both tests after DST. In 8 of 14 patients AG-CDC antibodies continued to be detectable even after C-CDC antibodies became undetectable as time passed and with plasmapheresis. Thus, AG-CDC tests are more sensitive compared to C-CDC tests and can extend the detection rate of DST-sensitized patients. Except for two DST patients (highly sensitized), 12 of 14 DST-sensitized patients were given transplants from specific blood donors at the time when their C-CDC tests became negative. One graft failed, another one had impaired function, and ten of them functioned. It should be noted that DST patients were transplanted successfully with or without plasmapheresis across a positive AG-CDC test if the titer was less than 1:4 at the time of transplant. All four DST recipients who developed antibodies detected only by AG-CDC tests after DST experienced severe accelerated rejections. In contrast, two of eight patients who were positive by both tests had "severe" accelerated rejections. The incidence of severe accelerated rejections was shown to be highly associated with the presence of AG-CDC antibodies. These facts suggest that AG-CDC antibodies may damage kidney grafts and result in severe accelerated rejections; and that AG-CDC tests are useful for predicting occurrence of severe accelerated rejections in DST recipients.

Blood Transfusion↗
PubMed1986

Mechanism of central hyperglycemic effect of cholinergic agonists in fasted rats.

The influence of cholinergic agonists on central nervous system (CNS) regulation of blood sugar homeostasis was studied in fasted rats. When carbachol, muscarine, bethanechol, methacholine, or neostigmine was injected into the third cerebral ventricle, it caused a dose-dependent increase in the hepatic venous plasma glucose concentration. However, in the case of 1,1-dimethylphenyl-4-piperazinium iodide (DMPP) or nicotine, the level of hepatic venous glucose did not differ from that of the saline-treated control rats. The increase in glucose level caused by neostigmine was dose-dependently suppressed by coadministration of atropine. These facts suggest that cholinergic activation of muscarinic receptors in the CNS plays a role in increasing hepatic glucose output. Injection of neostigmine (5 X 10(-8) mol), an inhibitor of cholinesterase, into the ventricle resulted in the increase of not only glucose, but also glucagon, epinephrine, and norepinephrine in the hepatic venous plasma. However, constant infusion of somatostatin through a femoral vein completely prevented the increase of glucagon after administration of neostigmine, although the increase of hepatic venous glucose and epinephrine levels were still observed. Neostigmine-induced increments in glucose did not occur in adrenalectomized rats. This suggests that the secreted epinephrine acts directly on the liver to increase hepatic glucose output.

Adrenalectomy↗
PubMed1986

Increase in plasma glucose concentration after intracerebroventricular injection of N,O'-dibutyryl cyclic adenosine 3',5'-monophosphate.

The effect of chemical stimulation of the central nervous system was studied in anesthetized rats. (Bu)2 cAMP, cAMP, 5'-adenosine monophosphate (AMP), ATP, and (Bu)2 N6,O2-dibutyryl guanosine-3'5'-cyclic monophosphate sodium salt were injected directly into the third cerebral ventricle, and changes in hepatic venous plasma glucose, immunoreactive glucagon, and insulin concentrations were studied. The injection of (Bu)2cAMP (1 X 10(-8) to 5 X 10(-7) mol/microliter saline) into the third cerebral ventricle caused a dose-dependent hyperglycemia associated with increased immunoreactive glucagon. (Bu)2cAMP-induced hyperglycemia and hyperglucagonemia were inhibited by prior bilateral adrenalectomy. The injection of somatostatin (1 X 10(-9) mol) with (Bu)2cAMP (5 X 10(-7) mol) into the third cerebral ventricle abolished both (Bu)2cAMP-induced hyperglycemia and an increase of glucagon secretion. These results suggest that cAMP may act intracellularly within the central nervous system to increase hepatic glucose output, and this appears to depend on the adrenal gland. Epinephrine secreted from the adrenal gland may directly act on the liver or enhance glucagon secretion, which in turn increases hepatic glucose output.

Adenosine Triphosphate↗
PubMed1986

Determination of safe interval of circulatory arrest from the cerebral metabolic aspect.

To determine the safe interval of hypothermic total circulatory arrest, the cerebral metabolic state was evaluated in 30 dogs. Surface cooling was achieved by deep ether anesthesia and the animals were assigned to three equal groups. Group I: 30 min circulatory arrest and surface rewarming. Group II: 60 min circulatory arrest and surface rewarming. Group III: 60 min circulatory arrest and perfusion rewarming. Brain tissue gas tension was monitored and cerebral O2 consumption was calculated. Cerebral O2 consumption reduced with cooling, parallel to the decrease in cerebral blood flow. Rapid increase in Po2, elevation of PCO2, and decrease of pH in the brain tissue were observed during circulatory arrest. Brain tissue PO2 increased significantly after circulatory arrest in Group I, but it remained low during rewarming in Groups II and III. Cerebral O2 consumption was at reduced levels in all groups during rewarming and it remained at 29% of the precooling control level in Group II at the end of rewarming, whereas it recovered to 71% and 57% of the precooling levels in Groups I and III, respectively. It was estimated that cerebral metabolism may be recovered after 30 min circulatory arrest, despite a transient reduction in cerebral O2 consumption. On the other hand, after 60 min circulatory arrest, the recovery of cerebral metabolism was delayed in Group II and organic failure might have occurred in this group. However, even after circulatory arrest for 60 min, cerebral metabolism was recovered in Group III. The safe period of circulatory arrest is considered to be prolonged by use of extra-corporeal circulation.

Animals↗
PubMed1986

Hypoglycemic activity of MTP-1403 (2-amino-7,8-dihydro-4-piperazinyl-6H-thiopyrano 3,2-d pyrimidine), a new hypoglycemic agent.

2-Amino-7,8-dihydro-4-piperazinyl-6H-thiopyrano 3,2-d pyrimidine (MTP-1403) is a new oral hypoglycemic agent structurally different from any existing hypoglycemic drugs. MTP-1403 lowered fasting plasma level and dose-dependently improved glucose tolerance test without increasing insulin secretory response to glucose. MTP-1403 caused a decrease in fasting plasma glucose level in mild alloxan-induced diabetic rats but not in the rats suffering from ketosis. MTP-1403 markedly improved the oral glucose tolerance test in the genetically diabetic KK mice. These results suggest that hypoglycemic activity of MTP-1403 may be mechanically different from sulfonylureas and biguanides and beneficial to type II diabetics with hyperinsulinemia and insulin resistance.

Animals↗
PubMed1985

Intrasinusal pyelocalicotomy with lower pole nephrotomy for removal of renal stones.

A small renal sinus often limits exposure of the intrarenal pelvis and restrains the sinus approach for removal of renal stones. For 14 such cases, we used a lower pole nephrotomy combined with extended pyelolithotomy. Incision of the renal parenchyma through the intersegmental avascular plane greatly facilitated exposure of the intrarenal collecting system and enabled stone removal through the longitudinal incision of the collecting system. The indication for operative technique and results of the procedure are described.

Humans↗
PubMed1985

Influence of microinjection of insulin into ventromedial hypothalamus on acetate metabolism in liver slices of rabbit.

Insulin was injected directly into the ventromedial hypothalamic nuclei (VMH) of rabbits, and changes in hepatic acetate metabolism were studied. The injection of 50 microU insulin into the VMH of intact rabbits decreased the rates of 14C transfer from 14C-1-acetate into glucose and cholesterol ester in liver slices. But after insulin injection into the parietal cortex of intact rabbits and into the VMH of rabbits with VMH lesions, hepatic acetate metabolism did not differ from that of the control rabbits, which received saline injection into the same brain regions. These observations support the hypothesis that the VMH are parts of an insulin-sensitive brain regulator system in the hepatic acetate metabolism.

Acetates↗
PubMed1985

Central hyperglycaemic effect of adrenaline and carbachol.

The effect of chemical stimulation of the brain on glucoregulation was studied in anaesthetized rats. Adrenaline, noradrenaline, acetylcholine, dopamine and carbachol (5 X 10(-8) mol/microliter saline) were injected directly into the third cerebral ventricle and changes in hepatic venous plasma glucose, immunoreactive glucagon and insulin concentrations were studied. The injection of adrenaline and carbachol into the third cerebral ventricle resulted in a marked hyperglycaemia associated with increased immunoreactive glucagon. Adrenaline-induced hyperglycaemia was not affected by bilateral adrenalectomy, while carbachol-induced hyperglycaemia was completely inhibited by adrenalectomy. The injection of somatostatin (1 X 10(-9) mol) with adrenaline into the third cerebral ventricle did not influence adrenaline-induced hyperglycaemia, while carbachol-induced hyperglycaemia was inhibited by co-administration with somatostatin. These results suggest that adrenergic and cholinergic neurons in the central nervous system may increase hepatic glucose output by different mechanism.

Acetylcholine↗
PubMed1984

The effects of streptozotocin diabetes on tissue specific lipase activities in the rat.

Fasting in normal rats produced a fall in hepatic triglyceride lipase (H-TGL) activity as well as lipoprotein lipase (LPL) activities of adipose tissue and psoas minor muscle. On the other hand, LPL activities of heart and diaphragm were not decreased by fasting; the former, in fact, was increased significantly. Changes in tissue specific lipase activity caused by withdrawal of insulin from insulin-treated diabetic animals paralleled in direction the changes induced by starvation of normal rats. Furthermore, it was shown in the present paper that the tissue specific lipase activity of diabetic rats became stuck in the starve phase of the starve-feed cycle regardless of dietary intake. The changes of the tissue specific lipase activities, especially of liver, adipose tissue and heart, appeared to coincide with those of plasma insulin levels. These results strongly suggest that the tissue specific lipase system is under hormonal regulation by insulin. Streptozotocin diabetes produced hypertriglyceridemia. The possible mechanism of the hypertriglyceridemia in diabetic animals was discussed in connection with the role of the tissue specific lipase system in the serum triglyceride metabolism.

Adipose Tissue↗
PubMed1984

Biochemical determination of training effects using insulin clamp technique.

Tissue sensitivity to insulin was evaluated in 6 trained athletes and 9 untrained controls using the euglycemic insulin clamp technique. The amount of glucose metabolism is a measure of overall tissue sensitivity to insulin. During insulin clamp study comparable plasma glucose (80-90 mg/dl) and insulin (90-100 microU/ml) were achieved in both groups. The glucose infusion rate in the athletes (10.70 +/- 0.32 mg/kg/min) was significantly higher than in the controls (7.37 +/- 0.23 mg/kg/min). During euglycemic hyperinsulinemia plasma FFA decreased by 80% while glycerol showed only a 20% reduction in both groups. Urinary catecholamine concentrations in the athletes were similar to those in the controls, and these levels did not change during the insulin clamp period. From these results, it might be concluded that tissue sensitivity to exogenous insulin is 45% higher in trained athletes and that physical exercise can reduce the insulin requirements in insulin-dependent diabetic patients in addition to being beneficial to noninsulin-dependent diabetics.

Adolescent↗