Biomedical subjects
Publications and source records attributed to F Goto.
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Highly pure polymorphonuclear leucocytes (PMN) were prepared from peritoneal exudate cells which were induced by an i.p. injection of casein into C3H mice and rabbits. The PMN were tested for the production of a lymphocyte proliferation potentiating factor with various stimulations in vitro. In both animal species, the purified PMN from the inflammatory site 3 hr after injection (3-hr PMN) produced the factor upon stimulation with kaolin, while the purified PMN from the lesion 24 hr after injection (24-hr PMN) did not. The 3-hr PMN produced the potentiating factor during a relatively earlier period after in vitro stimulation with kaolin. Protein synthesis inhibitors did not inhibit the factor production, suggesting the release of a preformed factor from 3-hr PMN. The effect of kaolin did not appear to be simply due to its cytotoxicity, because the release was dependent on the metabolism of 3-hr PMN and not parallel with 51Cr-release from the PMN. The factor produced by mouse PMN had an MW of about 15,000-25,000; it consisted of two isoelectrophoretically distinct factors, i.e. pI 9.4 and 5.4. The rabbit PMN factor was slightly smaller (MW ranging between 10,000 and 20,000) than the mouse PMN factor and was composed of three pI species, i.e. 7.2, 5.4, and 4.5.
Basic pharmacologic evidences have suggested the effects of dihydroergotoxine mesylate (DEM) on neurotransmitters. In its clinical use, however, various therapeutic effects and side effects are observed when the dose is changed, because of the complexity of this compound and the delicate mechanism of neurotransmitters in the brain, especially when modified by aging and vascular lesions. In order to investigate the optimal dose, a double-blind study in 550 patients with cerebrovascular disorders was carried out at 68 centers under observation by experienced specialists. Dihydroergotoxine mesylate in sublingual tablets, 3 mg daily, and in oral tablets, 6 mg daily, respectively, was given for 12 weeks, and therapeutic effects at those doses were compared by a double-blind method. In utility ratings for subjective and psychiatric symptoms, the effects in the oral tablet group at a daily dose of 6 mg were significantly superior to those in sublingual tablet group at a daily dose of 3 mg. There was no significant difference between those two groups in the comparison of side effects. These results show that the daily oral administration of 6 mg of DEM is more suitable for the improvement of subjective and psychiatric symptoms due to cerebrovascular disorders than is the daily sublingual administration of 3 mg. These results suggest that, despite much complexity in the neurohumoral transmitter mechanism in the brain, relatively simple dose-dependent efficacy of the drug in the range of the therapeutic doses was confirmed for many subjective and psychiatric symptoms of patients with cerebrovascular disorders.
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Hypotension induced by prostaglandin E1 (PGE1) infusion (100-150 ng/kg/minute) during halothane anaesthesia to reduce operative blood loss during mastectomy was investigated. PGE1 decreased systolic arterial pressure approximately 34% from pre-administration values. The duration of induced hypotension was about 75 minutes. When the infusion was stopped, blood pressure returned to within 15% of the control with 15 minutes. Heart rate did not change significantly during PGE1 infusion; the pre-ejection period and left ventricular ejection period were shortened. Renal function during the hypotensive period was well maintained. Blood loss during surgery was significantly decreased. These findings suggest that PGE1 can be used safely to control arterial pressure during surgery.
The effect of indomethacin, a prostaglandin (PG) synthetase inhibitor, on renal function was studied, and the relationship between PGE2 excretion in urine and renal function in laparotomized female patients was clarified. The PGE2 excretion rate significantly increased from 16.6 +/- 5.7 to 25.9 +/- 4.8 ng/h during surgery. This rate remained high during recovery. In patients who received 2 mg/kg of indomethacin (rectally) for postoperative analgesia following surgery, urine flow decreased from 67.8 +/- 5.4 to 42.2 +/- 6.4 ml/h 3.5-4.5 h. Para-aminohippurate clearance and creatinine clearance did not change following administration of indomethacin; however, sodium fractional excretion (FE Na) decreased significantly concomitant with depression of PGE2 excretion from 37.0 +/- 4.7 to 10.9 +/- 3.2 ng/h 3.5-4.5 h. This change in PGE2 excretion and FE Na was closely correlated (Y = 0.87 X + 13.8, r = 0.75, P less than 0.01). Plasma aldosterone levels did not change significantly after administration of indomethacin. These results suggest that PGE2 in the kidney contributes to the maintenance of sodium excretion in the post-operative period in surgical patients.
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Effects of gaseous nitrogen dioxide (NO2) on chromosomal morphology of cultured Chinese hamster V79-H3 cells were investigated. Chinese hamster cells were exposed to NO2 gas in N2 gas at NO2 concentrations of 0, 5, 10, 20, 50 and 100 ppm (v/v) for 10 min at a gas flow rate of 1000 ml/min. Both chromosomal aberrations and sister-chromatid exchanges were increased depending on the NO2 concentration. The effects of sodium nitrite (NaNO2) were also examined in comparison with those of gaseous NO2, and it was found that the effects of gaseous NO2 could not be ascribed to those of nitrous acid. The gas-exposure apparatus used in this experiments seems to be useful for quantitative investigation of the effects of various gaseous materials on cultured mammalian cells or bacterial cells.
The effect of indomethacin, a prostaglandin (PG) synthesis inhibitor, on the hemodynamics and survival rates of Escherichia coli endotoxin-administered animals (dog and Rat) was studied. Indomethacin post-treatment significantly elevated aortic pressure, cardiac output, and left ventricular isometric tension elevated aortic pressure, cardiac output, and left ventricular isometric tension rise (LVP dp/dt max) following endotoxin administration in the dog. In dogs in a hyperdynamic state due to indomethacin administration treated with phenoxybenzamine (COB) and alprenolol, aortic pressure and cardiac output fell to pre-indomethacin administration values. In reserpine-administered and bilaterally adrenalectomized dogs, hemodynamic states were not altered by indomethacin administration during endotoxin shock. These results suggest that indomethacin potentiates the responses of catecholamines induced by endotoxin shock. Pretreatment with indomethacin alone did not increase the survival rates in endotoxin-administered rats. However, pretreatment and posttreatment with indomethacin combined with POB significantly increased the survival rate over untreated controls (LD 80) given endotoxin alone. Cyclic adenosine monophosphate (cAMP) levels in liver tissue decreased significantly in untreated controls and rats pretreated with indomethacin alone. In contrast, tissue cAMP levels remained within normal values in rats pretreated with indomethacin combined with POB. These results indicate that indomethacin may make a significant contribution as an antishock agent when peripheral circulation is maintained.
The DNA synthesis potentiation of a mouse polymorphonuclear leukocyte (PMN) factor was studied by using phytohemagglutinin (PHA)-stimulated syngeneic thymocytes. The partially purified PMN factor was nonmitogenic and exhibited maximum potentiation of thymocytes when added within 3 hr of PHA stimulation. PHA-stimulated, but not nonstimulated thymocytes absorbed PMN potentiation factor. 125I-labeled factor binding to stimulated thymocytes was observed. Our results suggest that an acceptor site for PMN factor may be generated on the thymocyte surface only after PHA stimulation.
The effects of dopamine 0.5--6.0 microgram kg-1 min-1 on urine flow and the excretion of sodium and inorganic phosphate were studied in patients and dogs. In both the patients and the animals the diuretic effect of dopamine was augmented by the i.v. administration of droperidol 0.25 mg kg-1. Similarly, the excretion of sodium and inorganic phosphate was increased by droperidol.
With dopamine (0.5 microgram/kg/min) infusion into the renal artery of thyroparathyroidectomized dogs, urine output and inorganic phosphate excretion increased significantly (p less than 0.05), but the increase in sodium excretion was low and not statistically significant. However, natriuresis and phosphaturia due to the infusion of dopamine were accelerated more markedly by the pretreatment with phenoxybenzamine. Dopamine was infused into the renal artery indoses too small to affect renal hemodynamics (0.02-0.05 microgram/kg/min) after the treatment with phenoxybenzamine and alprenolol with the result that phosphate and sodium excretion increased significantly (p less than 0.05). The excretion rate of cAMP did not change. This suggests that the effect of dopamine on sodium and phosphate excretion is directly influenced by alpha adrenergic activity in the kidney. The mechanism of natriuresis and phosphaturia by dopamine is, however, independent of changes in parathyroid hormone and the adenyl cyclase-cAMP system.
Ninety-one patients suffering from idiopathic sudden hearing loss are presented. Twenty-two patients were given medical treatment (vasodilators, steroid hormones and vitamins) alone (group 1). Forty-nine patients were treated with stellate ganglion block (SGB) plus oxygen hyperbaric therapy (OHP) (group 2) and 20 patients were treated with SGB plus OHP along with medical treatment (group 3). The SGB plus OHP treated patients were given bupivacaine, which induced Moor's anterior approach of SGB and then exposed to oxygen at a pressure of 2.4 ATA for 90 min. In group 1, 69% of the patients treated within one week after onset exhibited over 10 dB pure tone average improvement, with only 33% patients treated one to two weeks after onset experiencing over 10 dB. However, 74% of the patients in group 2 and 100% of the patients in group 3 who were treated within two weeks after onset exhibited over 10 dB improvement. More significantly, of the patients which experienced complete loss of hearing, 83% in group 2 and 100% in group 3, exhibited over 10 dB improvement, compared to only 33% in group 1. Moreover, 8 (40%) patients in group 3 recovered to within 20 dB of their normal hearing levels. In group 2, 17 patients were treated two to six weeks after onset and 12 (71%) patients had over 10 dB improvement. SGB plus OHP therapy was shown effective in the treatment of sudden idiopathic hearing loss even when patients were treated more than two weeks after onset.
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