[A comparative study of the accuracy in locating adrenal lesions between CT, adrenal imaging and angiography].
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Biomedical subjects
Publications and source records attributed to K Ohkubo.
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A 54-year-old man had a leiomyosarcoma of the jejunum, 8 X 6 X 5 cm in size resected, on December 17, 1982 and died of liver metastases with hemorrhagic ascites (4,000 ml) on July 5, 1984. The malignant potential of a smooth muscle tumor based on the mitotic index of tumor cells has been stressed for many years. However, our biologically malignant autopsy case showed not only an exceptionally low mitotic index in tumor cells of the surgical specimen but also in those of the autopsy specimen. In this report, the fact that the degree of mitotic figures sometimes fail to indicate biological behavior is discussed.
The participation of central noradrenergic neurons in the pressor responses to intracerebroventricular (i.c.v.) administration of prostaglandin (PG) E2 was studied in anaesthetized rabbits. The hypertensive effect induced by i.c.v. injection of PGE2 was inhibited by i.c.v. pretreatment with 6-hydroxydopamine and phentolamine, but not propranolol. These findings suggest that the cerebral noradrenergic neurons may be involved in the development of hypertensive effect of PGE2 through the adrenergic alpha-receptors.
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The effects of dl-erythro-4-benzyl-alpha-(4-hydroxyphenyl)-beta-methyl-l-piperidine-eth anol tartrate (ifenprodil tartrate) on rabbit platelet aggregation in vitro and ex vivo were studied. Ifenprodil tartrate inhibited platelet aggregation in vitro induced by ADP, collagen and epinephrine. It also inhibited 5-hydroxytryptamine (5-HT) uptake into platelets and 5-HT release from platelets. Since these inhibitory effects of ifenprodil tartrate on the functions of rabbit platelets were similar to the effects of imipramine, the effects of ifenprodil tartrate may be due to the stabilizing action of ifenprodil tartrate on the platelet membrane. The platelet aggregation by ADP was significantly inhibited in rabbits after oral administration of ifenprodil tartrate, the maximal plasma level of ifenprodil being reached at 20 ng/ml ex vivo, while the maximal level was only 1/40 of the minimal concentration of ifenprodil tartrate necessary to inhibit platelet aggregation in vitro. These results indicate that factors other than ifenprodil tartrate acting directly on the platelets (e.g., PGI2 which is an endogenous inhibitor of platelet aggregation) are involved in inducing the inhibitory effects of ifenprodil tartrate on platelet aggregation ex vivo. The effects of ifenprodil tartrate on both PGI2 release from the aorta and the inhibitory effects of PGI2 on platelet aggregation in vitro were investigated: PGI2 was found to intensify the inhibitory effects of ifenprodil tartrate on platelet aggregation in vitro, but there was little effect, if any, on PGI2 release. Therefore, it is considered that the ex vivo effects of ifenprodil tartrate might be due to its interaction with endogenous PGI2 in the blood.
Effects of choline salicylate, sodium salicylate, choline chloride and acetylsalicylic acid on platelet aggregation in vivo, ex vivo and in vitro in mice were studied. These drugs all inhibited adenosine diphosphate (ADP)-induced respiratory depression, which is closely related to platelet aggregation in vivo, with choline salicylate showing the strongest inhibitory effect. Choline salicylate had a tendency to reduce the mortality of animals injected intravenously with endotoxin, but the other drugs had no such effect. The inhibitory effects of these drugs on ADP-induced platelet aggregation ex vivo were in the order of choline salicylate greater than acetylsalicylic acid congruent to sodium salicylate greater than choline chloride congruent to no effect, and plasma concentrations of protein-unbound salicylic acid at 1 hr after oral administration of drugs were in the order of choline salicylate greater than acetylsalicylic acid congruent to sodium salicylate. The in vitro effects of these drugs were in the order of choline salicylate congruent to sodium salicylate greater than choline chloride congruent to acetylsalicylic acid congruent to no effect. Therefore, it was considered that salicylic acid played an important role on the in vivo, ex vivo and in vitro effects of choline salicylate and that choline increased plasma concentrations of salicylic acid and consequently enhanced the in vivo and ex vivo effects of salicylic acid. Furthermore, the ex vivo effects of choline salicylate were found when ADP-induced platelet aggregation was measured with platelet-rich plasma prepared from blood collected with heparin as anti-coagulant, but not when blood was collected with citrate.(ABSTRACT TRUNCATED AT 250 WORDS)
In anesthetized rabbits, intracerebroventricular (ICV) administration of the alpha-adrenoceptor agonist, guanfacine, like clonidine, elicited dose-related falls in arterial blood pressure and heart rate. ICV pretreatment with the histamine H2-receptor antagonist, metiamide, significantly reduced the hypotensive and bradycardic responses caused by ICV injection of either guanfacine or clonidine. The present results seem to indicate that the antagonistic effect of metiamide against either guanfacine or clonidine is probably due to its alpha-adrenoceptor blocking action rather than its histamine H2-receptor blocking action, suggesting that these interactions might be of central origin.
Definite ultrastructural changes of the neuromuscular receptor organs were demonstrated in the young and adult rat masseter muscles either on the operated or unoperated side following the unilateral transection of the infraorbital nerve. The grade of the degeneration was intensive but quite similar in having no relation to the age of the rat when the operation was performed, while it increased drastically with time after the operation. On this base, it may be suggested that the sensory input coming from the various kinds of sensory receptors in the snout field do rather affect bilaterally the minor reflexive movements of the jaw. In other words, it can be said that the minor reflexive movements of the jaw might have been controlled by the sensory inputs coming from the snout sensory receptor organs. The definitely degenerated changes of the neuromuscular receptor organs in the masseter muscles should be regarded as disuse atrophy following the interception of the snout sensory input.
The effect of fourteen plant lectins on human peripheral blood lymphocytes in rosette formation with sheep red blood cells (SRBC) was examined. Among the lectins used, phytohemagglutinin (PHA), lens culinalis (LCH), wheat germ agglutinin (WGA), and ricinus communis I (RCAI) showed a significant increase in active T rosette counts when the results were compared with the effect of other lectins. This enhancement in active T rosette forming cells is found within one hour after the treatment with lectin and is dependent upon the concentration of lectin. The results suggest that the changes in lymphocyte membrane dynamics via stimulation by certain lectins increases the capacity to form active T rosettes.
The effect of various cellular metabolic inhibitors on the active T rosette formation of human peripheral blood lymphocytes with sheep red blood cells (SRBC) was studied. Cytochalasin B greatly inhibited SRBC rosette formation. However, colchicine, mytomycin C, cyclohexamide, and sodium azide had no effect. These results suggest that the ability of the lymphocyte to form active T rosettes is dependent on the lattice microfilament network, but not on the cellular metabolism. The effect of cytochalasin B on human peripheral blood lymphocytes activated by phytohemagglutinin (PHA), wheat germ agglutinin (WGA), lens culinalis (LCH), or ricinus communis agglutinin I (RCAI) was also examined. Cytochalasin B significantly inhibited the active T rosette formation induced by LCH or RCAI, but did not inhibit that induced by PHA or WGA. This suggests that different cellular mechanisms are involved in the activation of lymphocytes by either PHA and WGA or LCH and RCAI.
Penetrating keratoplasty combined lens extraction was employed in 4 cases at the Department of Ophthalmology Hospital, University of Occupational and Environmental Health from January 1981 through May 1983. The visual acuity of the treated eye in all of the four cases has improved from before surgery. The operative procedure employed in our cases was very effective in preventing complications that might occur during and after surgery. We performed the extracapsular lens extraction by using the open sky method and A/I tip under a surgical microscope without difficulty. We concluded that the keratoplasty combined with extracapsular lens extraction can be safely and reliably performed by employing the above method and that it is a very effective and useful operation in cases of which visual impairment is due to corneal opacity and cataracts.
A seven-year-old case with chronic dacryocystitis resulting from congenital obstruction of the nasolacrimal duct was cured not by a dacryocystorhinostomy but by probing of the duct. Our results show that even in case of planned dacryocystorhinostomy, probing of the duct should be performed at least once.
A method for monitoring ADP-induced thromboembolism in mice by means of the measurement of respiratory rate and depth was studied. The measurement were accurately carried out with a new method devised by us. In mice intravenously injected with 5-40 mg ADP/kg, it was found that the respiratory rate decreased transiently and dose-responsively, and that the platelet count also decreased transiently. On the other hand, no decrease in respiratory rate after administration of ADP was observed in neuraminidase-pretreated mice, in which the platelet count was significantly reduced. In the histological examination, platelet thrombi formed in the pulmonary vessels were observed 10 sec after administration of 10 and 40 mg/kg of ADP in mice which had not been treated with neuraminidase. The extent of thromboembolism at the dose of 40 mg/kg showed a tendency to be more marked than that at 10 mg/kg. Pretreatment with 300 mg dipyridamole/kg p.o. prevented the respiratory depression at 40 mg ADP/kg. However, with 10 mg dimorpholamine/kg i.v. or 30 mg warfarin/kg p.o., no preventive effect was observed. Therefore, it was concluded that it is possible to monitor ADP-induced thromboembolism in mice by means of the accurate measurement of the respiratory rate and depth.
A highly sensitive apparatus and method for measuring respiratory changes in conscious mice and rats is described. The apparatus is constructed from readily available components and consists of three sections: 1) mouse housing capsule and respiratory-sensitive part; 2) air supplying part; and 3) data recording part. Changes in the respiration of an encapsuled mouse can be accurately detected by means of changes in pressure exerted on the respiratory-sensitive part attached to the capsule. In our study, the rapid increases and decreases in the respiratory rates of these animals after the i.v. administration of respiratory depressing agents (morphine and arachidonate) and a respiratory stimulant (dimorpholamine) were recorded with exceptional accuracy by this procedure.
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Experiments were carried out in the blood-perfused canine papillary muscle preparation to evaluate the protective effect of a cardioplegic solution, Young's solution (YNG solution), on the myocardial function. Both in spontaneously contracting preparations and in electrically paced (2 Hz) preparations, the time to the cardiac arrest and the time to the maximum blood flow were found to be significantly shorter when the cardiac arrest was induced with cardioplegic solutions than when it was induced with the cold modified Krebs-Ringer's solution (cold cardioplegia). The maximum blood flow of the paced preparation tended to be greater with cardioplegic solutions. The time to resumption of regular contractions was significantly shorter with YNG solution as compared with cold cardioplegia. The developed tension and the blood flow at the time of resumption of the regular contractions tended to approach the control value more quickly with YNG solution, as compared with other cardioplegic solutions and cold cardioplegia. It is concluded that YNG solution represents an optimal cardioplegic solution.
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