Biomedical subjects
Publications and source records attributed to K Tsuruta.
Posterior tibial somatosensory evoked potentials were recorded from 10 patients with Duchenne-type progressive muscular dystrophy (DMD). The results of the patients were compared with age-matched controls. The ratio of height to latency (H/P38 and H/N22-P38) decreased significantly in DMD, which indicated central conduction disturbances in DMD.
A 22-year-old man was hospitalized because of hypertension, hypokalemic alkalosis and suppressed plasma renin activity. Although these findings were similar to hyperaldosteronism, plasma aldosterone concentration and urinary aldosterone excretion were lower than the normal range. Adrenocortical function also was normal except for aldosterone. Treatment with spironolactone, salt restriction and potassium supplementation improved the hypokalemia but not the hypertension. Blood pressure decreased markedly after administration of triamterene.
A case of a 68-year-old female patient with hypokalemic myopathy is presented. Her persistent diarrhea due to radiation enteropathy with a total dose of 8,400 rad for the treatment of cervical cancer caused potassium loss in the stool. It finally induced generalized muscle weakness with hypokalemia as low as 1.6 mEq/l with elevated CK 3,845 IU/l. The muscle biopsy of the left vastus lateralis demonstrated typical findings of hypokalemic myopathy. Radiation to the pelvic space can cause damage of the terminal ileum. Hypokalemic myopathy associated with radiation enteropathy is very rare in the literature.
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The present study was undertaken to determine the influence of indomethacin, a potent inhibitor of prostaglandin synthetase, on the intrauterine fetal growth of rats. All experimental rats administered indomethacin on various days of gestation were sacrificed on day 22 of gestation. The following results were obtained. The intrauterine fetal growth retardation (IUGR) and maternal weight loss were found following intramuscular administration of indomethacin 2mg on day 19 of gestation. IUGR and maternal weight loss were also found after fasting from day 19 of gestation to day 22. IUGR was induced by the administration of indomethacin on days 15 to 21 of gestation, while not by that on day 10. The mean fetal weight of rats which received indomethacin on day 19 of gestation was 3.57 +/- 0.44g, which was as low as 67.9% of normal fetal weight. There seemed to be a critical period for the occurrence of IUGR in rat due to indomethacin. The possible jeopardy of fetal development due to the administration of indomethacin to pregnant women in the late pregnancy should be warned against.
The effects of intra-aortic administrations of prostaglandin (PG) E2 and I2 on the renal regional blood flow were investigated in rabbits. Mean arterial blood pressure (MABP) was monitored by the direct method and total renal blood flow (TRBF) was measured using the electromagnetic method. Renal cortical and medullary blood flows (RCBF and RMBF) were measured by the hydrogen gas clearance method. Both PGE2 and PGI2 caused a dose-dependent reduction of MABP. At doses having no significant effect on MABP, PGE2, and PGI2 increased TRBF and decreased renal vascular resistance (RVR). The maximum reduction in RVR induced by PGI2 was significantly greater than that by PGE2. PGE2, produced significant increases in RCBF and in particular in RMBF, while PGI2 induced similar changes in RCBF and RMBF. The results suggest that PGE2, which is a weaker vasodilator than PGI2, mainly acts as a medullary vasodilator, and that PGI2 has similar vasodilatory effects on the cortex and medulla.
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Sensory and autonomic polyneuropathy is a rare disease characterized by a sensory nerve disorder and postganglionic autonomic dysfunction. The etiology of this disease is unknown. We described a 51-year-old woman who had a chronic sensory dominant polyneuropathy and dysautonomia associated with hypergammaglobulinemia. In the previous reports of sensory and autonomic polyneuropathy, not much attention was given to coexisting hypergammaglobulinemia. By reviewing the literatures, hypergammaglobulinemia was frequently present in these case reports. This fact leads us to consider that an immunological mechanism may be playing a role in the pathogenesis of this disorder.
A rare case of solitary neurofibroma located in the esophagus is reported. A large (4.2 X 4.0 X 3.0 cm) submucosal tumor was surgically removed from the midportion of the esophagus of a 64-year-old woman. Light and electron microscopic examination, and immunohistochemistry of S-100 protein in the tumor tissue confirmed neurofibroma. The patient had no evidence of von Recklinghausen's neurofibromatosis. A review of literature failed to find other reports of solitary neurofibroma of the esophagus with reliable histological diagnosis.
The high activity of 15-hydroxyprostaglandin dehydrogenase (PGDH) which catalyzes the first step in prostaglandin metabolism has been demonstrated in the human placenta. To investigate the role of placental PGDH (p-PGDH) in the perinatal period, PGDH activity was measured in 167 placentas of gestational ages 37 to 41 weeks. The activity was expressed as n mole/min/non heme protein of 15-keto-PGE2 which was produced by incubation of PGE2 and placental homogenate supernatant. The following data were obtained. p-PGDH activity was significantly lower at the 40 weeks of gestation than at other weeks. There was no difference in placental PGDH activity between cesarean section and vaginal delivery, and between the periods before and after onset labor of cesarean section. p-PGDH activity in the PGs administered group was higher than that in the non PGs group. p-PGDH activity of a male fetus was higher than that of a female. This suggests that p-PGDH activity is under the control of hormones. No relationship was observed between p-PGDH activity and other perinatal factors such as toxemia of pregnancy, parity, Apgar score, birth weight, placental weight, blood loss, and duration of labor.
The intermediate lobe (IL) of the rat pituitary gland responds to catecholamines. Catecholamines interacting with the beta-adrenoceptor stimulate adenylate cyclase activity, enhance cyclic AMP formation and thereby trigger the release of alpha-melanocyte-stimulating hormone (alpha-MSH). Catecholamines interacting with a D-2 dopamine receptor (in the classification schema of Kebabian and Calne) diminish adenylate cyclase activity and thereby decrease the capacity of IL cells to synthesize cyclic AMP. Dopaminergic agonists also inhibit the release of alpha-MSH from IL cells. The homogeneity of the IL facilitates biochemical investigations of this tissue.
After treatment with cholera toxin, homogenates of intact intermediate lobe (IL) tissue of rat pituitary gland synthesized more cAMP than did homogenates of untreated IL tissue, and only in the presence of GTP did dopamine or apomorphine diminish the elevated adenylate cyclase activity in homogenates of cholera toxin-treated IL tissue. Furthermore, when tested on cholera toxin-treated IL tissue, 5'-guanylyl imidodiphosphate [Gpp(NH)p] and two other nonhydrolyzable analogs of GTP inhibited adenylate cyclase activity in the absence of either a dopaminergic agonist or GTP; GTP reversed the Gpp(NH)p-induced inhibition of adenylate cyclase activity. Apomorphine, a dopaminergic agonist, abolished the ability of GTP to reverse the inhibition by Gpp(NH)p; this effect of apomorphine was prevented by fluphenazine, a dopaminergic antagonist. Sodium fluoride inhibited adenylate cyclase activity to approximately the same level obtained with GTP and apomorphine. In addition, apomorphine decreased cAMP accumulation and alpha MSH release from dispersed IL cells pretreated with cholera toxin.
Stimulation of the release of alpha MSH from dispersed rat melanotrophs by L-isoproterenol, 8-bromo-cAMP, or cholera toxin requires calcium ion (Ca++) in the incubation medium; the stimulatory effect of each of these agents is attenuated by D-600, a Ca++ antagonist. In contrast, stimulation of the formation of cAMP by L-isoproterenol, isobutyl methylxanthine, or cholera toxin does not require Ca++ in the incubation medium. Ca++ diminishes the amount of cAMP formed by cholera toxin-treated melanotrophs. Ca++ inhibits adenylate cyclase activity and enhances cyclic nucleotide phosphodiesterase activity in cell-free homogenates of intermediate lobe tissue. A23187, a calcium ionophore, increases the accumulation of 45Ca by melanotrophs and enhances the release of alpha MSH. Furthermore, when tested upon cholera toxin-treated melanotrophs, A23187 potentiates the Ca++-induced inhibition of cAMP formation. The results indicate that Ca++ is essential for the release of alpha MSH, and that cAMP in some way enhances the effects of Ca++ upon the release process.
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To study the role of renal prostaglandins (PGs) in renovascular hypertension, PGE2 and PGF2 alpha concentrations in both inner and outer medullae of the kidney were measured by radioimmunoassay in rabbits with hypertension produced by left renal artery constriction. In the acute phase, a week after surgery, PGE2 in the inner and outer medullae and PGF2 alpha in the inner medulla were significantly increased in both the constricted and opposite kidneys (p less than 0.01). In chronic phase, 5 weeks after surgery, PGs returned to normal concentrations with the exceptions of PGE2 in the outer medulla and PGF2 alpha in the inner medulla of the constricted kidney. These results suggest that increased renal PGs may not be the cause of hypertension but a defensive reaction to renal ischemia, hypertension and sodium load.
The dopamine receptor in the intermediate lobe (IL) of the hypophysis of the rat is characterized on the basis of the ability of dopamine and other dopaminergic agonists to decrease the consequences of activation of the beta-adrenoceptor. Stimulation of the dopamine receptor diminishes the L-isoproterenol-induced accumulation of cAMP and the catecholamine-stimulated enhancement of adenylate cyclase activity. The dopamine receptor in the IL can be assigned to the category of dopamine receptor designated D-2 on the basis of the following criteria: 1) occupancy of the dopamine receptor does not result in enhancement of adenylate cyclase activity or an accumulation of cAMP, 2) the dopaminergic ergots and apomorphine mimic the inhibitory effect of dopamine upon cAMP formation or alpha MSH release, and 3) metoclopramide and sulpiride, substituted benzamides, block the inhibitory effect of dopamine. The sympathetic neurotransmitter, norepinephrine, interacts with the dopamine receptor and the beta-adrenoceptor in the IL.