[Two cases of pulmonary embolism associated with iliac compression syndrome].
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Biomedical subjects
Publications and source records attributed to K Honda.
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We prepared human urinary glycopeptides from the supernatant liquid remaining after precipitation of the nondialyzable fraction with cetylpyridinium chloride. Using cation exchange and affinity chromatographies and gel filtration, we obtained 28 glycopeptide subfractions. By compositional analyses of sugar and amino acid, and by reducing-terminal analyses after reduction with NaBH4, we determined the size of the carbohydrate moiety and the types of carbohydrate-peptide linkage involved. We isolated several glycopeptides not previously described: six with sialic acid, two with fucose, two with glucose, and one with N-acetylgalactosamine. The sialic acid glycopeptides had a short carbohydrate chain of the O-glycoside type. The fucose-containing glycopeptides were fucosyllactosaminoglycans. The glucose glycopeptides were polymers linked to a small peptide moiety. The N-acetylgalactosamine-rich glycopeptide was found in an N-glycoside-type fraction, with N-acetylgalactosamine at the nonreducing terminal.
The hydroxyproline concentration in both the soluble and insoluble material from trichloroacetic acid-treated serum from postpartum mice was determined. The hydroxyproline concentration in the insoluble material increased, but that in the soluble material did not increase during the uterine involuting period.
Upon exposure to heat shock, HeLa cells synthesize a small set of proteins having the molecular weights of 70,000, 73,000, 78,000, 85,000, 92,000, and 105,000. In addition to these proteins, we found an unusual heat shock protein induced by heat shock at 42 degrees C, but not at 45 degrees C. The 42 degrees C-specific protein, the molecular weight of which was 90,000, was not produced in control cells and the induction of the protein was completely inhibited by actinomycin D. The protein was not induced by other treatments that induced most heat shock proteins. Thus, this 42 degrees C-specific protein seems to have a peculiar induction mechanism and a specific function in the cells.
A sensitive and selective method for the simultaneous determination of acetylcholine (ACh) and choline (Ch) is reported. ACh and Ch were separated on a reversed-phase column, passed through an immobilized enzymes (acetylcholine esterase and choline oxidase) column, and converted to hydrogen peroxide. The generated hydrogen peroxide was detected by the peroxyoxalate chemiluminescence reaction. The linear determination ranges were from 10 pmol to 10 nmol. The detection limit for both cholines was 1 pmol.
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An unusual case of pheochromocytoma associated with renal artery stenosis is described. Despite the removal of bilateral adrenal pheochromocytoma, laboratory findings suggested the presence of residual pheochromocytoma and abdominal aortography revealed more pronounced stenosis of the right renal artery. Two months later, the undetected residual pheochromocytoma underwent hemorrhagic necrosis with acute cessation of catecholamine release. Thereafter, the patient's blood pressure decreased to a normal level with marked improvement in hypertensive symptoms. No remaining stenosis was demonstrated on follow up renal angiography. Our case suggests that constant local secretion of catecholamines may be responsible for the development of renal artery stenosis.
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In isolated tracheal muscles of the guinea-pig, effects of several relaxants were studied by simultaneously recording the membrane potential and mechanical response. Intracellular recordings showed regular slow waves in most preparations. There was a close correlation between membrane potential and slow wave amplitude. The linear regression line of the slow wave amplitude (Y mV) on the membrane potential (X mV) could be expressed by Y = -0.35X-5.9. The mean values of resting potential and slow wave amplitude were -50.6 +/- 0.6 mV and 11.9 +/- 0.5 mV, respectively. Relaxant drugs used (isoprenaline, terbutaline, adrenaline, noradrenaline, theophylline, forskolin and dibutyryl cyclic AMP) all produced hyperpolarization of the membrane and abolished the slow wave. The degree of relaxation was closely related to these electrical responses, although the recovery of electrical responses was faster than the mechanical response. It was concluded that the relaxation caused by the agents, which are known to increase the intracellular cyclic AMP level, was accompanied by a clear hyperpolarization and suppression of slow waves.
This report deals with the effect of cholecystokinin octapeptide (CCK-8) on the regulation of the behavior stimulated by dopaminergic drugs. Bilateral injection of CCK-8 (1 microgram per side) into the nucleus caudatus significantly reduced the locomotor hyperactivity induced by methamphetamine. Stereotyped sniffing and yawning occurred after intrastriatal administration of apomorphine (20 micrograms per side). Injections of CCK-8 into the nucleus caudatus completely inhibited the sniffing, but did not affect the yawning induced by apomorphine. It also had no effect on the basal dopamine (DA) level or the methamphetamine-induced DA level in the striatum. These results suggest that the injection of CCK-8 into the nucleus caudatus selectively inhibited the function of the dopaminergic system in the striatum, and blocked post-synaptic DA receptors.
The pharmacological activities of the enantiomers of amosulalol (YM-09538), a combined alpha- and beta-adrenoceptor antagonist, and the corresponding desoxy derivative (YM-11133) were investigated in the cardiovascular system of rats. The optical isomers of amosulalol and YM-11133 antagonized the vasopressor effect of phenylephrine and the positive chronotropic effect of isoproterenol in normotensive pithed rats. Based on DR2 values (micrograms/kg, i.v.) obtained from Schild plots, (+)-amosulalol and YM-11133 (DR2 = 30) were approximately 10 times more potent than (-)-amosulalol (DR2 = 324) in blocking alpha 1-adrenoceptors. For beta 1-adrenoceptors, in contrast, (-)-amosulalol (DR2 = 107) was approximately 60 times more potent than (+)-amosulalol (DR2 = 6460), which was almost equipotent with YM-11133 (DR2 = 3250). The results indicate that the optical isomers of amosulalol interact differently with alpha 1- and beta 1-adrenoceptors. The effects of these phenethylamines on blood pressure and heart rate were studied in urethane-anesthetized rats (i.v.). The rank order of hypotensive potency in anesthetized rats [+)- = desoxy greater than (-)-form) was consistent with the rank order of alpha 1-adrenoceptor antagonism in pithed rats. In contrast, (-)-amosulalol having a more potent beta 1-adrenoceptor antagonist activity than (+)-amosulalol and YM-11133 only produced dose-dependent bradycardia at the hypotensive doses. The results indicate that the vascular alpha 1- and cardiac beta 1-adrenoceptor blocking activities of the optical isomers of amosulalol contribute to their hypotensive and bradycardia, respectively. Thus, the racemate of amosulalol appears to exert an overall activity reflecting the activities of the individual isomers.
Blood levels of oxytocin during parturition in pelvic-neurectomized rats were determined by radioimmunoassay. Four out of 29 pelvic-neurectomized rats completed parturition within 23 days of pregnancy. These rats exhibited an increase in blood levels of oxytocin during parturition similar to those of shamoperated control rats, but delivery took longer and there was a higher percentage of still-births. The rise in blood levels of oxytocin was smaller in the 16 rats in which the first fetus was expelled but where delivery did not end within day 23 of gestation than that in sham-operated controls. Levels did not increase in the other nine rats which failed to deliver the first fetus within 23 days of pregnancy. They did, however, show signs indicating delivery, such as stretch movements, vaginal bleeding and/or excretion of mucus within 23 days of gestation. Oxytocin infusion (2 mu./min) for 2-4 h increased uterine contractions in the pelvic-neurectomized rats but failed to reduce the percentage of still-births or the duration of delivery. Immunoneutralization of circulating oxytocin by anti-oxytocin serum in intact pregnant rats resulted in a significant but much smaller prolongation of the duration of delivery compared with that observed in pelvic-neurectomized rats. The rise in blood levels of oxytocin during pregnancy may be induced, at least in part, by the Ferguson reflex via the pelvic nerve and may thus facilitate the process of delivery. A shortage of oxytocin secretion may not, however, be the main cause of the dystocia in pelvic-neurectomized rats.
The influence of oestrogen on LH and oxytocin responses to immobilization stress, and the involvement of noradrenergic afferent neurones in these responses, was examined in ovariectomized rats with or without pretreatment with oestrogen or after noradrenergic transmitter blockade. Immobilization of the rats on a board in a supine position for 1 h brought about a rapid decrease in LH levels and an increase in oxytocin levels in the blood of ovariectomized rats. Oestradiol benzoate (20 micrograms) injected s.c. the day before immobilization, decreased basal LH levels but had no effect on basal oxytocin levels. Immobilization stress applied to oestrogen-treated rats induced a small but significant increase in LH concentrations and a rise in oxytocin concentrations similar to that in rats without oestrogen pretreatment. A dopamine-beta-hydroxylase inhibitor or phenoxybenzamine (alpha-adrenoceptor blocker) injected into ovariectomized rats reduced basal LH levels and increased basal oxytocin levels in the blood. Immobilization stress induced an increase in LH levels in rats treated with dopamine-beta-hydroxylase inhibitor, but had no effect in rats treated with phenoxybenzamine. Stress induced a larger increase in blood oxytocin levels in rats treated with either drug compared with that in control rats injected with vehicle. On the other hand, propranolol (beta-adrenoceptor blocker) had no effect on basal or stress-induced changes in LH or oxytocin levels in the blood. These results indicate that the LH response to stress, which might be mediated through alpha-adrenergic neurones, depends on the circulating oestrogen or LH levels before the stress. In contrast, the oxytocin response to stress may not be mediated by noradrenergic neurones and may not be influenced by oestrogen.
A detailed secretory profile of oxytocin during suckling and parturition was determined in unanaesthetized freely moving rats. Ten pups were reunited with their mothers after 12-15 h of separation. Unless the milk-ejection reflex occurred, there was no difference in serum oxytocin levels before separation and during the suckling of either four or five, or nine or ten pups. Serum oxytocin levels increased abruptly by 50.1 +/- 4.2 (S.E.M.) pmol/l (n = 9) at milk ejection, and declined rapidly with a half-life of about 1.5 min. The peak concentration of blood oxytocin at each milk ejection was independent of the previous suckling period; values from the first three milk-ejection reflexes following the introduction of the pups and those observed 3-5 h after introduction were similar. The process of parturition was monitored by recording intra-uterine pressure with a balloon implanted in the uterus. On day 22 or 23 of pregnancy, continuous and rhythmical contractions of the uterus occurred (onset of parturition), but serum levels of oxytocin (21.1 +/- 1.9 pmol/l; n = 13) did not alter until the expulsive phase. During the expulsive phase, fetuses were delivered after fetus-expulsion reflexes which were recorded as sudden large increases in intra-uterine pressure. Basal levels of oxytocin in the blood increased during this phase (32.5 +/- 4.4 pmol/l; n = 13) and, in addition, rose by about 15 pmol/l and declined slowly after fetus-expulsion reflexes. The increase, however, was quite different from that seen at milk-ejection reflexes.
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