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M Sakata

Publications and source records attributed to M Sakata.

At least 199 records · Page 11Linked to original sources
PubMed1988

Placental anticoagulant proteins: isolation and comparative characterization four members of the lipocortin family.

Previously we isolated and characterized a placental anticoagulant protein (PAP or PAP-I), which is a Ca2+-dependent phospholipid binding protein [Funakoshi et al. (1987) Biochemistry 26, 5572] and a member of the lipocortin family [Funakoshi et al. (1987) Biochemistry 26, 8087]. In this study, three additional anticoagulant proteins (PAP-II, PAP-III, and PAP-IV) were simultaneously isolated from human placental homogenates prepared in the presence of 5 mM ethylenediaminetetraacetic acid. The isoelectric points of PAP-I, PAP-II, PAP-III, and PAP-IV were 4.8, 6.1, 5.9, and 8.1, respectively, and their apparent molecular weights were 32,000, 33,000, 34,000, and 34,500, respectively. Amino acid sequences of cyanogen bromide fragments of these proteins showed that PAP-III was a previously unrecognized member of the lipocortin family, while PAP-II was probably the human homologue of porcine protein II and PAP-IV was a derivative of lipocortin II truncated near the amino terminus. Comparative studies showed that all four proteins inhibited blood clotting and phospholipase A2 activity with potencies consistent with their measured relative affinities for anionic phospholipid vesicles. However, PAP-IV bound to phospholipid vesicles approximately 160-fold more weakly than PAP-I, while PAP-II and PAP-III bound only 2-fold and 3-fold more weakly. These results increase to six the number of lipocortin-like proteins known to exist in human placenta. The observed differences in phospholipid binding may indicate functional differences among the members of the lipocortin family despite their considerable structural similarities.

Amino Acid Sequence↗
PubMed1988

Distribution of lidocaine and disopyramide in human blood and tissue, a case report of death caused by spinal anesthesia.

An 11-year-old girl was anesthetized with hyper-baric solution of lidocaine as spinal anesthesia for an appendectomy in a surgical clinic. Respiratory arrest which occurred soon after the injection, was not discovered for a period of time. Since spontaneous respiration recovered within 2 h of intensive resuscitation, the patient was transferred to a community hospital for intensive care. Ten hours after the spinal anesthesia, she died of cardiac failure. The concentration of lidocaine in the brain was 5-10 times more than that in other tissues. The relationship between the possibility of malpractice of spinal anesthesia and tissue distribution of the drug was discussed. In addition to lidocaine, a toxic amount of disopyramide, an antiarrhythmic drug, was detected in the body. The distribution of disopyramide was also estimated, and the pharmacokinetics of disopyramide in plasma and tissues were studied experimentally in rats.

Anesthesia, Spinal↗
PubMed1988

Paradoxical relationship between atriopeptin plasma levels and diuresis-natriuresis induced by acute volume expansion.

Surgical removal of one or both atrial appendages was employed in rats to reduce the intrinsic stores of atriopeptin (AP). In conscious rats (with intact baroreceptor reflexes), bilateral or unilateral atrial appendectomy suppressed the diuresis and natriuresis produced by acute volume expansion. Surprisingly, volume expansion (with 4% bovine serum albumin in saline at 1.5 ml/kg per min for 15 min) did not result in an increase in plasma AP immunoreactivity (APir) in control or atrial-appendectomized conscious rats. Previous studies demonstrated that acute volume expansion in anesthetized animals caused increased plasma APir. Indeed, we found that volume expansion causes comparable diuresis-natriuresis in conscious and chloral hydrate-anesthetized rats, but only the latter group exhibits an increase in plasma APir. Brattleboro rats, which are deficient in vasopressin, exhibit the same response as Long-Evans controls in that acute volume expansion in conscious animals produces a pronounced diuresis and natriuresis but no APir release, but when these same animals are anesthetized, there is a simultaneous induction of diuresis-natriuresis and APir release by volume expansion. Plasma AP does not increase in conscious rats despite a large volume load, 30-40% of the total blood volume given in 15 min, and the natriuresis-diuresis appears to also be independent of vasopressin. On the other hand, the diuresis induced by acute volume expansion in anesthetized rats seems dependent on the elevated APir, since rats made autoimmune to AP (which are nonresponsive to exogenous AP infusions) exhibit a diuresis in conscious but not anesthetized rats. We therefore conclude that the participation of AP in volume homeostasis is more likely in pathophysiological states and that another mechanism or possibly another atrial factor mediates the diuresis-natriuresis induced by volume expansion in conscious rats.

Anesthesia↗
PubMed1988

Is atriopeptin a physiological or pathophysiological substance? Studies in the autoimmune rat.

Atriopeptin (AP), a natriuretic-diuretic and vasodilatory peptide, is synthesized and secreted from mammalian atria. The definitive role of this peptide on cardiovascular physiology and pathophysiology has yet to be determined. We developed a population of autoimmune rats sensitized against their own AP to evaluate the consequences of prolonged AP deficiency on physiological and pathophysiological processes. Natriuresis in response to acute intravenous volume expansion was inhibited in the autoimmune rat, however, natriuresis produced by chronic oral salt loading was not suppressed in these animals. Plasma AP increased threefold in the spontaneously hypertensive rat when evaluated as a function of blood pressure. Immunization of these rats had no effect on the rate of development, magnitude of their developing hypertension, or their daily sodium excretion when compared with nonimmunized controls. Mineralocorticoid escape occurred during desoxycorticosterone acetate administration to rats. The ability of rats to escape from the sodium-retaining effects of this steroid was not affected by prior immunization against AP. These results suggest that AP is an important natriuretic substance in response to acute intravascular volume loading. However, atriopeptin does not appear to be involved in the natriuretic response to chronic intravascular volume loading, blood pressure regulation, or mineralocorticoid escape.

Animals↗
PubMed1987

Toxicity of D, L-mandelonitrile-beta-D-glucoside, "prulaurasin" in rat.

Toxicity of cyanogenetic glucoside was studied with rats using synthesized D, L-mandelonitrile-beta-D-glucoside. Considering from blood cyanide level, the cause of death was presumed to be cyanide intoxication. Hydrolysis of cyanogenetic glucoside occurred mainly in small and large intestines. Cyanide level in the intestine seemed to be independent of the amount of glucoside present. LD50 value was calculated to 560 mg/kg but good dose dependent result was not obtained. Relatively rapid absorption of the glucoside from the gastrointestinal tract was observed with the highest absorption rate of 53.4% within 165 min. About 30-45% of the administered glucoside was excreted within 24 hr without alteration and dose dependence appeared in an excreted ratio. The ratio of D-mandelonitrile-beta-D-glucoside to L-form excreted in the urine or remained in the gastrointestinal tract was almost in the same as at administration, and hence biological behaviors, such as absorption, excretion and hydrolysis, of both D- and L-forms of glucoside were almost the same.

Animals↗
PubMed1987

Studies on the distribution of lidocaine in tissue after spinal and intravenous application in rabbits: clinical and forensic toxicological aspects.

Distribution of lidocaine in tissue was investigated after spinal anesthesia and intravenous application in rabbits to examine aspects of forensic and clinical toxicology. Respiratory arrest occurred at 5-15 min after injection of 5 mg/kg hyper-baric lidocaine solution into the subarachnoid space followed by standing in the head down position. The minimum concentration of lidocaine in the middle part of the cervical spinal cord of the dead rabbits was 197 micrograms/g. On the other hand, maximum concentration in the same site at the critical state of almost complete respiratory arrest was 175 micrograms/g. The time at which the concentration of lidocaine reached a maximum in plasma and various tissues after subarachnoid administration was 10-15 min. The concentrations in the lumbar spinal cord, a site of administration, were 1200-1500 micrograms/g 5 min after the injection, which decreased gradually to about 180-250 micrograms/g at 60 min when paralysis of the hind legs began to recover. According to these data, the concentration of lidocaine in the spinal cord of rabbits required for neural blockade was presumed to be about 200 micrograms/g. Since the maximum concentrations of lidocaine in each tissue was already observed at 2.5 min after intravenous injection, transport of lidocaine from plasma to tissues was considered to be very rapid. Lidocaine accumulates most rapidly in the spleen and kidney, followed by the brain, lung, heart, spinal cord and plasma. The concentration in the liver was the least because of its hepatic metabolism. Distribution to adipose tissue was slower than that to other tissues, but the highest accumulation was observed at the late stage. Elimination rates of plasma and tissues other than adipose were almost the same.

Animals↗
PubMed1986

Prolactin in severe toxemia of pregnancy.

Plasma PRL levels were measured in 111 normal pregnant women and in 21 patients with severe toxemia of pregnancy. Twelve of 21 patients with severe toxemia of pregnancy showed high PRL levels in zone A (greater than mean value + 1 S.D. of PRL values in normal pregnancy). These 12 were significantly lower (P less than 0.02) in the Ccre rate, at 70.2 +/- 19.2 ml/min, than 5 toxemia patients (101.4 +/- 26.7 ml/min) in zone B (mean + 1 S.D. approximately mean) and 4 toxemia patients (110.0 +/- 35.3 ml/ml) in zone C (mean approximately mean -1 S.D.). Also, BUN, proteinuria and uric acid levels in zone A patients were higher than in those in zone B and C. However, no correlation was found between PRL levels and mean diastolic and systolic blood pressure. These results suggest that high PRL concentrations in toxemia of pregnancy may be associated with renal dysfunction.

Blood Urea Nitrogen↗
PubMed1986

Immunotherapy of cancer patients with BCG: summary of ten years experience in Japan.

Two thousand and four patients with various types of late stage cancer were treated with living BCG immunotherapy from 1972 to 1982. Fourty-five out of 1,112 patients were able to survive more than 5 years after initiation of this immunotherapy. All of these patients were noncurative operation except for 2 cases of hepatoma who received no surgery. We report the immunological and clinical aspects of the long term survivors of this treatment.

BCG Vaccine↗
PubMed1986

[Concentrations of growth hormone, prolactin and thyroid-stimulating hormone in the maternal, fetal and amniotic compartments].

GH, PRL and TSH in the maternal, fetal and amniotic compartments were measured by radioimmunoassay in normal pregnant women (group I, n = 16) and patients with anencephalic fetuses (group II, n = 10). The concentrations of GH (20.6 +/- 8.5 ng/ml, mean +/- SD) in cord blood of normal fetuses were significantly higher (p less than 0.001) than those (5.1 +/- 3.5 ng/ml) in anencephalic fetuses. Both maternal PRL levels in group I and group II were lower than their respective cord bloods. The concentrations of PRL (283.1 +/- 127.5 ng/ml) in normal fetuses were higher, but not significantly, than those (199.4 +/- 111.8 ng/ml) in anencephalic fetuses. Also, compared with PRL levels in the maternal and cord blood, those in amniotic fluid were significantly higher (p less than 0.001) in both groups. On the contrary, GH and TSH levels in amniotic fluid were much lower than those in the maternal and fetal blood. The concentration of TSH (10.2 +/- 4.6 microU/ml) in normal fetuses was significantly higher (p less than 0.05) than those (7.1 +/- 3.1 microU/ml) in maternal blood, but not significantly different from those (11.3 +/- 3.6 microU/ml) in anencephalic fetuses. These results suggest that GH, PRL and TSH do not cross human placenta and biosyntheses of these hormones in the maternal and fetal pituitaries are independent.

Adult↗