Biomedical subjects
Publications and source records attributed to K Ikegami.
Two triterpenoid saponins (1 and 2) were isolated from Desmodii Herba [the dried whole plants of Desmodium styracifolium (Osbeck) Merr. (Leguminosae)] and their chemical structures were characterized as soyasaponin I and a new saponin, 3-O-[alpha-L-rhamnopyranosyl-(1----2)-beta-D-galactopyranosyl- (1----2)-beta-D-glucuronopyranosyl]soyasapogenol E, respectively, by chemical and spectroscopic means.
We have reviewed 38 patients with invasive candidiasis and examined its predisposing factors, usefulness and limitation of cultural study in its diagnosis, and effective usage of amphotericin B in its treatment. Invasive candidiasis was diagnosed in 2.4% of the patients admitted during the past 5 years. One of the most important predisposing factors for development of invasive candidiasis was extensive use of antibiotics. Destruction of the mechanical barrier against bacteria and fungi caused by endotracheal intubations and various catheterization was another important factor. Mucosal lesion of the gastrointestinal tract, including stress ulcer, non-specific inflammatory bowel disease and esophageal ulcer, was seen in 30% of the patients. These lesions were thought to be the portal of entry for candida to systemic dissemination. AMPH is the most effective antifungal agent. Total dose of 300 to 1000 mg was effective in the patients. Dosage over 1000 mg was associated with progressive decrease in creatinine clearance. This decrease was irreversible even after discontinuation of AMPH. Candidal overgrowth within the G1 tract was considered to precede invasive candidiasis. Oral AMPH administration was effective in such conditions.
To investigate the role of prostaglandin E2 in urinary stone formation, urinary prostaglandin E2 was measured by radioimmunoassay in 28 men with recurrent idiopathic urolithiasis (14 normocalciuric and 14 hypercalciuric patients) and 6 healthy male volunteers. Urinary prostaglandin E2 levels were significantly higher (p less than 0.01) in the hypercalciuric group than in the normocalciuric and healthy control groups, and they showed a positive correlation with urinary calcium excretion. Urinary prostaglandin E2 and calcium excretions in the hypercalciuric and normocalciuric groups were suppressed significantly by indomethacin. Creatinine clearance was not reduced by indomethacin. The results suggest that renal prostaglandin E2 may participate in calcium stone formation by regulating the renal tubular handling of calcium.
Since beta-1,3-glucan is a common component of fungal cell wall, its detection might be useful in diagnosing invasive candidiasis. Not only endotoxin but beta-1,3-glucan activates proclotting enzyme contained in a conventional chromogenic limulus test (CCLT). Endotoxin activates this enzyme through factor C, while the beta-1,3-glucan activates through factor G. Since endotoxin specific test (EST) contains factor C, endotoxin would be quantified. By subtracting EST value from CCLT value, beta-1,3-glucan would be quantified. We named this value Fungal Index (FI), and examined if it actually reflects the candidal infection. Ninety-two patients were tested for CCLT and EST prospectively. FI increased significantly in candidal infection (p less than 0.05) but remained low in GNR infection. Moreover, FI increased proportionally to the severity of candidal infection. Elevated FI decreased when antifungal therapy was successful. Thus FI was a useful index not only in the diagnosis of invasive candidiasis but also in the evaluation of antifungal therapy.
To study the role of sodium and renal prostaglandin E2 in the chronic phase of two-kidney one-clip renovascular hypertension, urinary excretion rates of sodium and prostaglandin E2 were measured in rabbits with hypertension induced by left renal artery constriction during alteration in sodium intake. The arterial blood pressure, the increasing rate of body weight and sodium balance during alteration in sodium intake were directly proportional to the amount of sodium intake in the hypertensive rabbits, but not in the control ones. Plasma renin activity and plasma aldosterone concentration, which had no significant difference between hypertensive and control rabbits, were inversely proportional to the amount of sodium intake in both rabbits. Urinary excretion rates of sodium in the clipped kidneys of the hypertensive rabbits were significantly lower than the control values in all dietary regimens (p less than 0.01). Urinary excretion rates of sodium in the nonclipped kidneys were not significantly higher and in the total kidneys were significantly lower than the corresponding control values during sodium load (p less than 0.01). Urinary excretion rates of prostaglandin E2 were inversely proportional to the amount of sodium intake in both groups. Urinary excretion rates of prostaglandin E2 in the clipped kidneys were significantly lower than the control values in all dietary regimens (p less than 0.001). Urinary excretion rates of prostaglandin E2 in the nonclipped kidneys were significantly higher during sodium restriction (p less than 0.01) but not during sodium load than the control values. Furthermore, urinary excretion rates of prostaglandin E2 in the total kidneys were significantly lower than the control values in all dietary regimens (p less than 0.01). These results suggest that two-kidney one-clip renovascular hypertension in rabbits seems to be partly sodium-dependent in the chronic phase because the nonclipped kidney fails to excrete sodium sufficiently. There may also be disorders of renal prostaglandin E2 metabolism influencing these disorders of sodium in the nonclipped kidneys.
L-Cysteine ethylester hydrochloride (ethylcysteine; 30 mg/kg, p.o.) increased the number of la-positive cells (antigen presenting cells) in spleen adherent cells (SAC) and that of Lyt 1.2-positive cells (helper T cells), but not that of Lyt 2.2-positive cells (suppressor T cells) of C57BL/6 mice immunized with sheep red blood cells. The production of hemolytic plaque forming cells (HPFC) in spleens of syngeneic recipient mice was enhanced by the transfer of SAC or spleen lymphocytes of the donor mice pretreated with ethylcysteine. This drug augmented phagocytosis of yeast particles by peritoneal macrophages of ICR mice at concentrations of 1-100 microM. In ex vivo experiments, this drug (30 mg/kg, p.o.) augmented the phagocytosis of yeast particles by mouse macrophages and showed a tendency to increase the macrophage number in the peritoneal cavity. Ethylcysteine (30 mg/kg, p.o.) significantly accelerated the decrease of viable E. coli number in the liver of normal mice 2 and 48 hr after challenge. Furthermore, this drug at the same dose restored the suppression of the decrease of E. coli number in the blood and liver of mice treated with cyclophosphamide (200 mg/kg, i.p.). These results suggest that ethylcysteine augments the functions of macrophages in vitro and ex vivo, and these enhancing effects may lead to the enhancement of host resistance to infections in compromised hosts.
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Strips of bladder neck smooth muscle were isolated from the dog and noradrenaline stores in the peripheral sympathetic nerve terminals were labelled with (-)3H-noradrenaline. Transmural electrical stimulation was applied and the released radiolabeled noradrenaline in the superfusate was measured with a liquid scintillation counter. Autonomic drugs were administered in the superfusate to examine their effect on noradrenaline release evoked by electrical stimulation. The general conclusions drawn from the data are that: there are two autonomic receptor systems on sympathetic nerve terminals of bladder neck--alpha-adrenergic receptors and muscarinic receptors, the activation of alpha-adrenergic receptors or muscarinic receptors depresses noradrenaline release and parasympathetic nerve excitement inhibits noradrenaline release in bladder neck.
The change of the response to angiotensin II (AII) and norepinephrine (NE) was evaluated in vivo and vitro in the chronic phase of two-kidney, one-clip renovascular hypertensive rabbits. In the constricted group, systemic blood pressure (BP) was significantly higher and plasma renin activity (PRA) was significantly lower than in the control group. Subpressor doses of AII and NE injections in the constricted group produced significant elevations of BP. In the aortic, renal and iliac arterial strips, the reactivity to AII (10(-10) to 10(-8) M) and NE (10(-10) to 10(-7) M) was significantly increased in the constricted group as compared to the control group. In the constricted group, sodium loading produced BP elevation with decreased PRA and shifted the dose-response curves by AII and NE to the left, whereas sodium restriction decreased BP and shifted the curves to the right. In the control group, altered sodium intake did not affect BP but affected only the dose-response curves by AII. These results suggested that in the chronic phase of renovascular hypertensive rabbits, the increased reactivity to AII and NE may contribute to the maintenance of hypertension.
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Although present day progressive respiratory management has decreased the tetanus mortality rate, tetanus-related autonomic overactivity remains a lethal condition. The cause, pathophysiology, and treatment of this condition are controversial and no animal model has ever been reported. So we tried to make a rabbit model of this condition. At first we injected 30 micrograms of purified tetanus toxin intravenously. Blood pressure oscillation occurred, but the degree of oscillation was smaller than that was seen in the clinical cases. The degree of oscillation had not changed by addition of 30 micrograms purified toxin 12 hours after first injection. Secondly, 7 days before the experiment we injected 0.5 micrograms of purified tetanus toxin intravenously. On the experiment day, we injected 30 micrograms of purified toxin again. By this method there occurred blood pressure oscillation as same as that was seen in the clinical cases. But no rabbits progressed to circulatory collapse by purified toxin. Then to the last group of rabbits, we injected crude tetanus toxin for purified toxin. The degree of blood pressure oscillation was same as that of cases in which purified toxin was injected, and all rabbits progressed to circulatory collapse.
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.
To investigate the role of renal prostaglandin E2 (PGE2) in renovascular hypertension, urinary PGE2 was measured in rabbits with hypertension produced by left renal artery constriction. In the acute phase of renovascular hypertension (1 week after the constriction), urinary excretions of PGE2 and sodium were significantly increased without correlations with changes in the systemic blood pressure (delta BP). In this phase, delta BP was directly proportional to plasma renin activity and plasma aldosterone concentration (p less than 0.001). In the intermediate phase (5 weeks), delta BP lost significant correlations with plasma renin activity and plasma aldosterone concentration and had a inverse correlation with urinary sodium excretion (p less than 0.01). In the maintenance phase (10 weeks), delta BP showed inverse correlations (p less than 0.01) with both PGE2 and sodium excretions, although their excretions decreased to normal levels. In the clipped kidney, only urinary PGE2 excretion in the acute phase was significantly elevated (p less than 0.02), and both sodium and PGE2 excretions were significantly decreased (p less than 0.01) in the maintenance phase. In the nonclipped kidney, urinary PGE2 and sodium excretions were elevated in the acute and intermediate phases, but decreased to the control levels in the maintenance phase. In this phase, delta BP showed inverse correlation (p less than 0.01) with both PGE2 and sodium excretions from the nonclipped kidney. The infusion of saralasin, an angiotensin II analogue, dose dependently reduced the blood pressure in the acute phase, but showed no effect in the intermediate and maintenance phases.(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of prostaglandins (PGE1, PGE2, PGF2 alpha, and PGI2) on the isolated human minor calyceal strips were isometrically investigated in vitro. PGE2 and PGF2 alpha, 10(-7) to 10(-6) g/ml, increased the basal tone of spontaneous contractions. PGE1 and PGI2 did not affect the contractions of the isolated human minor calyceal strips. The increases on the basal tone induced by PGE2 and PGF2 alpha were not affected by the pretreatment with atropine, hexamethonium, and phentolamine. Following incubation in a Ca2+-free medium, spontaneous contractions and the responses to PGE2 and PGF2 alpha were abolished. The results suggest that the contractile effects of PGE2 and PGF2 alpha may not be mediated by activation of muscarinic, nicotinic, or alpha-adrenergic receptors and result from a consequent increase of the transmembrane Ca2+ influx.
The production of hemolytic plaque forming cells (HPFC) in the spleen of BALB/c mice immunized with sheep red blood cells was significantly inhibited by carrageenan treatment (0.3 mg/kg, i.p.; on days -3 and -1). Cysteine ethylester hydrochloride (ethylcysteine) restored the inhibition of the HPFC production by carrageenan treatment in a dose-dependent manner (10-100 mg/kg, p.o.). Ia positive cells (antigen-presenting cells) increased in the spleen adherent cells (SAC) obtained from immunized mice, whereas they decreased in the SAC obtained from carrageenan-treated mice. An increase of Ia positive cells occurred in the SAC of carrageenan-treated mice given ethylcysteine. Ethylcysteine (10-100 mg/kg, p.o.; on days -2 and -1) prevented both the suppression of the HPFC production and the decrease of the number of thymus lymphocytes and peripheral leukocytes induced by cyclophosphamide treatment (30 mg/kg, i.p.; on days -1 and 0). Lyt 1.2 positive cells (helper T cells) decreased in the spleen T cells of cyclophosphamide-treated mice, but increased in the spleen T cells from cyclophosphamide-treated mice give ethylcysteine. On the other hand, Thy 1.2 negative cells (B cells) did not increase in the spleen cells of cyclophosphamide-treated mice with or without ethylcysteine. These results suggest that ethylcysteine restores the immune response in immunosuppressed mice through the functions of macrophages and/or helper T cells.
ICR mice were treated orally with cysteine ethylester hydrochloride (ethylcysteine, 10 and 100 mg/kg) immediately before the intraperitoneal injection of yeast particles. This agent significantly potentiated phagocytosis of yeast particles by peritoneal polymorphonuclear leukocytes in mice obtained 2 hr after the yeast injection, and the treatment with this agent (3 and 30 mg/kg, p.o.) 4 hr before the injection of yeast potentiated phagocytosis of yeast particles by mouse peritoneal leukocytes. This agent (30 mg/kg, p.o.) restored the suppression of phagocytosis of mouse leukocytes by the intraperitoneal administration of cyclophosphamide (30 mg/kg, i.p.) 24 hr before the yeast injection. This agent (10-100 mg/kg, p.o.) had no effect on the decrease of peripheral leukocyte number in irradiated mice (560 rad), but restored the suppression of phagocytosis, nitroblue tetrazolium (NBT) reduction and stimulated NBT reduction by the addition of lipopolysaccharide. Furthermore, this agent (3-30 mg/kg, p.o.) potentiated phagocytosis, NBT reduction and stimulated NBT reduction of peripheral leukocytes obtained from guinea pigs 2 and 6 hr after ethylcysteine treatment. It is suggested that ethylcysteine potentiates phagocytosis and NBT reduction of leukocytes in animals, and it restores phagocytosis and NBT reduction inhibited by the treatment with cyclophosphamide or X-ray irradiation. It may be possible that this stimulating effect of ethylcysteine could be at least in part involved in the stimulation of nonspecific resistance to infection in the compromised host.
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