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Biomedical subjects

H Higashino

Publications and source records attributed to H Higashino.

At least 73 records · Page 4Linked to original sources
PubMed1989

[Clinical and pharmacokinetic evaluation of cefodizime in children].

Cefodizime (CDZM, THR-221), a new cephem antibiotic, was investigated for its clinical efficacy and pharmacokinetics in children. The results obtained are summarized as follows. 1. Antimicrobial activities Antimicrobial activities of CDZM against clinically isolated organisms were determined. MICs of CDZM against 1 strain each of Streptococcus pneumoniae, Escherichia coli and Klebsiella pneumoniae were 0.05 micrograms/ml to 0.10 micrograms/ml. Especially, MIC against all 6 strains of Haemophilus influenzae was less than or equal to 0.024 micrograms/ml. This MIC value was lower than those of other antibiotics such as cefotaxime, cefotiam, cefazolin, piperacillin. 2. Pharmacokinetics CDZM was given to 1 case at a dose of 20 mg/kg by a 60-minute intravenous drip infusion. The peak value of serum concentration of CDZM was 207.80 micrograms/ml at the end of the infusion. The half-life was 2.15 hours. The mean urinary excretion rate was 68.5% in the first 4 hours, 79.2% in 6 hours and 76.5% in 8 hours after the 30-minute drip infusion. 3. Clinical efficacy CDZM was given to a total of 27 patients, 13 with pneumonia, 1 with bronchitis, 2 with acute pharyngitis, 1 with purulent tonsillitis, 5 with urinary tract infection, 1 each with retrograde cholangitis, acute enteritis, pericementitis, phlegmon and inguinal lymphadenitis. Overall clinical efficacies were excellent in 5 cases, good in 17 and the efficacy rate was 81%. Bacteriological effects were investigated in 13 cases and the eradication rate was 85%. No adverse reactions were observed in any case. As abnormal laboratory findings, elevated GOT, GPT, A1-P, LAP and gamma-GTP, were noted in 1 out of the 28 cases examined.

Adolescent↗
PubMed1988

[A study on pharmacokinetics, antimicrobial activity and clinical efficacy of sultamicillin in children].

Sultamicillin (SBTPC), a mutual prodrug for ampicillin (ABPC) and beta-lactamase inhibitor sulbactam (SBT), was evaluated for its antibacterial activity, pharmacokinetics and clinical efficacy. Pharmacokinetic studies were done in 2 subjects (a male and a female) following single oral administrations of 5 mg/kg and 10 mg/kg SBTPC fine granules after meal. Peak serum concentrations of ABPC and SBT in the 2 cases were 0.85 and 0.38 micrograms/ml and 3.74 and 3.79 micrograms/ml, respectively. Urinary excretion rates in 6 hours were 43.5-58.1% for ABPC and 33.6-53.6% for SBT. A total of 20 patients including 14 with respiratory infections, 1 with urinary tract infection and 5 with skin and soft tissue infections were treated with daily oral dose of 15.4-39.3 mg/kg SBTPC fine granules t.i.d. for 4 to 13 days. Responses were excellent in 5, good in 13 and fair in 2, hence the overall efficacy rate was 90.0%. Bacteriological responses were confirmed on 5 (62.5%) out of 8 strains which were eradicated by the treatment. SBTPC showed strong antibacterial activities against an ABPC-resistant strain of Escherichia coli. Side effects of the drug were observed in 3 patients: diarrhea in 2 and loose stool in 1. An abnormal laboratory test value, eosinophilia, was observed in only one patient.

Adolescent↗
PubMed1987

Acute monocytic leukemia in children. Response to VP-16-213 as a single agent.

Three patients were studied: two infants with acute monocytic leukemia who failed to respond to the initial combination therapy of daunorubicin with cytosine arabinoside, and an adolescent with relapsed acute monocytic leukemia. They were intensively treated with epipodophyllotoxin (VP-16-213) alone and subsequently had complete remission. One patient showed apparently dose-dependent cytotoxic effect. All three patients have maintained complete remission for 6, 7, and 11 months, respectively. Toxicities, including myelosuppression, alopecia, nausea, vomiting, and renal dysfunction, were well tolerated. Intensive treatment with VP-16-213 alone was thus found to have a potent therapeutic effect on acute monocytic leukemia in children. VP-16-213 deserves a further assessment in the therapeutic protocol for patients with childhood acute monocytic leukemia.

Adolescent↗
PubMed1987

Congenital absence of lacrimal puncta and of all major salivary glands: case report and literature review.

A 7-year-old girl had dry mouth and recurrent infections of the lacrimal fistulae with decreased lacrimal secretion. All four puncta were absent, and a Schirmer test showed decreased lacrimal secretion. Salivary gland imaging with sodium pertechnetate 99mTcO4 showed absence of all major salivary glands. Lower lip biopsy disclosed normal structure of the salivary gland. No evidence of abnormal inheritance patterns could be demonstrated.

Abnormalities, Multiple↗
PubMed1987

Role of endothelial cells in responses of spontaneously hypertensive rat mesenteric arteries to norepinephrine and angiotensins.

The role of endothelial cells in the constrictor and dilator responses of mesenteric arteries to infused drugs was evaluated. Fifteen- to seventeen-week-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) were used. Periarterial sympathetic nerve stimulation (PNS, 6 Hz, 30 sec) elicited greater pressor responses in SHR than WKY. Acetylcholine (ACh, 1.0 microM) lowered the perfusion pressure elevated by norepinephrine (NE, 0.1 microM) significantly more in SHR than WKY. Angiotensin I and II (AI and AII, 1.0 nM) markedly potentiated the PNS-induced constriction in both animals. Collagenase perfusion (Type 1A, 2 mg/ml, 5 ml/min intermittently, for 23 min) significantly diminished the ACh-induced dilation, indicative of endothelium destruction. However, it greatly increased the constrictor effect of NE and AI and AII in SHR and the potentiating effects of AI and AII on PNS-evoked construction in both SHR and WKY, especially in SHR. These results suggest that, while endothelial cells mediate the dilator response to ACh, they are unnecessary for the constrictor and potentiating effects of NE, AI and AII and, in fact, counteract the latter two effects, particularly in the hypertensive rats. Furthermore, the endothelial cell functions promoting the effect of ACh or countering those of NE, AI and AII are in general greater in SHR than WKY.

Angiotensin I↗
PubMed1987

[Clinical and pharmacokinetics evaluation of flomoxef in pediatrics].

Flomoxef (FMOX, 6315-S), a new parenteral oxacephem antibiotic was investigated for its clinical efficacy and pharmacokinetics. The results obtained are summarized below. 1. Twenty-eight patients were treated with 39-152 mg/kg per day of FMOX by intravenous administration. Diagnosis of patients were pneumonia in 15 patients, acute upper respiratory tract infection in 5, acute enterocolitis in 3, urinary tract infection in 2 and cholangitis, suppurative lymphadenitis and suspicious sepsis in 1 patient each. Clinical effect was excellent in 7 cases, good in 8, fair in 5, poor in 2 and 6 cases were excluded because therapy periods were too short and other antibiotics were used together. Efficacy rate was 68% and the rate of bacterial disappearance was 83%. 2. Rash was found in 5 cases and thrombocytosis was found in 1 out of 28 cases. However, no severe adverse reaction was encountered. 3. The peak serum level of FMOX was 51.0 micrograms/ml after 20 mg/kg of drip infusion for 30 minutes and the half-life was 17.2 minutes in alpha-phase and 58.2 minutes in beta-phase.

Adolescent↗
PubMed1986

Alterations of presynaptic and endothelial functions in SHR: effects of adenosine.

The effects of adenosine on stimulation-evoked 3H-efflux from perfused mesenteric arteries pretreated with 3H-norepinephrine and on norepinephrine-induced contractile responses of the thoracic aorta before and after mechanical removal of endothelial cells were examined in spontaneously hypertensive rats (SHR) compared with Wistar-Kyoto rats (WKY). Adenosine inhibited the stimulation-evoked 3H-efflux; this inhibitory effect was smaller in young and adult SHR than age-matched WKY. Mechanical removal of endothelial cells rendered the SHR aorta much less responsive to adenosine, while in the WKY aorta endothelial removal had no influence on the relaxation response to adenosine. These results support the hypothesis that pre-synaptic factors are contributory whereas endothelial factors are compensatory to hypertension in SHR.

Adenosine↗
PubMed1983

Na+-K+-ATPase in rat vascular smooth muscle cell grown in vitro.

This study has focused on the characteristics of the Na+-K+-ATPase in in vitro preparations of vascular smooth muscle cells (VSMCs) derived from the rat carotid artery. The maximum velocity of enzyme reaction (Vmax) for the specific activity of the enzyme in the VSMCs' preparations was 2.36 +/- 0.04 (SE) mumol Pi X mg cell protein-1 X h-1 or 0.82 +/- 0.02 mumol Pi X 10(6) cells-1 X h-1. The activation of the enzyme by potassium, sodium and ATP has been investigated. The half-maximal values for potassium and sodium activation of the enzyme in the preparations were 1.18 and 10-20 meq/l, respectively. The respective Vmax values for potassium and sodium activation were reached at concentrations of 4-10 and 80-100 meq/l. The Michaelis constant for ATP was 0.83 mM. Calcium exerted a potent inhibition on the activity of the enzyme (I50 at 1 mM). It has been concluded that the Na+-K+-ATPase kinetic pattern in in vitro preparations of VSMCs is quite similar to that observed in homogenates or subcellular fractions of other tissues.

Animals↗
PubMed1983

Vanadium, Na-K-ATPase, and potassium adaptation in the rat.

Vanadate is a potent inhibitor of Na-K-ATPase in vitro. It has been suggested that vanadium may function as a cellular regulator of Na-K-ATPase in vivo. To examine this speculation, we studied in rats the effect of high vanadate intake on 1) the tissue levels and distribution of vanadium, 2) basal activity of Na-K-ATPase in various tissues, and 3) the activity of Na-K-ATPase in various organs under conditions of massive chronic potassium loading known to stimulate Na-K-ATPase in the kidney and colon. Despite extremely high tissue levels of vanadium there was no demonstrable effect of the element on the basal activity of Na-K-ATPase. When subjected to chronic potassium loading, rats with high tissue vanadium concentrations underwent potassium adaptation that was associated with a rise in Na-K-ATPase activity in the renal cortex, renal medulla, and colonic mucosa. Further studies are needed to support or refute the thesis that vanadium might be an intracellular regulator of Na-K-ATPase in vivo.

Animals↗
PubMed1983

Vanadate effect on the Na,K-ATPase and the Na-K pump in in vitro-grown rat vascular smooth muscle cells.

The impact of vanadate on the Na,K-ATPase system in the vascular smooth muscle cell is poorly understood. The present study describes the kinetics of the effect of vanadate on Na,K-ATPase and the Na-K pump in in vitro grown rat VSMC's. Vanadate interaction with the Na,K-ATPase system in vascular smooth muscle cells was examined by observing its influence on ouabain-sensitive adenosine triphosphate hydrolysis in disrupted cells rendered permeable by osmotic shock, and the uptake of rubidium by intact cells. The I50 for vanadate inhibition of ouabain-sensitive hydrolysis of adenosine triphosphate occurred at vanadate concentrations of 10(-6) to 10(-7) M. This inhibition was potassium dependent. The maximal inhibitory effect of vanadate occurred at potassium concentrations of 10-20 mEq/liter. Sodium exerted a moderate antagonistic influence on vanadate inhibition of ouabain-sensitive adenosine triphosphate hydrolysis. Rubidium uptake by vascular smooth muscle cells was not altered within 120 minutes when 10(-5) M vanadate was added to the medium containing intact vascular smooth muscle cells. Yet, vanadium concentrations in the vascular smooth muscle cells within this incubation period reached levels 1.48-fold higher than the extracellular vanadate concentrations of 10(-5) M. These observations indicate that vanadate is a potent inhibitor of the VSMC Na,K-ATPase in disrupted vascular smooth muscle cells. However, in intact vascular smooth muscle cells vanadium gaining access into the vascular smooth muscle cell's interior does not inhibit the Na-K pump, probably because of its binding to intracellular proteins and/or conversion from the vanadate to the vanadyl ion.

Animals↗
PubMed1982

Balance and tissue distribution of vanadium after short-term ingestion of vanadate.

Forty-six female Sprague-Dawley rats (170-200 g) were randomly assigned to one of six treatment groups receiving 0.1, 5.0, or 25.0 ppm dietary vanadium with either normal (0.13 mEq/g) or high (1.82 mEq/g) dietary potassium. Supplemental vanadium was administered as sodium metavanadate. These diets were fed for 2 weeks, and all feces and urine collected. At the end of the treatment period, brain, liver, renal cortex and medulla, whole blood, and plasma were obtained and analyzed for vanadium by atomic absorption spectrophotometry, as were the urine and feces samples. Tissue vanadium concentration increased significantly (P less than 0.00001) with increasing food vanadium content, but were not affected by dietary potassium in spite of the polyuria induced in animals on the high potassium diets. The highest vanadium concentrations were found in the renal cortex and the lowest, in the brain. Although urinary vanadium excretion was higher in animals fed the high potassium diets, a relatively small percentage of ingested vanadium was excreted in the urine. Rats fed diets containing no supplemental sodium metavanadate (0.1 ppm vanadium) were in negative vanadium balance, but their growth was not inhibited. Animals receiving 5.0 and 25.0 ppm vanadium diets retained 39.7 +/- 18.5% of ingested vanadium and excreted 59.1 +/- 18.8% of ingested vanadium in the feces. These values indicate greater absorption and retention of ingested vanadium than found In previously reported investigations.

Animals↗
PubMed1982

Chronic sodium deficit in the immature rat: its effect on adaptation to sodium excess.

The impact of chronic low-sodium intake during early development on body sodium homeostasis is not sufficiently known. To explore this effect, we have investigated the influence of chronic sodium deficit during the rapid growth period of rats (first phase, age 3-7 wk) and the short-term effect of sodium repletion (second phase, age 8-9 wk) on parameters such as growth rate, urinary aldosterone excretion, 22Na volume of distribution (space), and various renal functions. Three groups were studied: group I (control) and groups II and III. During the first phase the respective sodium intake values for these groups were 8.9, 3.1, and 1.5 meq.kg body wt-1.day-1. During the second phase, all groups had sodium intake of 8.7-8.8 meq.kg body wt-1.day-1. At the end of the first phase, group II showed weight gain and 22Na space values similar to those of group I. Group III demonstrated severe growth retardation and reduced 22Na space. During the second phase, both groups II and III demonstrated expansion of the 22Na space and persistently elevated urinary "acid-labile" aldosterone excretions. Despite the 2 wk of sodium repletion, group III failed to catch up with the body weight of groups I and II. It is concluded that chronic sodium deficit during early development transition is made to a higher sodium intake.

Aging↗
PubMed1982

The intestinal profile of Na-K-ATPase in two rat models of acute renal failure.

The specific activity of mucosal Na-K-ATPase in segments of the small intestine and colon was examined after BN or BUL. BN resulted in a surge of the specific activity of the enzyme throughout the mucosa of the intestinal tract (duodenum 26%, jejunum 33%, ileum 37%, and colon 68%). BUL induced to significant change in the specific activity of Na-K-ATPase in the small intestinal mucosa and a small rise (32%) in the specific activity of the enzyme in the colon. Kinetic analyses of potassium activation of the enzyme in the two models of ARF indicate that the increase in the specific activity of the enzyme in the colonic mucosa was a function of increased Vmax rather than a change in the apparent Km for potassium by the Na-K-ATPase. It is theorized that the kidney modifies the response of intestinal Na-K-ATPase in AFR.

Acute Kidney Injury↗