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K Ishida

Publications and source records attributed to K Ishida.

At least 523 records · Page 29Linked to original sources
PubMed1985

The significance of plasma gastrointestinal glucagon in endotoxemia.

Hyperglucagonemia has been reported during endotoxemia. Increases in plasma glucagon concentration may serve as an important mediator and be influential in modifying metabolism during endotoxin shock. Increases in the plasma concentration of glucagon are brought about by both pancreatic and gastrointestinal release of glucagon during endotoxemia. The purpose of the present study was to determine the importance of gastrointestinal-derived glucagon (glucagon-like immunoreactivity; GLI) during endotoxin shock. LD100 endotoxin (3.0 mg/kg) was injected via the auricular vein into fasted rabbits. Emphasis was focused on total glucagon and gastrointestinal glucagon (GLI) concentrations, but measurements of these parameters were supplemented by determinations of glucose and triglyceride. The results were as follows: 1) gastrointestinal glucagon concentration increased threefold over that of pancreatic glucagon concentration and 27-fold over that of the control group at 6 hr after endotoxin administration and 2) significant increases of both serum glucose and triglyceride concentrations were observed after endotoxin was injected. Findings suggest that gastrointestinal glucagon may be one of the factors responsible for evoking the abnormal metabolism caused by endotoxin shock. In hyperglucagonemia resulting from endotoxemia, it is suggested that attention should be paid not only to the glucagon originating from the pancreas but also to that derived from the intestine.

Animals↗
PubMed1985

[A study on transference of cefmenoxime into the cerebrospinal fluid].

Two grams of cefmenoxime (CMX) was administered by one-shot intravenous injection to the patients in normal pressure hydrocephalus without meningitis, and the transference of CMX into the cerebrospinal fluid (CSF) from blood was investigated. After the injection of CMX, CSF and serum were serially taken, and the concentrations of CMX were measured by agar-well method using E. coli. The conclusions drawn from this study are summarized as follows: The concentrations of CMX in CSF were more slowly decreased than those in serum. The mean ratio of transference of CMX into CSF from the serum was 1.4%. After the intravenous injection of 2 g CMX, the mean maximum concentration of CMX in CSF was 0.36 microgram/ml, which exceeded 80% MIC (minimal inhibitory concentration) against several Gram-positive cocci and Gram-negative rods, and higher concentrations than the 80% MIC were kept over 4 hours in CSF. The efficacy of CMX may be kept by its injections less than 4 times a day.

Aged↗
PubMed1985

[Studies of plasma gastrointestinal glucagon after LD100 E. coli infusion].

We postulate that high plasma concentrations of gastrointestinal-derived glucagon may be used to identify severe sepsis and correlate with the effect of therapy. Eighteen adult dogs were separated into three groups: Group I-LD100 E. coli alone, group II-LD100 E. coli + tobramycin (TOB) and group III-LD100 E. coli + TOB + methylprednisolone sodium succinate (MPSS). E. coli was infused intravenously for one hour. Each animal was monitored for six hours and observed for a 7-day recovery period. Percent survival (greater than 7 days): I = 0%, II = 17% and III = 83%. Concentrations of gastrointestinal glucagon were 3417 pg/ml in group I, 5167 pg/ml in group II and 1081 pg/ml in group III at six hours after E. coli infusion. In group III these concentration returned to control values by 7 days after E. coli infusion. Increases in gastrointestinal glucagon were more readily induced by E. coli infusion than those of pancreatic glucagon. Gastrointestinal glucagon concentrations were related to the severity of E. coli induced shock and the beneficial effects of MPSS/TOB therapy. Therefore, plasma gastrointestinal glucagon concentrations may be useful in recognizing the presence of severe sepsis and directly related to the beneficial effects of therapy.

Animals↗
PubMed1985

[Alanine metabolism in the skeletal muscle and plasma in endotoxemia].

Utilizing a 24 hour fasting rabbit (N = 30), we measured free amino acids in the femoral artery and vein and the quadriceps femoris muscle. The endotoxin E. coli 026, 3.0mg/kg (LD100) was injected and free amino acid plasma levels were monitored for 6 hours. Changes in free amino acid plasma levels were variable and marked after endotoxin injection. By 360 min. after endotoxin injection: (a) the rate of increase in free amino acid levels in the femoral artery was 366 mumole/l of alanine, 162 mumole/l of glycine and 85 mumole/l of proline; (b) the rate of increase in free amino acid of the quadriceps femoris muscle was 1376 nmole/g of alanine, 156 nmole/g of glycine and 109 nmole/g of serine; and (c) the femoral arteriovenous difference was -225 nmole/l of alanine, -118 nmole/l of glycine and -77nmole/l of proline. Within 10 min. after endotoxin injection, alanine concentration was higher in the femoral vein. This change in concentration became significant by 60 min. The results show the following: Skeletal muscle appears to be an important source of amino acids for amino acid metabolism during endotoxemia, especially plasma alanine which is closely connected with alanine levels in skeletal muscle.

Alanine↗
PubMed1984

Epidemic Shiga bacillus dysentery in Central Africa.

An outbreak of dysentery began late in 1979 in Central Africa and spread to involve a major portion of Zaire as well as Rwanda and Burundi. We traveled to a mission hospital in northeast Zaire during the epidemic and isolated Shigella dysenteriae, type 1, from most of the patients studied. All isolates were resistant to ampicillin, tetracycline, chloramphenicol, sulfathiazole, and streptomycin but sensitive to trimethoprim-sulfamethoxazole. Antimicrobial resistance was transferable to Escherichia coli, and at least three plasmids were identified in the donor Shigella isolates by using agarose gel electrophoresis. One was coded for ampicillin, tetracycline, and chloramphenicol resistance while a second conferred resistance to ampicillin and chloramphenicol but not tetracycline. A third large plasmid of approximately 120 megadaltons could not be transferred to E. coli recipients. All S. dysenteriae isolates yielded identical kinetic growth curves when analyzed on the Abbot MS-2 Research System. This is the most extensive outbreak of dysentery caused by S. dysenteriae reported since the Central American epidemic of 1969, and the first epidemic caused by a strain resistant to ampicillin.

Adolescent↗
PubMed1984

[Hepatic glycolytic intermediates and glucoregulatory enzymes in septic shock due to peritonitis: experimental study in rats].

The hypoglycemia in septic shock due to peritonitis indicates deranged carbohydrate metabolism. To determine if this metabolic failure could be attributed to changes of glucoregulatory enzymes and glycolytic intermediates, activities and changes of these substances in septic shock have been studied in rats. Liver tissue was sampled 5 hours after induction of peritonitis by cecal incision in fasted male rats. Hepatic glycolytic intermediates were assayed by UV-spectrophotometry. Peritonitis caused 33% decrease in glucose-6-phosphate (G6P), a 2.5 fold increase in fructose-1,6-diphosphate (FDP) and a 3.5 fold increase in lactate. Phosphoenolpyruvate (PEP) levels did not show a significant increase in peritonitis. We investigated activities of glucose-6-phosphatase (G6Pase), fructose-1,6-diphosphatase (FDPase), phosphofructokinase ( PFKase ) and pyruvate kinase ( PKase ) in mitochondria-free supernatants from rat liver homogenates. Tissue was sampled 5 hours after induction of peritonitis by cecal incision. Assays were conducted at optimal substrate levels at pH 7.4; NADH charges produced by coupled reactions were determined by UV-spectrophotometry. A significant increase of PFKase and PKase specific activity was observed. These changes were consistent with stimulated glycolysis. For gluconeogenesis to achieve maximum efficiency it would be necessary to inhibit PFKase and PKase completely.

Animals↗