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Biomedical subjects

Y Takasugi

Publications and source records attributed to Y Takasugi.

At least 19 recordsLinked to original sources
PubMed1998

Blood coagulation activity during microsurgery.

The authors investigated blood coagulation activity in patients who underwent microsurgery. Hemostatic parameters were measured in 9 patients (10 operations) who were undergoing free tissue transfers. These parameters included prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinopeptide A (FPA), prothrombin fragment 1 + 2 (F1 + 2), and thrombin-antithrombin complex (TAT). The flap totally necrosed owing to vasospasm in 1 patient with osteomyelitis of the heel, and the FPA, F1 + 2, and TAT values significantly increased. Reexploration was required because of flap cyanosis in 1 patient with a hemangioma on the wrist, and the F1 + 2 and TAT values increased during the salvage procedure. These molecular markers could be important in indicating hypercoagulable state sensitivity, and they serve as a warning of possible vascular compromise to a surgeon.

Adult↗
PubMed1995

[Intracystic infusion therapy of minocycline hydrochloride for benign hepatic cysts].

This paper describes ultrasonically-guided infusion of minocycline hydrochloride solution (MINO infusion therapy) in benign nonparasitic cysts of the liver. MINO infusion therapy was performed in 7 large hepatic cysts and successful results were obtained in 6 lesions. The infusion procedure in the initial 4 hepatic cysts a 7 Fr catheter was placed into the cyst and MINO solution was left in the cyst according to the procedure of ethanol infusion therapy. In the most recent 2 cases the cyst was punctured with a 21G needle, washed with physiologic saline and then infused MINO solution without placement of an indwelling drainage tube. This modified procedure is simple and safe and also yields a good therapeutic result. MINO infusion therapy for benign hepatic cyst is very useful and the modified procedure can be performed safely in elderly patients and in patients with several complications.

Adult↗
PubMed1993

Disseminated intravascular coagulation in a patient with acute myeloid leukemia. Ultrastructural evidence of hypercoagulation in bone marrow.

The bone marrow of a 53-year-old woman with acute myeloid leukemia (AML) with disseminated intravascular coagulation was investigated by transmission electron microscopy. The patient had a preceding granulocytic sarcoma, and subclinical disseminated intravascular coagulation occurred concomitantly with the development of AML. Ultrastructural findings of the bone marrow at the onset of AML revealed the following: (1) The cytoplasm of the leukemic cells showed frequent fragmentation, resulting in the formation of abundant cytoplasmic fragments. (2) These cytoplasmic fragments were surrounded by abundant fibrin fibers, forming the fibrin-cytoplasmic fragment complex (FCF complex). (3) Slight fibrin deposition was seen around the leukemic cells and in the intercellular space of the bone marrow. Fibrin deposition in the bone marrow is thought to represent morphologic evidence of disseminated intravascular coagulation. The damage on the leukemic cell surface due to the cytoplasmic fragmentation seems to be closely related to the development of disseminated intravascular coagulation.

Acute Disease↗
PubMed1993

[Arteriosclerosis obliterans that was improved by LDL apheresis].

We reported here a case of arteriosclerosis obliterans (ASO) in which clinical symptoms and signs were improved after repeated LDL apheresis. The patient was a 70-year-old man who was diagnosed as having ASO in 1989. Although drug treatment started for the arterial disease, such clinical manifestations as rubor and intermittent claudication were gradually worsening. In 1991, the patient was also found to have diabetes mellitus (DM), leading to admission for its treatment. Insulin therapy was initially required, but it finally became possible to maintain a good control of DM with diet therapy alone. Since hypercholesterolemia (402 mg/dl) was noted on admission, we began to give the patient pravastatin. In response to the medication, serum total cholesterol (TC) levels declined to 270 mg/dl, but no further improvement was obtained. We therefore decided to perform LDL apheresis on the patient, hoping the improvement of both ASO and hypercholesterolemia. After six series of LDL apheresis were performed during 4 weeks, ASO-related signs and symptoms (i. e., intermittent claudication) were remarkably improved, and serum TC levels were decreased below 200 mg/dl. Our experience in the present case suggested that this procedure would be useful as an effective choice of treatment for ASO, but further studies as to the indication and protocol of this therapeutic maneuver will be clearly needed.

Aged↗
PubMed1992

The gastric antisecretory action of lipopolysaccharide is blocked by indomethacin.

We have recently found that bacterial lipopolysaccharide (LPS) at minute doses inhibits the secretion of gastric acid and pepsin in rats. The present study was performed to examine the mechanism by which LPS exerts its antisecretory action. The i.p. injection of LPS resulted in a dose-dependent (40-4000 ng/kg) decrease in gastric acid output in pylorus-ligated rats. However, preinjection of indomethacin (2-10 mg/kg s.c.), an inhibitor of prostaglandin biosynthesis, prevented the LPS-induced inhibition of gastric secretion in a dose-related manner, while these concentrations of indomethacin by themselves did not affect gastric acid output. These results suggest that LPS requires an intact prostaglandin system to exhibit its inhibitory action on gastric secretion.

Animals↗
PubMed1992

Evidence that gastric antisecretory action of lipopolysaccharide is not due to a toxic effect on gastric parietal cells.

We have recently found that bacterial lipopolysaccharide (LPS) or endotoxin at minute doses inhibits the secretion of gastric acid and pepsin in rats. The present study was performed to determine whether this antisecretory action of LPS was a reversible biological response or a result of the destruction of gastric parietal cells by endotoxin. The intraperitoneal injection of LPS into pylorus-ligated rats resulted in a dose-related (40-4000 ng/kg) decrease in gastric acid secretion, with maximal inhibition being observed at a dose of 4000 ng/kg. The stomach then was examined both macroscopically and microscopically for the presence or absence of mucosal lesions or damaged gastric parietal cells. No morphological changes in the gastric mucosal structure including parietal cells were observed even in the rats injected with 4000 ng/kg of LPS. Next, basal gastric acid output was compared in the rats that had received LPS (4000 ng/kg, intraperitoneal) or saline alone 24 hr before. There was no significant difference in gastric acid secretion between the saline- and LPS-pretreated groups, indicating that the secretory capacity of gastric parietal cells returned to the control level at 24 hr after the injection of a maximal antisecretory dose of LPS. These results clearly suggest that the LPS-induced inhibition of gastric secretion results not from its toxic or destructive effect on the gastric secretory mechanism but from its reversible biological effect on gastric physiology.

Animals↗
PubMed1992

Gastric antisecretory and antiulcer actions of interleukin-1. Evidence for the presence of an "immune-brain-gut" axis.

Increasing evidence suggests that interleukin-1 (IL-1), a cytokine mainly produced by activated monocytes/macrophages, has various biological actions in addition to its immunological activities. In the present study, we examined the effect of IL-1 on gastric secretion and gastric ulcer formation in rats. Gastric secretion was assessed in conscious pylorus-ligated rats weighing approximately 200 g. The peripheral injection of IL-1 resulted in a dose-related inhibition of gastric acid output. The central injection of IL-1 similarly reduced gastric acid secretion at 100 times smaller doses than peripherally injected IL-1, suggesting that this gastric antisecretory action of IL-1 is mediated by the central nervous system. In addition, it was found that this inhibitory effect of IL-1, either peripherally or centrally administered, was still evident at 8 h after injection, indicating the long-lasting property of this IL-1 action. On the basis of these antisecretory actions of IL-1, we determined whether or not pretreatment with IL-1 would prevent experimentally induced gastric ulcer formation. As expected, the central administration of IL-1 dose-dependently suppressed the development of gastric mucosal lesions induced by water-immersion restraint stress, a well-established ulcerogenic procedure. These results clearly demonstrated that IL-1 has potent antisecretory and antiulcer effects that are mediated by the central nervous system. Moreover, these findings suggest that there may exist an "immune-brain-gut" axis, which is involved in the regulation of gastric secretion and mucosal homeostasis, especially under certain pathophysiological conditions that activate the immune system to release various cytokines including IL-1.

Animals↗
PubMed1991

Central basic fibroblast growth factor inhibits gastric ulcer formation in rats.

We have recently reported that basic fibroblast growth factor (bFGF) acts in the brain to inhibit the secretion of gastric acid and pepsin, two major aggressive factors in the pathogenesis of gastric ulcer formation. In the present study, we determined whether or not bFGF has an anti-ulcer action via the central nervous system, using male Wistar rats. The intracisternal injection of bFGF dose-dependently (0.1-1.0 microgram(s)/rat) inhibited the severity of gastric ulcers induced by water-immersion restraint stress or central thyrotropin-releasing hormone. The same doses of peripherally injected bFGF failed to protect the gastric mucosa from these ulcerogenic procedures. These results suggest for the first time that bFGF has a mucosal protective effect through a mechanism involving the central nervous system. It is speculated that this anti-ulcer action of bFGF is, at least in part, dependent upon its gastric antisecretory effect.

Animals↗
PubMed1991

Prevention by interleukin-1 of intracisternally injected thyrotropin-releasing hormone (TRH)-induced gastric mucosal lesions in rats.

We have recently found that interleukin-1 (IL-1) acts in the central nervous system to potently inhibit gastric acid and pepsin secretion in rats. In the present study, we examined the effects of IL-1 on the development of gastric mucosal lesions induced by intracisternal (i.c.) thyrotropin-releasing hormone (TRH), a neuropeptide known to centrally stimulate gastric secretion. Pretreatment with i.c. injected IL-1 (10 ng/rat) significantly suppressed the severity of TRH-induced gastric erosions. On the other hand, the same dose of i.c. injected IL-1 failed to exert a cytoprotective action for the gastric mucosa against orally administered absolute ethanol. These results suggest that IL-1 has an anti-ulcer effect mainly through its inhibitory action on gastric secretion.

Animals↗
PubMed1991

Central nervous system action of basic fibroblast growth factor: inhibition of gastric acid and pepsin secretion.

To examine the effects of basic fibroblast growth factor (bFGF) on gastric secretion, the present study was carried out using pylorus-ligated rats. Intracisternally injected bFGF inhibited the secretion of both gastric acid and pepsin, and this gastric antisecretory action of bFGF was a dose-related response. On the other hand, the intraperitoneal injection of bFGF did not change gastric secretion. These results strongly suggested for the first time that bFGF, a growth factor that promotes the proliferation of various cell types, might also be a chemical messenger that is involved in the central regulation of gastric secretion. This biological action of bFGF may be considered as a novel nonmitogenic activity of this growth factor.

Animals↗
PubMed1991

Indomethacin reverses interleukin-1-induced hyperinsulinemia in conscious and freely moving rats.

With the aim of studying the mechanism by which peripherally injected interleukin-1 increases the serum levels of insulin in conscious rats, the effects of indomethacin, a cyclooxygenase inhibitor, on interleukin-1-induced hyperinsulinemia were examined using male Wistar rats implanted with intra-atrial cannulas. The i.v. injection of interleukin-1 (1 microgram/rat) into conscious rats resulted in a significant increase in serum insulin levels with the peak response being observed 10 min after injection. It was also found that this insulin response to interleukin-1 was dose-related. Pretreatment with indomethacin (3 mg/kg body weight), however, completely blocked the interleukin-1-induced stimulation of insulin secretion. These findings suggest that i.v. injected interleukin-1 stimulates insulin release from the endocrine pancreas by a mechanism involving the prostaglandin system.

Anesthesia↗
PubMed1990

Interleukin-1: a cytokine that has potent antisecretory and anti-ulcer actions via the central nervous system.

The present study was performed to determine if interleukin-1 (IL-1) acts as a chemical messenger in the central nervous system (CNS) regulation of gastric secretion and ulcer formation, using male Wistar rats. The central injection of IL-1 dose-dependently inhibited gastric acid secretion in pylorus-ligated rats at 100 times smaller doses than the peripheral injection of the cytokine. The action of IL-1 was long-lasting because its antisecretory effect was still evident at 8 hr after injection. Furthermore, it was observed that pretreatment with central IL-1 dose-dependently suppressed the development of gastric ulcers induced by water-immersion restraint stress, a well-established ulcerogenic procedure. These results clearly suggested for the first time that IL-1, a cytokine produced by activated monocytes/macrophages, acts centrally in the brain to exert gastric antisecretory and anti-ulcer actions.

Animals↗
PubMed1990

Lipopolysaccharide-induced inhibition of gastric acid and pepsin secretion in rats.

We used male Wistar rats to determine the effects of lipopolysaccharide (LPS) on gastric secretion. After pylorus ligation, 24-h fasted rats received i.p. injections of different doses of LPS dissolved in sterile saline. The amounts of gastric acid and pepsin secreted were determined 2, 4 or 8 h after injection. Small doses of LPS (10-1000 ng/rat) significantly inhibited the release of both gastric secretants as compared with control animals, and this inhibitory effect of LPS on gastric secretion was dose-related. The gastric antisecretory effect of LPS was still evident 8 h after injection, indicating that this action of LPS was long-lasting. These results suggest that LPS might be involved in the regulation of gastric secretion under certain pathophysiological conditions such as acute bacterial infections.

Animals↗
PubMed1990

Inhibition of gastric pepsin secretion by peripherally or centrally injected interleukin-1 in rats.

The present study was carried out to investigate the effects of Interleukin-1 (IL-1) on gastric pepsin secretion in conscious pylorus-ligated rats. The intraperitoneal (ip) injection of IL-1 resulted in a dose-related inhibition of gastric pepsin output. The intracerebroventricular (icv) injection of IL-1 similarly reduced pepsin secretion at 100 times smaller doses than ip IL-1, suggesting that this inhibitory action of IL-1 is mediated by the central nervous system (CNS). In addition, it was found that the antisecretory action of IL-1, both peripherally and centrally administered, lasted throughout the periods observed (2 hr through 8 hr after injection). These results strongly indicate that IL-1 is involved in the CNS regulation of gastric secretion, especially under certain pathophysiological conditions which activate the immune system to release various cytokines including IL-1.

Animals↗
PubMed1989

Indomethacin blocks the anorexic action of interleukin-1.

It has been reported recently that the central nervous system actions of interleukin-1 are mediated by the prostaglandin system in the brain. The present study was therefore performed in order to examine the hypothesis that indomethacin, an inhibitor of prostaglandin biosynthesis, might alleviate the interleukin-1-induced suppression of food intake in rats. The i.p. injection of interleukin-1 (2 micrograms/rat) resulted in a significant decrease in food intake. The pre-injection of indomethacin (0.5 mg/rat), however, completely blocked the anorexic action of the monokine, while indomethacin on its own did not affect food intake. These results suggested that indomethacin might be clinically useful for improvement of the anorexic state of patients with acute infectious diseases.

Animals↗