Biomedical subjects

F Ueda

Publications and source records attributed to F Ueda.

At least 37 records · Page 2Linked to original sources

PubMed1998

Effect of YNS-15P, a new alpha-2 adrenoceptor antagonist, on stress-stimulated colonic propulsion in rats.

We studied effects of a novel alpha-2 adrenoceptor antagonist, YNS-15P (N-[(2R,11bS)-9-methoxy-1,3,4,6,7, 11b-hexahydro-2H-benzoquinolizin-2-yl]-N-methylmethanesulfonami de hydrochloride), on colonic propulsion stimulated by wrap-restraint stress (WRS) or bethanechol, on normal colonic propulsion and on diarrhea induced by castor oil in rats. Alpha-2 adrenoceptor antagonists, rauwolscine and RX821002, decreased the increase in the number and weight of fecal pellets induced by WRS. YNS-15P also inhibited WRS-stimulated fecal excretion in a dose-dependent manner. A 5-hydroxytryptamine3 receptor antagonist, granisetron, trimebutine and diazepam, but not a 5-hydroxytryptamine4 receptor antagonist, GR113808, significantly inhibited WRS-stimulated fecal excretion. YNS-15P inhibited WRS-stimulated colonic transit in a dose-dependent manner. However, YNS-15P had no significant effect on normal fecal excretion and colonic transit or on bethanechol-stimulated fecal excretion. YNS-15P also failed to inhibit castor-oil-induced diarrhea. These results indicate that YNS-15P selectively inhibits WRS-stimulated colonic propulsion, and that alpha-2 adrenoceptors may be involved in stress-induced colonic motor dysfunction in fed rats.

Adrenergic alpha-2 Receptor Antagonists↗

PubMed1997

Uptake of 26-Al and 67-Ga into brain and other tissues of normal and hypotransferrinaemic mice.

Aluminium uptake from blood into tissues of control and homozygous hypotransferrinaemic (hpx/hpx) mice, following continuous intravenous infusion of 26Al and 67Ga, has been compared with that of gallium, a proposed tracer for aluminium. 26Al uptake into tissues of control (hpx/+ and +/+) mice occurred in the order (expressed as a space): bone 464.7 ml 100 g-1; renal cortex 102.9 ml 100 g-1; liver 13.0 ml 100 g-1; spleen 8.4 ml 100 g-1 and brain 0.8 ml 100 g-1. 67Ga uptakes were similar in liver, spleen and brain, but smaller in the renal cortex and bone, at one-third and one-fifth of the values for 26Al, respectively. In the hypotransferrinaemic mice, uptake of 67Ga into all tissues was increased, especially in renal cortex (ninefold) and bone (twentyfold) as compared with the controls. Increases in 67Ga uptakes into cerebral hemisphere, cerebellum and brain stem of the hypotransferrinaemic mice were 3.8, 4.2 and 2.8 fold, respectively. 26Al uptake into tissues of the hypotransferrinaemic mice was similar to control values except in bone where it was three times greater. Pre-treatment of control animals with the anti-transferrin receptor antibody, RI7 208, enhanced 67Ga uptake in all tissues, the effect being greatest in renal cortex (tenfold) and bone (ninefold). 67Ga uptakes into cerebral hemisphere, cerebellum and brain stem in the mice pre-treated with RI7 208 were 6.4, 6 and 10 times greater than in untreated mice, respectively. No influence of antibody on 26AI uptake into mouse tissues was observed except in spleen where it was three times greater than in untreated mice. Hence, transport of aluminium and gallium into mouse tissues is not similar under all conditions. Non-transferrin mediated transport of each metal can occur into all tissues, especially in renal cortex and bone, where gallium may be a suitable marker for aluminium.

Aluminum↗

PubMed1997

Effect of Irsogladine on gap junctions in cerulein-induced acute pancreatitis in rats.

The capacity for intercellular communication (IC) via gap junctions is found in normal pancreatic acinar cells. The major role of IC is considered to be the maintenance of tissue homeostasis and the regulation of signal transmissions. Up to now, the participation of IC via gap junctions in acute pancreatitis has not been reported. We investigated the role of IC in cerulein (Cn)-induced acute pancreatitis in rats using irsogladine, an enhancer of IC via gap junction. Acute edematous pancreatitis was induced in rats by two intraperitoneal injections of 40 micrograms/kg Cn. Rats received various doses (25, 50, or 100 mg/kg body weight) of irsogladine orally, 15 and 2 h before the first Cn injection. The normal control group received only vehicle. The severity of pancreatitis was evaluated enzymatically and histologically 5 h after the first Cn injection. In Cn-induced acute pancreatitis, irsogladine significantly lowered the serum amylase level, the pancreatic wet weight, and the pancreatic amylase and DNA contents, in a dose-dependent manner. Particularly, the amylase content improved to the level of the normal controls. Histologically, the severity of pancreatitis was reduced significantly by treatment with irsogladine and no discernible vacuolization was seen in the group with 100 mg/kg irsogladine treatment. By immunofluorostaining pancreata with anti-connexin 32 (Cx32; a gap junction protein) antibody, we found that pancreatic acini were diffusely positive for Cx32 in the control group, but the number of Cx32-positive grains decreased markedly, to 19%, in the pancreatitis group. With 100 mg/kg irsogladine treatment, the number of Cx32 grains recovered to 70% of the normal control value. These findings indicate that IC via gap junction is disturbed in Cn-induced pancreatitis, which may result in the breakdown of tissue homeostasis and the progression of acute pancreatitis.

Acute Disease↗

PubMed1996

Tuberculous tenosynovitis in the elbow joint.

A 74-year-old woman was noted to have a mass lesion near the right elbow joint during medication for pulmonary tuberculosis. After discontinuation of medication, the mass gradually became enlarged with swelling and tenderness of the joint. Radiological evaluation disclosed tenosynovitis with an encapsulated abscess. Microscopic examination and culture of an aspiration biopsy specimen from the abscess showed no microorganisms. However, DNA extracted from the specimen contained mycobacterium tuberculosis DNA, permitting a diagnosis of tuberculous tenosynovitis. Mycobacterium is not always detected in biopsy specimens of tuberculous arthritis and tenosynovitis. In such cases, genetic diagnosis may be of great use.

Abscess↗

PubMed1995

Inhibition of intercellular communication via gap junction in cultured aortic endothelial cells by elevated glucose and phorbol ester.

Gap junctional intercellular communication (GJIC) is important in coordinating the cells in maintaining tissue homeostasis and in regulating signal transmission. We examined the effect of elevated glucose on GJIC activity in cultured bovine aortic endothelial cells. GJIC activity was assessed by quantitating the transfer from cell to cell of directly microinjected fluorescent dye molecules. GJIC was activated in the subconfluent monolayer. In this condition, exposing the cells to elevated glucose (400 mg/dl) for 24 hrs significantly inhibited GJIC activity, as compared with low glucose (100 mg/dl). This inhibition of GJIC activity induced by elevated glucose was mimicked by addition of 12-O-tetradecanoylphorbol-13-acetate and was restored by addition of staurosporin (10(-8)M), a PKC inhibitor. These results suggest that inhibition of GJIC activity induced by elevated glucose probably through activation of PKC may be involved in the vascular endothelial cell dysfunction associated with diabetes.

Alkaloids↗

PubMed1995

Quality of peptic ulcer healing induced by lansoprazole and roxatidine.

This study reports preliminary results of a controlled, multicenter trial on the quality of ulcer healing induced by lansoprazole (LPZ) or roxatidine (R) in gastric ulcer (GU) or duodenal ulcer (DU) patients. Group A received LPZ 30 mg q.d. and group B received R 75 mg b.i.d. All drugs were given for 8 weeks in GU and for 6 weeks in DU. Endoscopy and gastric biopsy were performed to detect Helicobacter pylori before and on completion of treatment. The healing rates of groups A and B were 100 and 69.2%, respectively, in GU and 100 and 70.0%, respectively, in DU. This difference (p < 0.01) was significant between the two groups in GU. There was no significant difference between the two groups in the S2 stage shift rate in GU and DU. The H. pylori clearance rates of groups A and B were 33.3 and 20.0%, respectively, in GU and 62.5 and 33.3%, respectively, in DU. The differences in treatment response (healing rates and S2 shift rates) between the LPZ group and the R group may be related to the differences in suppression of acid secretion and in bactericidal effects on H. pylori.

2-Pyridinylmethylsulfinylbenzimidazoles↗

PubMed1995

[Ameliorating effect of lactitol on experimental hepatic encephalopathy in Eck fistula dogs].

Eck fistula (portacaval shunted) dogs were prepared for use as an experimental model of chronic hepatic encephalopathy. The effect of lactitol on hepatic encephalopathy was investigated by observing the behavior, electroencephalograms (EEGs) and visually evoked potentials (VEPs) of the experimental dogs. Lactitol was administered intragastrically once a day for 12 weeks from the third week after the portacaval-shunt operation and the behavior, EEGs and VEPs of the dogs were observed every two weeks. Dogs not given lactitol became sluggish, then apparently blind, and eventually fell into a coma, over a period of several weeks after the operation. Some dogs died. The EEGs revealed low-voltage slow waves and, at a later stage, displayed flattening in some dogs. The VEPs displayed prolonged latency of both the positive and the negative component as well as an increased amplitude. Lactitol at 1 or 3 g/kg/day suppressed the behavioral symptoms and the changes in the EEGs and the VEPs. These results suggest that lactitol may be useful for the treatment of various nervous symptoms in patients with hepatic encephalopathy accompanied by hyperammonemia.

Animals↗

PubMed1995

Mechanism for lowering blood ammonia levels by lactitol.

Lactitol has been reported to decrease the blood ammonia concentration in various experimental hyperammonemia models such as portacaval shunted rats. The mechanism responsible for this lowering of blood ammonia levels was investigated in rats. When lactitol was given orally twice a day for 7 days at doses of 3 and 10 g/kg/day and at half that daily dose on day 8, it significantly decreased the ammonium concentration of the portal blood by 27.3-43.2%, cecal ammonia contents by 49.2-57.6% and the pH of the cecal contents from 6.52 to 5.92-5.54, 4 hr after the final administration. Lactitol also inhibited increases in the portal ammonia concentration induced by the intracecal administration of ammonium acetate (300 mg/kg) 4 hr after the final administration. When lactitol was given orally at bolus doses of 1 and 3 g/kg simultaneously with a charcoal meal, lactitol significantly facilitated small intestinal transit by 12-13%. At a bolus dose of 3 g/kg, given 1 hr before the administration of a charcoal meal into the proximal colon, lactitol significantly facilitated colonic transit by 29.5%. These effects of lactitol were similar to those of lactulose. These findings suggest that lactitol decreases blood ammonia concentration by inhibiting both the production and the absorption of ammonia through reducing intestinal pH and shortening the residence time of intestinal contents in the intestinal tract.

Acetates↗

PubMed1995

Irsogladine inhibits ionomycin-induced decrease in intercellular communication in cultured rabbit gastric epithelial cells.

Effects of irsogladine on ionomycin-induced decrease in intercellular communication and increase in intracellular concentration of Ca2+ ([Ca2+]i) were investigated in cultured rabbit gastric epithelial cells. Ionomycin (10(-7)-10(-6) M) transiently and concentration-dependently inhibited intercellular communication concomitantly with the elevation of [Ca2+]i in the presence and absence of extracellular Ca2+. Irsogladine (10(-5) M), which has been shown to facilitate intercellular communication, suppressed the ionomycin-induced elevation of [Ca2+]i and decrease in intercellular communication. The suppression of the ionomycin effects by irsogladine was independent of extracellular Ca2+. TMB-8 [8-(diethylamino)octyl-3,4,5-trimethoxy-benzoate hydrochloride] (10(-6) M) also suppressed the ionomycin-induced elevation of [Ca2+]i and decrease in intercellular communication. These results indicate that the ionomycin-induced decrease in intercellular communication may be due to Ca2+ mobilization from intracellular stores. Inhibitory effects of irsogladine and TMB-8 on the ionomycin-induced decrease in intercellular communication may be produced by suppressing Ca2+ mobilization.

Animals↗

PubMed1995

Irsogladine activates gap-junctional intercellular communication through M1 muscarinic acetylcholine receptor.

Irsogladine, an agent that protects gastric mucosa against various ulcerogenic stimuli through increasing cyclic AMP in surface mucous cells, has been reported to dose-dependently (10(-7) to 10(-5) M) facilitate gap-junctional intercellular communication (GJIC) in gastric epithelial cells. The beta adrenergic agonist, isoproterenol, stimulates GJIC in resting cells and inhibits GJIC in cells activated by 3-isobutyl-1-methylxanthine. In this study, we investigated whether irsogladine acts on GJIC in a manner similar to that shown by isoproterenol. Irsogladine, which bound to M1 muscarinic acetylcholine receptors (mAChR), did not inhibit, but failed to further facilitate the 3-isobutyl-1-methylxanthine-enhanced GJIC, measured by Lucifer yellow transfer. The enhancement of GJIC by irsogladine was inhibited by the M1 mAChR antagonist, pirenzepine. A selective M1 mAChR agonist, McN-A-343, enhanced GJIC. Isoproterenol (10(-8) to 10(-6) M), which alone did not affect GJIC, inhibited the GJIC enhanced by 10(-5) M irsogladine. Conversely, 10(-10) to 10(-6) M irsogladine, which alone did not affect GJIC, inhibited the GJIC enhanced by 10(-5) M isoproterenol. McN-A-343 also converted the action of 10(-5) M isoproterenol from facilitation to inhibition of GJIC. These results indicate that GJIC is heterologously down-regulated by cross-talk between M1 mAChR and beta adrenergic receptors. In addition, the effects of irsogladine and isoproterenol at low concentrations suggest the involvement of another mechanism for down-regulating GJIC.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗

PubMed1994

Contrasting uptakes of 59Fe into spleen, liver, kidney and some other soft tissues in normal and hypotransferrinaemic mice. Influence of an antibody against the transferrin receptor.

Uptake of iron-59 from blood into various soft tissues of anaesthetized mice was investigated by continuous intravenous infusion of the radiotracer during 2 hr. The 59Fe was given either as ferrous chloride with ascorbate or as 59Fe-transferrin. Infusions were made into adult mice with and without pretreatment with a monoclonal antibody against transferrin receptors, and into hypotransferrinaemic mice and appropriate controls. In normal mice, 59Fe uptake into spleen was much higher than into other tissues and was 94-96% inhibited by the antibody. Inhibitions due to the antibody were less complete in liver and renal cortex, and there was evidence of some non-transferrin-mediated transport during infusion of 59Fe/ascorbate. In the hypotransferrinaemic mice, tissue uptakes of 59Fe during infusion of 59Fe/ascorbate were enormous, being two to three orders of magnitude greater than in the normal controls. The rank order for size of uptake was liver > renal cortex > pancreas > spleen > other tissues. All tissues examined have a considerable potential capacity for uptake of non-transferrin-bound iron, this being greatest in liver and renal cortex.

Animals↗

PubMed1994

Effect of anti-inflammatory agent etodolac on antigen-induced contractions of the trachea and lung parenchyma of guinea pigs.

Etodolac, which inhibits the activity of cyclooxygenase, did not affect antigen-induced contractions of the trachea and lung parenchyma of guinea pigs. Indomethacin tended to enhance antigen-induced contractions of the trachea and significantly enhanced contractions of the lung parenchyma. The inhibitory activity of AA-861, a 5-lipoxygenase inhibitor, in antigen-induced contractions of the trachea and lung parenchyma was more potent than that of ozagrel, a thromboxane A2 (TXA2) inhibitor. Thus, lipoxygenase products played a more important role than TXA2 in antigen-induced contractions of the trachea and lung parenchyma. These results suggest that the enhancement of antigen-induced contractions by indomethacin might be due to an increase in anaphylactic release of lipoxygenase products through the inhibition of cyclooxygenase. Since etodolac did not enhance antigen-induced contractions, we attempted to determine whether or not etodolac inhibits 5-lipoxygenase. Etodolac was found to have no effect on 5-lipoxygenase activity. Therefore, the low adverse effect of etodolac on antigen-induced contractions of the airway may be due to its weak inhibition of cyclooxygenase in the airway. These results suggest that etodolac would have only a very slight, if any, adverse effect on the airway in patients with asthma.

Animals↗

PubMed1994

Effect of etodolac on prostaglandin E2 biosynthesis, active oxygen generation and bradykinin formation.

The inhibitory actions of etodolac on prostaglandin (PG) E2 biosynthesis, active oxygen generation and bradykinin formation were compared with those of indomethacin, diclofenac Na, piroxicam, naproxen, ketoprofen and aspirin. The inhibitory action (IC50 5.35 x 10(-8) M) of etodolac on PGE2 biosynthesis in rabbit articular chondrocytes stimulated by interleukin-1 (IL-1) beta was about 1/5 that of indomethacin. The inhibitory action of etodolac on spontaneous PGE2 biosynthesis in rabbit gastric epithelial cells (RGEs) (IC50 2.27 x 10(-5) M) and Madin-Darby canine kidney cells (MDCKs) (IC50 4.54 x 10(-7) M) was much less than that in rabbit articular chondrocytes stimulated by IL-1 beta and about 1/19 and 1/9 that of indomethacin in rabbit gastric epithelial cells (RGEs) and Madin-Darby canine kidney cells (MDCKs), respectively. The inhibitory action of etodolac on active oxygen generation was similar to that of indomethacin and piroxicam, and more potent than that of naproxen, ketoprofen and aspirin. The inhibitory action of etodolac on bradykinin formation was the most potent among the seven anti-inflammatory drugs tested. Both etodolac and bromelain inhibited the inflammatory pain in concanavalin A-treated paws of rats in a dose-dependent manner, but indomethacin did not. These results indicate that etodolac is an anti-inflammatory drug which suppress IL-1 beta-stimulated PGE2 biosynthesis in rabbit articular chondrocytes, active oxygen generation and bradykinin formation. It has less suppressive action against spontaneous PGE2 biosynthesis in RGEs and MDCKs. Thus, etodolac is considered to be a safe anti-inflammatory drug for clinical use.

Animals↗

PubMed1994

Transport of zinc-65 at the blood-brain barrier during short cerebrovascular perfusion in the rat: its enhancement by histidine.

Zinc-65 transport into different regions of rat brain has been measured during short vascular perfusion of one cerebral hemisphere with an oxygenated HEPES-containing physiological saline at pH 7.40. The [Zn2+] was buffered with either bovine serum albumin or histidine. In each case uptake was linear with time up to 90 s. 65Zn flux into brain in the presence of albumin followed Michaelis-Menten kinetics and for parietal cortex had a Km of 16 nM and a Vmax of 44 nmol/kg/min. Increasing concentrations of L-histidine enhanced 65Zn flux into brain at [Zn2+] values between 1 and 1,000 nM. The combined effect of [histidine] and [Zn2+] was best accounted for by a function of [ZnHis+], i.e., flux = 64.4.[ZnHis+]/(390 + [ZnHis+]) + 0.00378.[ZnHis+], with concentrations being nanomolar. D-Histidine had an influence similar to that of L-histidine. 65Zn flux in the presence of 100 microM L-histidine was not affected by either 500 microM L-arginine or 500 microM L-phenylanine. The results indicate specific transport of Zn2+ across the plasma membranes of brain endothelium. The enhancement due to histidine has been attributed to diffusion of ZnHis+ across unstirred layers "ferrying" zinc to and from transport sites.

Animals↗

PubMed1994

Anti-inflammatory effects of etodolac: comparison with other non-steroidal anti-inflammatory drugs.

The anti-inflammatory effects of etodolac (Eto) were compared with those of 6 other anti-inflammatory drugs: indomethacin (Ind), diclofenac Na (Dic), piroxicam (Pir), naproxen (Nap), ketoprofen (Ket) and aspirin (Asp). Eto inhibited carrageenin-induced edema in rats, adjuvant-induced arthritis in rats, acetic acid-induced writhing in mice and brewer's yeast-induced hyperalgesia and fever in rats. In the adjuvant arthritis test, the ED30 value (1.88 mg/kg) on day 3 and ED50 values (adjuvant-injected paw: 1.18 mg/kg and non-injected paw: 0.96 mg/kg) on day 18 for Eto were comparable to those for Dic (2.16, 1.72 and 1.28) when given prophylactically and the ED50 values for Eto (adjuvant-injected paw: 1.61 and non-injected paw: 1.20 mg/kg) were comparable to those for Ket (1.24 and 1.22) when used therapeutically. The analgesic activity of Eto (ED50 value: 3.67 mg/kg) in the acetic acid-induced writhing test was greater than that of Nap (9.83) or Asp (31.6) and less than that of Ind (0.71), Dic (1.54), Pir (0.92) or Ket (1.34). In the antipyretic test, the minimum effective dose (MED: 1 mg/kg) for Eto was comparable to that for Ind (1.0), Nap (1.0) or Ket (1.0). Eto was less potent in inhibiting carrageenin-induced edema (ED30 value: 6.99 mg/kg) and inflammatory pain (ED50 value: 9.24 mg/kg) than the other drugs (Ind: 2.32 and 3.47, Dic: 0.69 and 3.80, Pir: 1.31 and 1.94, Nap: 1.83 and 2.78, Ket: 1.12 and 0.63), except for Asp (167 and 51.8).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗

PubMed1994

Adrenergic regulation of prostaglandin biosynthesis in cultured rabbit gastric epithelial cells.

Adrenergic regulation of prostaglandin (PG) biosynthesis was investigated in 1-14C-arachidonic acid-prelabeled cultured rabbit gastric epithelial cells (RGECs). RGECs expressed adrenergic alpha 1- and beta-receptors and muscarinic receptors. Norepinephrine facilitated the synthesis of PGs I2 (determined as the stable metabolite 6-keto PGF1 alpha) and E2 and hydroxyfatty acids, while epinephrine facilitated the synthesis of PGI2 and hydroxyfatty acids, but not PGE2. However, isoproterenol did not affect PG biosynthesis. The effects of norepinephrine and epinephrine on PG biosynthesis were markedly suppressed by the non-selective alpha-blocker phentolamine and/or the selective alpha 1-blocker prazosin. In combination with epinephrine, the selective alpha 2-blocker yohimbine or the beta-blocker propranolol facilitated PGE2 synthesis. Acetylcholine did not affect PG biosynthesis. These results indicate that norepinephrine and epinephrine act on PG biosynthesis as adrenergic agonists in these cultured RGECs and that an alpha 1-receptor couples PGI2 and PGE2 synthesis.

6-Ketoprostaglandin F1 alpha↗

PubMed1994

Beta-adrenergic regulation of gap-junctional intercellular communication in cultured rabbit gastric epithelial cells.

The effect of a beta-adrenergic agonist, isoproterenol, on gap-junctional intercellular communication (GJIC) and intracellular cyclic AMP (cAMP) content was investigated in cultured rabbit gastric epithelial cells. Isoproterenol rapidly enhanced GJIC determined by the Lucifer yellow transfer at 10(-6) and 10(-5) M but the effect at 10(-6) M was variable. The enhancement of GJIC by 10(-5) M isoproterenol, which disappeared within 10 or 30 min, was inhibited by a beta blocker, propranolol. Isoproterenol (10(-6) M) greatly increased cAMP at 5 min and much more so at 20 min after its addition. Colforsin (also known as forskolin) and 3-isobutyl-1-methylxanthine (IBMX) enhanced GJIC until 16 and 20 min after their addition, respectively. Both colforsin and IBMX increased the cAMP content by a lesser extent than 10(-6) M isoproterenol. Isoproterenol (10(-5) M) inhibited the GJIC enhanced by colforsin or IBMX. Propranolol abolished the inhibition of GJIC by isoproterenol in the presence of IBMX. Both amiloride, an inhibitor of the Na+/H+ exchanger, and nigericin, a K+/H+ antiporter, inhibited the GJIC enhanced by isoproterenol, IBMX, colforsin and irsogladine. An inhibitor of cAMP-dependent protein kinase A, H-89 (N-[2-((3-(4- bromophenyl)-2-propenyl)-amino)-ethyl]-5-isoquinolinesulfonamide), abolished the enhancement of GJIC by colforsin and IBMX but did not abolish that by isoproterenol.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗

PubMed1993

[MR imaging of postoperative change of dura mater of rabbits--effect of contrast enhancement of dura mater & correlation with pathological findings].

To explain the mechanism of benign postoperative dural enhancement, the author made experimental model of rabbit's subdural hematoma and performed magnetic resonance (MR) imaging with gadolinium-diethylenetriaminepentaacetic acid (Gd-DTPA). On plain T1-weighted images, infused blood or red blood cells could not be detected immediately after surgery. On follow up plain T1-weighted images, the infused blood could be identified in only a case with 1 cc blood infusion. Marked dural enhancement could be seen immediately after surgery and continued three to fourteen days after 1 cc or 0.1 cc blood or 0.1 cc red blood cells infusion. To the contrary, no definite dural enhancement could be seen in the cases with plasma or saline infusion. Subdural red blood cells were required for dural enhancement immediately after surgery. Pathological findings revealed three types of reaction to infused blood: newly formed capillarization with fresh hemorrhage from the capillaries; subdural hematoma and no reaction. After vanishment of dural enhancement, pathological findings of the specimens were identical to that of normal dura. Dural enhancement may be induced by increased permeability of the dura associated with subdural hematoma and/or the extravasation of the contrast from newly formed capillaries.

Animals↗