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Volume 107 (1996)
- Issue 6 Pages 259-
- Issue 5 Pages 213-
- Issue 4 Pages 173-
- Issue 3 Pages 97-
- Issue 2 Pages 47-
- Issue 1 Pages 1-
Volume 107, Issue 4
Displaying 1-3 of 3 articles from this issue
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Takaki YAMAMURA1996 Volume 107 Issue 4 Pages 173-182
Published: 1996
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSDespite being small and simple in structure the nitric oxide free radical (NO·) is now proving to be of vital physiological significance, and it has been shown to play important roles in complex processes such as vasodilatation, inflammation, thrombosis, immunity and neurotransmission. To conduct meaningful research into the role of NO·, it is necessary to accurately determine its concentration. Its direct and quantitative measurement, however, has been little discussed inspite of the abundance of studies on this compound. Generally most authors refer to indirect qualitative measurements, such as employment of NO-synthase inhibitors, measurement of cGMP or citrulline, and the detection of NO·-induced physiological effects such as vascular relaxation. The primary difficulties in the direct measurement of NO stem from its short lifetime and very low concentrations. Notwithstanding these problems, several quantitative methods for measuring NO· have been established. The most commonly used techniques are as follows: 1) UV-visible spectrophotometry of the diazotization product of the nitrite, NO-hemoglobin or methemoglobin, 2) fluorometry of the fluorescent product of the nitrite, 3) detection of chemiluminescence by its reaction with ozone or luminol/H2O2, 4) amperometric microelectrode assay, and 5) electron spin resonance spectrometry. All the aforementioned techniques have certain limitations that should be considered carefully prior to each application.View full abstractDownload PDF (8039K) -
Mamoru KOBAYASHI, Kazuhiko SHINAGAWA, Masaru SUGIURA, Tatsuya NAGASAWA ...1996 Volume 107 Issue 4 Pages 183-195
Published: 1996
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSWe investigated the protective and/or therapeutic effects of a new cholecystokinin receptor antagonist, KSG-504, on different types of experimental pancreatitis in the rat and mouse. The intravenous injection of KSG-504 (10, 25, 50 and 100 mg/kg) before caerulein administration to the rat inhibited the increases in plasma amylase, lipase and of pancreatic wet weight in a dosedependent manner. The histological changes due to caerulein-induced acute pancreatitis were also decreased by KSG-504 when KSG-504 (25, 50 and 100 mg/kg) was administered after the induction of acute pancreatitis; the increases in plasma amylase, lipase and pancreatic wet weight were reduced, but the histological changes of the pancreas were not decreased significantly. In the second experiment, acute pancreatitis was induced in rats by injecting 0.3 ml of 6% sodium taurocholate into the pancreatic interstitial tissue. KSG-504 administered immediately and 1.5 hr after sodium-taurocholate injection at 100 mg/kg reduced the increases of pancreatic enzymes in the plasma, pancreatic wet weight and ascites. Moreover, KSG-504 (50 and 100 mg/kg, i.v., × 2) mitigated the histological changes of taurocholate-induced acute pancreatitis. Another type of acute pancreatitis was induced in mice by dl-ethionine (0.5 g/kg, p.o., ×4) and a choline-deficient diet. KSG-504 (10, 30 and 100 mg/kg) was subcutaneously administered five times every 12 hr during the experiment. KSG-504 elongated the survival of mice in a dose-dependent manner. These findings suggest that KSG-504 has potent protective and/or therapeutic effects against acute pancreatitis and that cholecystokinin may be involved in the development of pancreatitis.View full abstractDownload PDF (11980K) -
Chikako MORI, Reiko NATSUKI1996 Volume 107 Issue 4 Pages 197-203
Published: 1996
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSThe effect of ethanol on nitric oxide synthase (NOS) activity was examined histochemically and biochemically in cultured cerebral cells of chick embryos. The cells were isolated from 13- to 14-day-old chick embryos to which 10% ethanol (ethanol group) or saline (control) had been injected on the 3rd day of embryogenesis. Expression of NADPH diaphorase in cultured cells was stained using nitro blue tetrazolium (NBT). The activity of NOS was observed by the following 2 assays: NADPH diaphorase activity was determined using the substrate NBT with the cofactor NADPH, and NOS activity was determined by measurement as radiochemical activity of the conversion of [3H] L-arginine to [3H] L-citrulline. The number of isolated cells and viability from one cerebrum of chick embryo were 3 ?? 4 × 106 and more than 97%, respectively. In the neuronal cells, moderately positive expression of NADPH diaphorase was first detected on about the 3rd day of culture in both the control and ethanol group. The NADPH diaphorase and NOS activities in the isolated cells were higher in the ethanol group than in the control group. The NADPH diaphorase and NOS activities were significantly higher in the ethanol group than in the control group on the 4th and 2nd day of culture, respectively. These findings suggest that NO-released by elevated NADPH diaphorase activity and NOS activity is responsible for the induction of neuronal cell disorders attributed to chronic ethanol damage.View full abstractDownload PDF (5162K)
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