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  • 1
    Electronic Resource
    Electronic Resource
    Effects of dimethyl sulfoxide on heavy chain monoclonal antibody production from plant cell culture (1995)
    Springer
    Biotechnology letters 17 (1995), S. 463-468 
    Details
    ISSN: 1573-6776
    Source: Springer Online Journal Archives 1860-2000
    Topics: Process Engineering, Biotechnology, Nutrition Technology
    Notes: Summary The addition of 4% (v/v) dimethyl sulfoxide (DMSO) increased the total production of heavy chain monoclonal antibody (HC MAb) in suspension culture of genetically modified Nicotiana tabacum by three fold. This may be due to stabilization of HC MAb in the presence of DMSO by forming hydrogen bonds with proton-donor groups on protein molecules.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00132011
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  • 2
    Electronic Resource
    Electronic Resource
    The effects of pinacidil and tolbutamide in feline pial arteries in situ (1989)
    Springer
    Pflügers Archiv 415 (1989), S. 250-252 
    Details
    ISSN: 1432-2013
    Keywords: Pinacidil ; tolbutamide ; K+ channels ; cerebral arteries ; microapplication ; cerebral circulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The vasomotor effect of the K+ channel opener pinacidil was investigated in feline pial arteries of the parietal cortex. Perivascular microapplication (5μl in 40 sec) and an image splitting method for the measurement of vascular diameter were employed. Pinacidil (10−11 –10−7 M) induced concentration-dependent dilatations at 10−9 M and higher concentrations. A maximal dilatation of about 42% was achieved at 10−8 M, the dilatation at 10−7 M was reduced to 22%. The sulphonylurea tolbutamide exerted per se no effect in pial arteries but it blocked concentration-dependently the pinacidil induced dilatation. This is consistent with the presence of ATP-sensitive K+ channels in pial arteries which are closed under resting conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00370602
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  • 3
    Electronic Resource
    Electronic Resource
    pH-microclimate at the luminal surface of the intestinal mucosa of guinea pig and rat (1986)
    Springer
    Pflügers Archiv 407 (1986), S. 33-40 
    Details
    ISSN: 1432-2013
    Keywords: pH-Microclimate ; pH-Microelectrodes ; Colon ; Jejunum ; Guinea pig ; Rat ; in vitro ; in vivo
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Segments of guinea pig jejunum, proximal and distal colon and of rat jejunum were superfused either in vivo or in vitro with different electrolyte solutions. The pH in the bulk phase solution and at the surface of the epithelium was measured with two different types of glass pH-microelectrodes, a pointed tip (Hinke-type) and a flat membrane electrode (Dubuisson-type); both types of electrodes gave the same results. The existence of a pH-microclimate at the surface of the mucosa was demonstrated under both in vivo and in vitro conditions. In vivo the pH-microclimate was stable and virtually independent of changes in the luminal bulk phase pH. When the bulk phase pH of the guinea pig colon was changed between pH 5 and pH 8.6, the mean pH in the microclimate was 7.08±0.15 (n=163) in the proximal colon and 6.91±0.14 (n=75) in the distal colon. In the guinea pig jejunum pH in the microclimate was 7.37±0.21 (n=10) while the luminal pH was 7.27±0.10. Under in vitro conditions, the pH in the microclimate was more acidic (guinea pig jejunum ΔpH 0.93, rat jejunum ΔpH 0.40, guinea pig proximal colon ΔpH 0.22). Addition of glucose (10 mM) or short-chain fatty acids (80–90 mM) to the luminal solution or replacement of sodium by lithium did not influence the pH in the microclimate significantly. Also the addition of acetazolamide, amiloride, SITS or sodium deoxycholate to the luminal solution, did not affect the pH in the microclimate in vivo. A temporary interruption of the blood supply caused acidification of the pH in the microclimate. Restoring the blood flow reversed the effect, and the pH returned to the original values within a few minutes. The originally proposed acid-microclimate could not be confirmed under in vivo experimental conditions either in the jejunum or in the colon by direct measurement with pH-sensitive glass-microelectrodes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00580717
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  • 4
    Electronic Resource
    Electronic Resource
    Analysis of cromakalim-, pinacidil-, and nicorandil-induced relaxation of the 5-hydroxytryptamine precontracted rat isolated basilar artery (1991)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 343 (1991), S. 377-383 
    Details
    ISSN: 1432-1912
    Keywords: K+ channel openers ; Glibenclamide ; Cerebral arteries ; 5-Hydroxytryptamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of the K+ channel activators cromakalim, pinacidil, and nicorandil were investigated in endothelium intact, 5-hydroxytryptamine (5-HT) precontracted rat isolated basilar artery. Cromakalim, pinacidil, and nicorandil produced concentration-dependent relaxation of rat isolated basilar artery precontracted with 5-HT with a rank order of potency of cromakalim 〉 pinacidil 〉 nicorandil. All compounds produced full or nearly full relaxation. The calculated Hill coefficients for cromakalim-, pinacidil-, and nicorandil-induced relaxation of 5-HT-precontracted rat isolated basilar artery were 2.20 ± 0.36, 1.30 ± 0.07, and 1.00 ± 0.01, respectively. Under conditions of increased tone produced by 50 mmol/1 KCl (which inhibits cromakalim-induced relaxation) pinacidil and nicorandil produced marked reversal of spasm, with pinacidil being more potent than nicorandil. In arteries precontracted with 5-HT, preincubation with glibenclamide (0.1–1 μmol/1) produced concentration-related inhibition of relaxation with calculated mean pA 2 values (and slopes of Schild regression) ± SEM of 6.84 ± 0.20 (1.1 ± 0.20) against cromakalim, 6.60 ± 0.14 (0.95 ± 0.23) against nicorandil,and6.57 ± 0.26(1.04 ± 0.18) against pinacidil. For cromakalim, pinacidil, and nicorandil the slopes of Schild regression were not significantly different from unity. Tolbutamide 10 μmol/l was without effect against the cromakalim-, pinacidil-, or nicorandil-induced relaxation. Tetraethylammonium (TEA; 1–10 mmol/l) produced noncompetitive inhibition of the cromakalim-induced relaxation, but appeared to produce competitive inhibition of the pinacidil- and nicorandil-induced relaxations. We conclude that cromakalim, pinacidil, and nicorandil produce relaxation of the 5-HT precontracted rat basilar artery by similar mechanisms to those identified in other peripheral vascular and visceral smooth muscle. Furthermore, pinacidil and nicorandil differ from cromakalim in possessing marked spasmolytic activity in 50 mmol/l KCl precontracted arteries.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00179042
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  • 5
    Electronic Resource
    Electronic Resource
    Comparison of cromakalim-induced relaxation of potassium precontracted rabbit, cat, and rat isolated cerebral arteries (1991)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 343 (1991), S. 384-392 
    Details
    ISSN: 1432-1912
    Keywords: Cromakalim ; Glibenclamide ; Cerebral arteries ; K+ channel opener ; Potassium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of cromakalim were investigated in KCl-precontracted cat, rabbit, and rat isolated cerebral arteries with intact endothelium. Potassium induced contraction of all cerebral arteries studied, but exhibited marked vessel and species variation with no spasm to 20 or 30 mmol/l KCl in the rat basilar artery or 20 mmol/l KCl in the rabbit middle cerebral artery. On sustained tension to 20 mmol/l KCl, cromakalim induced concentration-related relaxation in the rabbit basilar artery and the cat basilar and middle cerebral arteries with Hill coefficients greater than unity. Cromakalim was more potent in the rabbit basilar artery precontracted with 20 or 30 mmol/KCl than in the rabbit middle cerebral artery or the cat basilar or middle cerebral artery. Elevation of the KCl concentration to 50 mmol/l inhibited cromakalim-induced relaxation and produced a decrease in the Hill coefficient. Preincubation of cerebral arteries with glibenclamide (100 nmol/l–1 μmol/1) produced concentration-related inhibition of the cromakalim-induced relaxation in the rabbit basilar, cat basilar, and cat middle cerebral arteries precontracted with 20 mmol/l KCl. The degree of rightward shift of concentration-effect curves by glibenclamide was calculated at the EC25, EC50, and EC75 levels. A good correlation was observed between the shifts at the EC50 and EC50 levels. However, the shift in concentration — effect curves for cromakalim produced at the EC25 level was markedly less than the-EC50 or EC75 levels in the presence of 1 μmol/1 glibenclamide. The pA 2 values for glibenclamide calculated at the EC50 level were 6.6 ± 0.09, 7.1 ± 0.1, and 6.5 ± 0.5 in the rabbit basilar, cat basilar, and cat middle cerebral artery, respectively. The slope of the Schild regression for the inhibitory effect of glibenclamide in the rabbit basilar artery was significantly greater than unity but did not differ from unity in cat cerebral arteries. Glibenclamide (1 μmol/l) produced a similar degree of inhibition of the cromakalim-induced relaxation in the 30 mmol/l KCl precontracted rabbit middle cerebral artery and in the rabbit basilar artery exposed to 20 mmol/l KCl. In contrast, tolbutamide 10 μmol/l was essentially inactive against the cromakalim-induced relaxation in all vessels studied. It is concluded that cromakalim produces concentration-dependent relaxations of rabbit and cat isolated cerebral arteries by a mechanism that is similar to that identified in peripheral vasculature and visceral smooth muscle. In this study we were unable to demonstrate effects of cromakalim on the KCl precontracted rat basilar artery, possibly due to the low sensitivity of this preparation to KCl.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00179043
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  • 6
    Electronic Resource
    Electronic Resource
    The dilatatory action of adenosine on pial arteries of cats and its inhibition by theophylline (1976)
    Springer
    Pflügers Archiv 362 (1976), S. 55-59 
    Details
    ISSN: 1432-2013
    Keywords: Pial arterial resistance ; Arterial resting tone ; Metabolic factors ; Cerebral blood flow ; Local regulation of pial arterial diameter
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of adenosine upon pial resistance vessels was studied using local microapplication from the perivascular side and measurement of vascular diameter. Concentration-response curves revealed a concentration-dependent dilatatory effect of adenosine between 10−7 and 10−3 M. The degree of dilatation was independent of initial vessel size (47–260 μ). The dilatations due to adenosine could be reduced by theophylline in a reversible competitive antagonism. Concentration-response curves for theophylline yielded no vascular reaction at concentrations of up to 10−5 M theophylline. From these data it is concluded that the pial arterial resting tone is not influenced under our experimental conditions by adenosine formed and released by brain tissue. The dilatations measured at high theophylline concentrations are apparently due to a mechanism different from the adenosine antagonism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00588681
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  • 7
    Electronic Resource
    Electronic Resource
    Measurements of the perivascular PO2 in the vicinity of the pial vessels of the cat (1979)
    Springer
    Pflügers Archiv 383 (1979), S. 29-34 
    Details
    ISSN: 1432-2013
    Keywords: Microcirculation ; Local control ; Brain ; Arterioles ; Tissue $$P_{O_2 } $$
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract $$P_{O_2 } $$ 's in the environment of the pial microvessels of the cat were measured using recessed tip oxygen microelectrodes. Measurements were made on the surface of vessels with internal diameters ranging from 200μm to 22μm. Blood oxygen partial pressures were also measured inside these vessels by penetrating the vessels with sharpened electrodes. Both intravascular and extravascular $$P_{O_2 } $$ values decreased progressively from the large arterial vessels down to the small arterioles. The observed values of intravascular $$P_{O_2 } $$ showed a systematic longitudinal decrease from 98.5±10.7 (SEM) mm Hg in the largest vessels down to 72.6±3.6 mm Hg in the smallest vessels. In addition to the longitudinal gradient, a transmural gradient was observed across the walls of the microvessels. The difference between blood $$P_{O_2 } $$ and vessel surface $$P_{O_2 } $$ was 27.0±2.5 mm Hg in the largest vessels and 6.0±2.2 in the smallest. The mean wall thickness in these groups of vesseis were 27.0±1.5 and 7.5±0.8 μm respectively. Measurements of the minimum tissue $$P_{O_2 } $$ on the exposed surface of the cortex yielded a value of 25.4±6.6 mm Hg. Systemic arterial partial pressure of oxygen averaged 94.7±4.7 mm Hg. The data indicate that significant gradients for oxygen exist both longitudinally and radially in association with the pial vessels. The longitudinal gradients represent losses of oxygen from the precapillary vessels. The transmural gradients are apparently the result of both consumption by the microvessel wall and diffusional gradients due to oxygen flux into the extravascular space.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00584471
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