Faculty Opinions recommendation of Propentofylline, a CNS glial modulator does not decrease pain in post-herpetic neuralgia patients: in vitro evidence for differential responses in human and rodent microglia and macrophages.

Author(s):  
Odd-Geir Berge
Zygote ◽  
2000 ◽  
Vol 8 (3) ◽  
pp. 245-256 ◽  
Author(s):  
Michael B. Dinkins ◽  
Benjamin G. Brackett

Efforts to achieve complete chemical definition of media used for in vitro capacitation of bovine spermatozoa including removal of heparin purified from porcine intestinal mucosa are presented. Fluorescent staining with chlortetracycline (CTC), known to reflect changes coincident with sperm capacitation in certain species, was studied following treatments of frozen-thawed bull spermatozoa with β-cyclodextrins, dibutyryl cAMP (dbcAMP) and progesterone in comparison with heparin. The CTC staining patterns (F, B and AR) were confirmed to correlate with known conditions that effectively prepare cryopreserved bull spermatozoa for fertilisation in vitro. In the absence of glucose, the routinely employed heparin-containing capacitating medium caused an increase in spermatozoa displaying the AR pattern. Both progesterone (100 μM) and dbcAMP (0.01–0.1 mM) were able to increase the proportion of B pattern stained sperm cells more than after exposure to control (mDM) conditions without a significant reduction in motility. Exposure to either dbcAMP or β-cyclodextrins was accompanied by an increase in proportions of spermatozoa displaying the AR pattern over those seen in controls. Exposure to β-cyclodextrins did not increase the proportion of B pattern stained spermatozoa. Comparison of spermatozoa from two bulls revealed differential responses of spermatozoa from different males to treatments with heparin and progesterone. In vitro fertilisation results demonstrated that previously cryopreserved bull spermatozoa could be capacitated in chemically defined conditions devoid of heparin or other biological components.


1996 ◽  
Vol 271 (1) ◽  
pp. F87-F93 ◽  
Author(s):  
J. D. Imig ◽  
L. G. Navar

Arachidonic acid (AA) metabolites have been implicated in the control of renal hemodynamics, but the nature of the metabolites produced by renal cells when AA is released has remained uncertain. Experiments were performed using the in vitro perfused juxtamedullary nephron preparation to examine the effects of perfusion and superfusion of AA on the renal microvasculature. Extraluminal exposure of the vessels by superfusion with solutions containing 0.1, 1.0, and 10 microM AA decreased afferent arteriolar diameter by 8 +/- 2, 16 +/- 3, and 20 +/- 3%, respectively. The same doses of AA added to the perfusate produced a similar afferent arteriolar vasoconstriction. Inhibition of the major enzymatic pathways unmasked differential responses of AA that were dependent on the direction from which the vasculature was exposed to AA. 17-Octadecynoic acid (1 microM), an inhibitor of the cytochrome P-450 pathway, eliminated the vasoconstrictor response to superfused AA but had little effect on the response to perfused AA. Lipoxygenase inhibition with baicalein (0.5 microM) did not alter the afferent arteriolar vasoconstriction during superfusion with AA but did attenuate the vasoconstrictor response to perfused AA by 34%. Cyclooxygenase inhibition with 10 microM indomethacin reduced the afferent arteriolar response to superfusion with 10 microM AA by 46%, but the responses to perfusion with AA were reversed, leading to the unmasking of a 17% afferent arteriolar dilation. The AA-induced vasorelaxation observed during cyclooxygenase inhibition was prevented by the subsequent addition of a P-450 inhibitor. Additionally, after endothelial removal with 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate (CHAPS), the vasodilatory response reverted to a vasoconstriction. The results of this study demonstrate that in the rat, AA metabolites exert predominant actions on afferent arterioles, but differential responses are mediated via different enzymatic pathways depending on the origin of AA. Increased AA availability of intraluminal origin leads to production of cyclooxygenase-derived vasoconstrictor metabolites and also to endothelial-derived cytochrome P-450 vasodilatory metabolites. In contrast, increased AA availability of interstitial origin leads to production of vasoconstrictor cytochrome P-450 metabolites.


1990 ◽  
Vol 259 (1) ◽  
pp. F176-F185 ◽  
Author(s):  
C. E. Ruegg ◽  
L. J. Mandel

Innate biochemical responses of rabbit renal proximal convoluted (PCT) and straight (PST) segments following in vitro exposure to anoxia or hypoxia were investigated to delineate the mechanisms responsible for segment-selective injury in vivo. After bulk isolation, suspensions (1 mg/ml) enriched in either PCT or PST were preincubated in Dulbecco's modified Eagle's-Ham's F-12 medium for 1 h before being exposed to either 40 min of anoxia (N2) or 120 min of hypoxia (1% O2) and 1 h of recovery under air-CO2 conditions. After recovery from anoxia, the percent of control values for each viability indicator in PCT and PST, respectively, were as follows: O2 consumption (QO2), 30/50; ATP content, 22/49; K+ content, 60/70; and percent lactate dehydrogenase (LDH) release, 66/45. Likewise, following recovery from hypoxia, the percent of control values for PCT and PST, respectively, were as follows: QO2, 50/90; ATP, 16/57; K+, 52/79; LDH, 45/17. These differential responses indicate that PCT segments were innately more susceptible to anoxic and hypoxic injury than PST segments. Because ATP content was significantly higher in PST segments immediately after anoxia and hypoxia, we investigated glucose-dependent responses during anoxia by exposing these segments to 30 min of anoxia in nutrient buffer with or without glucose. Results from these experiments demonstrate that the PST protection from anoxia was glucose dependent because removal of glucose from the nutrient buffers during anoxia abolishes the differential responses between PCT and PST. The in vitro PCT sensitivity observed here contrasts with the PST sensitivity observed following in vivo ischemia, suggesting that hemodynamic factors present in vivo may ultimately determine the overall susceptibility of PST segments in situ.


2001 ◽  
Vol 85 (3) ◽  
pp. 207-214 ◽  
Author(s):  
Martina Dörger ◽  
Silvia Münzing ◽  
Anne-Marie Allmeling ◽  
Konrad Messmer ◽  
Fritz Krombach

1994 ◽  
Vol 72 (9) ◽  
pp. 1007-1012 ◽  
Author(s):  
N. Woodley ◽  
J. K. Barclay

Nous avons comparé la capacité des cellules endothéliales isolées de l'aorte, de la veine cave, de la chambre ventriculaire et du système microvasculaire pulmonaire du lapin de produire un ou des facteurs de relaxation en réponse à l'acetylcholine (ACh) et à la bradykinine (BK). Des anneaux aortiques de lapin dépouillés d'endothélium ont été précontractés avec 1 μM de phényléphrine et superfusés à 2 mL/min avec une solution tampon bicarbonatée de Krebs–Henseleit. Les anneaux ont été exposées à des épreuves témoins d'embols de 3 mL de 1 μM d'ACh ou 1 μM de BK. Les embols d'ACh et de BK ont été ajoutés à des cultures de cellules endothéliales qui avaient été incubées pendant 45 min dans des milieux contenant ou non 10 μM de NG-nitro-L-arginine (NNLA). La solution ainsi obtenue a été répandue sur les anneaux en moins de 8 s. Seules les cellules endothéliales ventriculaires gauches stimulées avec ACh et BK et les cellules endothéliales microvasculaires pulmonaires stimulées avec BK ont donné des produits qui ont relaxé les anneaux d'approximativement 6 ± 2%. L'incubation avec la NNLA a atténué ces relaxations. Nos résultats indiquent qu'il existe des différences dans la capacité des cellules endothéliales de divers sites anatomiques de libérer des facteurs de relaxation dérivés de l'oxyde nitrique en réponse à l'ACh et à la BK. Mots clés : facteur de relaxation dérivé de l'endothélium, aorte, dosage biologique in vitro, acétylcholine, bradykinine, superoxyde dismutase, nitroprussiate de sodium.[Traduit par la rédaction]


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