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F Crews

Publications and source records attributed to F Crews.

6 recordsLinked to original sources
PubMed1993

Chronic ethanol exposure potentiates NMDA excitotoxicity in cerebral cortical neurons.

The effect of acute and chronic ethanol exposure on excitotoxicity in cultured rat cerebral cortical neurons was examined. Neuronal death was quantitated by measuring the accumulation of lactate dehydrogenase (LDH) in the culture media 20 h after exposure to NMDA. Addition of NMDA (25-100 microM) to the culture dishes for 25 min in Mg(2+)-free buffer resulted in a dose-dependent increase in LDH accumulation. Phase-contrast microscopy revealed obvious signs of cellular injury as evidenced by granulation and disintegration of cell bodies and neuritic processes. Chronic exposure of neuronal cultures to ethanol (100 mM) for 96 h followed by its removal before NMDA exposure, significantly increased NMDA-stimulated LDH release by 36 and 22% in response to 25 microM and 50 microM NMDA, respectively. Neither basal LDH release nor that in response to maximal NMDA (100 microM) stimulation was altered by chronic alcohol exposure. In contrast to the effects of chronic ethanol on NMDA neurotoxicity, inclusion of ethanol (100 mM) only during the NMDA exposure period significantly reduced LDH release by approximately 50% in both control and chronically treated dishes. This reduction by acute ethanol was also observed under phase-contrast microscopy as a lack of development of granulation and a sparing of disintegration of neuritic processes. These results indicate that chronic exposure of ethanol to cerebral cortical neurons in culture can sensitize neurons to excitotoxic NMDA receptor activation.

Animals↗
PubMed1983

Effects of verapamil on platelet aggregation, ATP release and thromboxane generation.

We examined the effects of verapamil on platelet function. Verapamil (0.5 micrograms/ml) in this study inhibited platelet aggregation induced by threshold amounts of ADP, AA, and epinephrine. With higher concentrations of aggregating stimuli, verapamil caused a dose-dependent inhibition of aggregation. Verapamil reduced the extent of epinephrine-induced primary wave, but not that by ADP. Ristocetin-induced aggregation was not affected at any concentration of verapamil. Platelet ATP release induced by AA and ADP was also inhibited. In vitro platelet TXA2 generation was inhibited by verapamil in concentrations lower than those required for inhibition of aggregation.

Adenosine Triphosphate↗
PubMed1982

Comparison of umbilical vein models for measurement of relative prostacyclin and thromboxane production.

There is growing evidence that blood vessels generate TXA2 in addition to PGI2. We examined effluents from continuously perfused human umbilical vein and supernatants from umbilical vein rings for TXB2 and 6-keto-PGF1 alpha measurements (stable metabolites of TXA2 and PGI2, respectively). TXB2 and 6-keto-PGF1 alpha were identified in all samples. 6-keto-PGF1 alpha to TXB2 ratio was higher in intact vein effluents than in the venous ring supernatants (112:1 and 28:1, respectively, P less than 0.01). Arachidonate stimulation increased 6-keto-PGF1 alpha and TXB2 levels similarly in the intact vein effluent. In contrast, stimulation of the venous rings resulted in a relatively larger increase in TXB2 than in 6-keto-PGF1 alpha. This caused 6-keto-PGF1 alpha to TXB2 ratio to decline (p less than 0.01). The identity of TXB2 was confirmed in several different ways. These data suggest that 1) human umbilical veins produce TXA2 in addition to PGI2, 2) TXA2 release is more by venous rings than by the intact vein probably reflecting contribution from non-endothelial layers, and 3) arachidonate stimulation causes relatively greater release of TXA2 than of PGI2 from the venous rings, whereas release of PGI2 and TXA2 is similar from the intact vein.

6-Ketoprostaglandin F1 alpha↗
PubMed1974

Anxious energetics.

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History, Modern 1601-↗