1. |
- Belfrage, Per, et al.
(author)
-
Dispersion of viable pig liver cells with collagenase
- 1975
-
In: Life Sciences. - : Elsevier BV. - 1879-0631 .- 0024-3205. ; 17:8, s. 1219-1225
-
Journal article (peer-reviewed)abstract
- Viable suspended hepatocytes were prepared from surgical biopsy specimens of pig and human liver by digestion with collagenase. Initial perfusion of the tissue through cannulated blood vessels with 0.5 mM EGTA followed by 0.2% collagenase gave the best results. 20−870 × 106 cells of which 60–95 % excluded trypan blue were obtained from 5–30 g pig liver pieces, while results with human liver specimens were usually less satisfactory. In some experiments, however, viable cells, as judged by vital stain exclusion and ability to synthesize lipids were obtained in sufficient yield. In the pig hepatocytes glycerolipid synthesis from [3H] glycerol and oxidation and esterification of [14C] oleic acid had the same characteristics as those observed earlier in rat hepatocytes.
|
|
2. |
- Björkman, Sven, et al.
(author)
-
Cerebral uptake of morphine in the pig calculated from arterio-venous plasma concentration gradients: an alternative to tissue microdialysis
- 1995
-
In: Life Sciences. - 1879-0631 .- 0024-3205. ; 57:25, s. 2335-2345
-
Journal article (peer-reviewed)abstract
- The aim of this study was to characterize the reversible cerebral uptake of morphine in the pig by measuring the changing arterio-venous plasma concentration gradient over the brain. Seven pigs were anaesthetized by continuous infusions of ketamine and pancuronium and ventilated with oxygen in nitrous oxide. During and after 5-min intravenous infusions of morphine hydrochloride, blood samples were drawn from a central artery and from the internal jugular vein. Concomitantly, cerebral blood flow (CBF) was repeatedly measured as clearance of 133Xe from the brain after intracarotid injection. Plasma concentrations of morphine and, in samples from two animals, morphine glucuronides were assayed by high-performance liquid chromatography. Drug flux (Jnet) from arterial blood to brain was calculated from the arterio-venous plasma concentration gradients, the blood:plasma concentration ratio and CBF. Uptake of morphine from arterial blood to brain was very rapid, with a maximal Jnet typically at 3 min after the beginning of the infusion. The initial cerebral extraction of morphine was close to 50%. When the arterial and jugular venous concentration curves crossed, 1-5 min after the end of the infusion, the initially rapid uptake of morphine changed into a slow and steady release. The cerebral extraction of morphine glucuronides was comparable to that of morphine, however, Jnet was lower due to lower plasma concentrations at time of maximal extraction. The findings demonstrate how the cerebral uptake and release of morphine and its metabolites can be studied with a method that is entirely non-invasive to the brain and permits very flexible sampling. Uptake and release of drug is observed directly and need not be inferred from cerebral concentration curves.
|
|
3. |
- Caron, Murielle, et al.
(author)
-
Effects of ethanol on phosphoinositide hydrolysis and muscarinic acetylcholine receptor number in SH-SY5Y cells
- 2000
-
In: Life Sciences. - : Elsevier BV. - 0024-3205. ; 67:4, s. 56-447
-
Journal article (peer-reviewed)abstract
- Previous studies suggest that the effects of ethanol on carbachol-stimulated I(1,4,5)P3 formation and on the number of mAChRs may be independent of each other. The aim of this work was to further study this hypothesis. Human neuroblastoma SH-SY5Y cells were used as a model system. Acute exposure of the cells to 100 mM ethanol induced a decrease in [3H]N-methylscopolamine ([3H]NMS) binding at 30 seconds which was of lower magnitude and of shorter duration than the previously described ethanol-induced inhibition of the peak of carbachol-stimulated I(1,4,5)P3 formation. Long-term ethanol treatment of the cells induced a time- and concentration-dependent increase in [3H]NMS binding. Three hours of 100 mM ethanol treatment were sufficient to increase the number of mAChRs at the cell surface but these receptors were not immediately functionally active, suggesting that they may be newly synthesized. Furthermore, the ethanol-induced potentiation of carbachol-stimulated I(1,4,5)P3 formation, after two days, was, for all ethanol concentrations tested, of higher magnitude than the ethanol-induced increase in mAChR number. Together, these data indicate that both acute and chronic ethanol-induced changes in carbachol-stimulated I(1,4,5)P3 formation may not only be explained by changes in mAChR density at the cell surface but may rather be the consequence of actions of ethanol down-stream of the receptor.
|
|
4. |
- Nilsson-Ehle, Peter, et al.
(author)
-
Specific conditions for enhancement of lipoprotein lipase activity by platelets
- 1975
-
In: Life Sciences. - : Elsevier BV. - 1879-0631 .- 0024-3205. ; 16:11, s. 1703-1709
-
Journal article (peer-reviewed)abstract
- Homogenates of human blood platelets, but not of red blood cells, have been found to stimulate lipoprotein lipase activity only when assayed against an emulsified triglyceride substrate sonicated for a short period of time. The degree of stimulation was inversely related to the time of sonication of the substrate. Using chylomicrons as substrate no stimulation of lipoprotein lipase activity by platelet homogenate was seen.
|
|
5. |
- Simonsson, Per, et al.
(author)
-
The 5-hydroxytryptamine stimulated formation of inositol phosphate is inhibited in platelets from alcoholics
- 1988
-
In: Life Sciences. - : Elsevier BV. - 1879-0631 .- 0024-3205. ; 42:4, s. 385-391
-
Journal article (peer-reviewed)abstract
- The accumulation of inositol monophosphate (IP1) was measured after stimulation of 5-hydroxytryptamine2 (5-HT2) receptors on platelets from alcoholics and healthy controls. In controls, 5-HT induced a dose-dependent response with an EC50 = 2 x 10(-6) M and a maximal response at 10(-5) M. Ritanserin, a selective 5-HT2 antagonist, markedly reduced the accumulation. The IP1 formation after stimulation by 10(-5) M 5-HT was significantly impaired in platelets from alcoholics as compared to controls. This study indicates that the 5-HT2 receptor function is inhibited in alcoholics. It also illustrates the possibility of using IP1 formation in peripheral cells as a mean of studying receptor function in disease.
|
|
6. |
|
|
7. |
|
|
8. |
|
|
9. |
|
|
10. |
|
|