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. 1997 Feb;120(4 Suppl):439-43; discussion 437-8.
doi: 10.1111/j.1476-5381.1997.tb06831.x.

Prostacyclin (PGI2) inhibits the formation of platelet thrombi in arterioles and venules of the hamster cheek pouch. 1977

E A Higgs, G A Higgs, S Moncada, J R Vane

Prostacyclin (PGI2) inhibits the formation of platelet thrombi in arterioles and venules of the hamster cheek pouch. 1977

E A Higgs et al. Br J Pharmacol. 1997 Feb.

Abstract

  1. Isolated rings of hamster aorta produced an unstable substance which inhibited platelet aggregation in vitro and had the same characteristics as prostacyclin.

  2. Prostacyclin inhibited adenosine diphosphate (ADP)-induced aggregation of hamster platelets in vitro.

  3. The effects of prostacyclin on ADP-induced platelet thrombi in the microcirculation of the hamster cheek pouch were studied with a television microscope.

  4. Prostacyclin caused a dose-dependent increase in the time of iontophoretic application of ADP which was required to induce platelet thrombi formation and embolization in venules (30 to 40 μm diameter).

  5. Prostacyclin caused a dose-dependent reduction in the total time during which ADP-induced thrombi were observed following local electrical damage to arterioles (40 to 80 μm diameter).

  6. Thrombus formation in venules and arterioles was abolished by 500 ng/ml prostacyclin in the Krebs solution superfusing the hamster cheek pouch.

  7. Prostacyclin was approximately twenty times more potent than prostaglandin E1 in preventing thrombus formation in the microcirculation.

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Figures

Figure 1
Figure 1
The time in seconds of iontophoretic application of adenosine diphosphate (ADP) to venules (30 to 40 μm) necessary to induce the formation and embolization of platelet thrombi in the presence of increasing concentrations of prostacyclin (PGI2) infused into the Krebs solution superfusing the hamster cheek pouch microcirculation. Each column represents the mean of 4–8 experiments and the bars are ± 1 s.e. mean. NS, P > 0.01; *P < 0.01.
Figure 2
Figure 2
Inhibition of adenosine diphosphate (ADP)-induced thrombus formation in electrically damaged arterioles (40 to 80 μm) by increasing concentrations of prostacyclin (PGI2) infused into the Krebs solution superfusing the hamster cheek pouch microcirculation. Inhibition is measured as a reduction in total thrombus time (see text) compared with control values. Each point is the mean of 4–7 experiments and the bars represent ± 1 s.e. mean. The straight line was fitted to the log dose-response curve by regression analysis. There is a highly significant linear regression (P > 0.001) and there is no significant deviation from linearity. NS, P > 0.01; *P < 0.0025, **P < 0.0005.
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References

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    1. Begent NA, Born GVR, Sharp DE. The initiation of platelet thrombi in normal venules and its acceleration by histamine. J. Physiol. 1972;223:229–242. - PMC - PubMed
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    1. Duling BR, Berne RM, Born GVR. Microiontophoretic application of vasoactive agents to the micro-circulation of the hamster cheek pouch. Microvascular Res. 1968;1:158–173.
    1. Emmons PR, Hampton JR, Harrison MJC, Honour AJ, Mitchell JRA. Effect of prostaglandin E1 on platelet behaviour in vitro and in vivo. Br. med. J. 1967;ii:468–472. - PMC - PubMed

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