Key result
In isolated rabbit ear arterial preparations, prostaglandin I2 slightly enhanced vasoconstrictor responses to adrenergic stimulation, while sympathetic nerve stimulation significantly reduced effluent levels of its metabolite 6-keto-PGF1α (p<0.01).
In rabbit ear perfused arterial preparations, PGI2 acts as a weak vasoconstrictor and its levels decrease following sympathetic nerve stimulation, suggesting potential endothelial damage by adrenergic transmitters.
PGI2 may weakly enhance adrenergic vasoconstriction in rabbit arteries; leaves open relevance to human endothelial function.
In the present study, the effects of prostaglandin I2 (PGI2) on the vasoconstrictor response to adrenergic nerve relating agents was examined using the perfused arterial preparations, i.e., the isolated perfused central artery of a rabbit ear and its perfused arterial segment. The following results were obtained.1. PGI2, 3.0 to 9.0ng/m/, slightly enhanced not only the vasoconstrictor response to electrical stimulation of the perivascular sympathetic nerve (VSNS), and that to the exogenously applied noradrenaline, but also the noradrenaline-induced contracture.2. In the experiment examining the effect of VSNS on 6-keto-PGF1α, a main metabolite of PGI2, levels in the effluent perfusate, it was clarified that 6-keto-PGF1α levels following VSNS were lower than those before VSNS.These results seem to suggest that PGI2 is a weak vasoconstrictor in a rabbit ear and the endothelium of vascular wall would be inclined to be damaged by the mobilization of an adrenergic nerve transmitter.
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T Michibayashi (1984) studied Healthy animal model (isolated arterial preparations). Prostaglandin I2 (PGI2) and perivascular sympathetic nerve stimulation (VSNS) vs. Baseline/Control was evaluated on 6-keto-PGF1α levels in effluent perfusate before and after VSNS (p=<0.01). In isolated rabbit ear arterial preparations, prostaglandin I2 slightly enhanced vasoconstrictor responses to adrenergic stimulation, while sympathetic nerve stimulation significantly reduced effluent levels of its metabolite 6-keto-PGF1α (p<0.01).
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