To assess the effect of prostaglandins and endothelium-derived relaxing factor (EDRF) on diaphragmatic microcirculation under basal conditions and after acetylcholine (ACh) stimulation, we studied a diaphragmatic preparation in anesthetized rats. With bicarbonate-buffered Ringer's solution suffusing the abdominal surface of the left costal diaphragm, laser-Doppler flowmetry was used to record microvascular blood flow (Q(LDF)). Microvascular conductance (C(LDF)) was derived from Q(LDF) by dividing by the systemic blood pressure. Drugs were applied to the surface of the diaphragm. Four series of experiments were performed. In Series 1 (n = 9), ACh (3 x 10-5-10-3 mol/L) elicited a concentration-dependent increase in Q(LDF) and C(LDF). In Series 2 (n = 11), ACh-induced Q(LDF) and C(LDF) changes were significantly attenuated after 30 minutes suffusion of indomethacin (10-5 mol/L), although baseline Q(LDF) and C(LDF) were little affected. In Series 3 (n = 7), following suffusion of N(ω)-nitro-L-arginine methyl ester (L-NAME) (10-4 mol/L) for 30 minutes, there was no change in baseline Q(LDF) and C(LDF). The ACh-induced Q(LDF) change was abolished, while there was still a slight increase in C(LDF) (172 ± 26%) at high concentrations of ACh (10-3 mol/L). In Series 4 (n = 5), co-administration of indomethacin (10-5 mol/L) and L-NAME (10-4 mol/L) for 30 minutes did not completely prevent the increase in C(LDF) (143 ± 13%) induced by high concentrations of ACh (10-5 mol/L). The data suggest low basal activities of both vasodilatory prostaglandins and EDRF in diaphragmatic microvascular beds of the anesthetized rat, while both mediators independently modulate microvascular response to ACh. Also, certain non-prostanoid, non-EDRF vasodilators probably play a role in this preparation only when exposed to high concentration of ACh.
|Number of pages||9|
|Journal||Journal of the Formosan Medical Association|
|Publication status||Published - 1995 Jan 1|
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