Kjeldsen S E, Weder A B, Egan B, Neubig R, Zweifler A J, Julius S
Department of Internal Medicine, Ullevaal University Hospital, Oslo, Norway.
Hypertension. 1995 May;25(5):1096-105. doi: 10.1161/01.hyp.25.5.1096.
We investigated the effect of raising arterial plasma epinephrine within the lower pathophysiological concentration range on various indicators of blood platelet function and hematocrit. Epinephrine was raised over 60 minutes by a stepwise increasing intravenous infusion in 40 healthy men aged 20 to 40 years. Platelet count increased progressively with increasing arterial epinephrine to a maximal change of 69 +/- 6 x 10(9)/L in EDTA-anticoagulated blood and a maximal change of 42 +/- 6 x 10(9)/L in acid-citrate-dextrose (ACD)-anticoagulated blood, and the weight of circulating platelets increased by 29% (P < .001). Platelet size increased significantly in EDTA and decreased in ACD, and the difference between EDTA and ACD was significant (P < .0001) for both count and size, suggesting that epinephrine not only recruits platelets into the circulation but also induces some microaggregation in vivo or adhesion ex vivo. Aggregation of platelets in vitro induced by epinephrine decreased (P < .003 for delta optical density and P = .038 for maximal optical density) after epinephrine infusion compared with saline but did not change when stimulated with ADP or collagen. These findings suggest a selective downregulation of the epinephrine-activating mechanisms concomitant with a rise in the platelet content of epinephrine by 81% (P < .001) and no change in the platelet sodium-proton membrane exchange. The release of granular content (beta-thromboglobulin and platelet factor 4) to the circulation in response to epinephrine was not significant. Thus, under acute conditions it seems that the platelets may protect themselves against inappropriate overstimulation by epinephrine. The importance of platelet epinephrine uptake is still unknown, but sodium-proton exchange does not seem to be involved in regulating the effects of circulating epinephrine on platelet function. Epinephrine has a pronounced effect on raising hematocrit (maximal change of 1.74 +/- 0.13 x 10(-2), P < .0001).
我们研究了在较低病理生理浓度范围内提高动脉血浆肾上腺素对血小板功能和血细胞比容各项指标的影响。通过逐步增加静脉输注肾上腺素60分钟,对40名年龄在20至40岁的健康男性进行了研究。随着动脉肾上腺素水平的升高,血小板计数逐渐增加,在乙二胺四乙酸(EDTA)抗凝血液中最大变化为69±6×10⁹/L,在枸橼酸-葡萄糖-酸(ACD)抗凝血液中最大变化为42±6×10⁹/L,循环血小板重量增加了29%(P<.001)。血小板大小在EDTA抗凝时显著增加,在ACD抗凝时减小,且在计数和大小方面,EDTA与ACD之间的差异均具有显著性(P<.0001),这表明肾上腺素不仅能使血小板进入循环,还能在体内诱导一定程度的微聚集或在体外诱导黏附。与输注生理盐水相比,肾上腺素输注后肾上腺素诱导的体外血小板聚集降低(光密度变化ΔP<.003,最大光密度P=.038),但在用二磷酸腺苷(ADP)或胶原刺激时无变化。这些发现表明,随着血小板中肾上腺素含量升高81%(P<.001),肾上腺素激活机制出现选择性下调,且血小板钠-质子膜交换无变化。肾上腺素刺激后颗粒内容物(β-血小板球蛋白和血小板因子4)向循环中的释放不显著。因此,在急性情况下,血小板似乎可以保护自身免受肾上腺素不适当的过度刺激。血小板摄取肾上腺素的重要性尚不清楚,但钠-质子交换似乎不参与调节循环肾上腺素对血小板功能的影响。肾上腺素对提高血细胞比容有显著作用(最大变化为1.74±0.13×10⁻²,P<.0001)。