Harris S N, Rinder C S, Rinder H M, Tracey J B, Smith B R, Hines R
Department of Anesthesiology, Yale University School of Medicine, New Haven, Connecticut 06520-8051, USA.
Anesthesiology. 1995 Dec;83(6):1145-52. doi: 10.1097/00000542-199512000-00003.
The time course and reversibility of sodium nitroprusside's in vivo inhibition of platelet function are unclear.
Platelet aggregation and P-selectin expression as measures of platelet dense and alpha-granule release, respectively, were examined before and after administration of sodium nitroprusside (18 mg) to human volunteers and in in vitro studies. Hypotension occurring with sodium nitroprusside administration was treated with intravenous crystalloid and/or phenylephrine.
Compared with preinfusion studies, platelet aggregation to epinephrine was significantly inhibited immediately and 4 min after discontinuation of the sodium nitroprusside infusion but returned to baseline at 8 and 12 min after discontinuing sodium nitroprusside. However, both dense and alpha-granule release to adenosine diphosphate after in vivo sodium nitroprusside were never significantly inhibited even at the time when sodium nitroprusside infusion was maximal. In contrast to our in vivo findings, in vitro incubation of platelet-rich plasma with sodium nitroprusside resulted in significant inhibition of dense and alpha-granule release to adenosine diphosphate. These in vitro inhibitory effects of sodium nitroprusside were reversed by pretreatment with epinephrine but not phenylephrine.
In normal volunteers, sodium nitroprusside inhibits platelet aggregation to epinephrine but not adenosine diphosphate; inhibition was reversed within 8-12 min after discontinuing sodium nitroprusside. Sodium nitroprusside in vitro inhibition of platelet function to adenosine diphosphate was reversed by epinephrine pretreatment. Because of the rapid reversibility of its antiplatelet effect, sodium nitroprusside may be clinically useful even when there is the potential for impaired coagulation.
硝普钠在体内对血小板功能的抑制作用的时间进程和可逆性尚不清楚。
分别以血小板聚集和P-选择素表达作为血小板致密颗粒和α颗粒释放的指标，在给人类志愿者输注硝普钠（18mg）前后以及体外研究中进行检测。输注硝普钠时出现的低血压用静脉晶体液和/或去氧肾上腺素治疗。
与输注前研究相比，输注硝普钠后立即及停药4分钟时，血小板对肾上腺素的聚集显著受抑制，但在停用硝普钠后8分钟和12分钟时恢复至基线水平。然而，即使在硝普钠输注量最大时，体内给予硝普钠后血小板对二磷酸腺苷的致密颗粒和α颗粒释放从未受到显著抑制。与我们的体内研究结果相反，富含血小板血浆与硝普钠进行体外孵育导致血小板对二磷酸腺苷的致密颗粒和α颗粒释放受到显著抑制。硝普钠的这些体外抑制作用可通过肾上腺素预处理而逆转，但不能通过去氧肾上腺素预处理逆转。
在正常志愿者中，硝普钠抑制血小板对肾上腺素的聚集，但不抑制对二磷酸腺苷的聚集；停药后8 - 12分钟内抑制作用逆转。肾上腺素预处理可逆转硝普钠在体外对血小板对二磷酸腺苷功能的抑制作用。由于其抗血小板作用的快速可逆性，即使存在凝血功能受损的可能性，硝普钠在临床上可能仍有用处。
