Klee A, Vater S, Schmid-Schönbein G W, Seiffge D
Hoechst AG, Werk Kalle-Albert, Wiesbaden, Germany.
Stroke. 1993 Oct;24(10):1528-33. doi: 10.1161/01.str.24.10.1528.
Platelet behavior of Sprague Dawley (SD), Wistar (WI), Wistar-Kyoto (WKY), spontaneously hypertensive (SHR), and stroke-prone spontaneously hypertensive rats (SHRSP) was studied in vivo to evaluate the importance of hypertension-related hemostatic disorders.
The study was based on the model of stimulus-induced pulmonary microembolization of labeled platelets. After injection of 51Cr-labeled homologous platelets into urethane-anesthetized rats, the organ distribution of the platelets was continuously monitored by gamma detectors. Count rates of two detectors--one placed above the animals' thoraxes (C1), the other above their abdomens (C2)-and the ratio of C1:C2 were calculated. The following platelet activators were applied intravenously: adenosine diphosphate (ADP; 50 micrograms/kg), collagen (100 micrograms/kg), and thrombin (50 IU/kg).
All three substances caused a reversible pulmonary accumulation of the labeled platelets and hence an increase in C1/C2 (delta C1/C2%). ADP induced a shift of 75% in SD, 52% in WI, 32% in WKY, 30% in SHR, and 31% in SHRSP. Thrombin-mediated shift was 79% in SD, 64% in WI, 58% in WKY, 48% in SHR, and 54% in SHRSP. Collagen induced a shift of 85% in SD, 96% in WI, 84% in WKY, 56% in SHR, and 62% in SHRSP.
Because indistinguishable results were observed in both hypertensive strains, we conclude that impaired platelet aggregation is not specific for SHRSP. Hence, it may not primarily be responsible for the increased occurrence of stroke in these animals.
对斯普拉格-道利（SD）大鼠、Wistar（WI）大鼠、Wistar-Kyoto（WKY）大鼠、自发性高血压（SHR）大鼠及易卒中型自发性高血压（SHRSP）大鼠的血小板行为进行体内研究，以评估高血压相关止血障碍的重要性。
本研究基于标记血小板刺激诱导肺微栓塞模型。将51Cr标记的同源血小板注入经乌拉坦麻醉的大鼠体内后，用γ探测器持续监测血小板的器官分布。计算两个探测器的计数率——一个置于动物胸部上方（C1），另一个置于腹部上方（C2）——以及C1:C2的比值。静脉注射以下血小板激活剂：二磷酸腺苷（ADP；50微克/千克）、胶原（100微克/千克）和凝血酶（50国际单位/千克）。
所有三种物质均导致标记血小板在肺部可逆性积聚，从而使C1/C2升高（ΔC1/C2%）。ADP诱导的变化在SD大鼠中为75%，WI大鼠中为52%，WKY大鼠中为32%，SHR大鼠中为30%，SHRSP大鼠中为31%。凝血酶介导的变化在SD大鼠中为79%，WI大鼠中为64%，WKY大鼠中为58%，SHR大鼠中为48%，SHRSP大鼠中为54%。胶原诱导的变化在SD大鼠中为85%，WI大鼠中为96%，WKY大鼠中为84%，SHR大鼠中为56%，SHRSP大鼠中为62%。
由于在两种高血压品系中观察到的结果无差异，我们得出结论，血小板聚集受损并非SHRSP所特有。因此，它可能不是这些动物中风发生率增加的主要原因。
