Haugan A, Kirkebø A
Circ Shock. 1986;20(1):13-23.
Intermittent patchy ischemia in the renal cortex during traumatic shock has previously been observed in dogs and rats. In recent experiments on rats a high rate of abrupt changes in local blood flow was observed after scalding. To try to reveal endogenous factors causing such ischemic episodes, we scalded six series of anesthetized rats (50% of body surface for 30 s in 80 degrees C water) and measured arterial pressure (AP), hematocrit (Hct), and local renal cortical blood flow (RCF). RCF was recorded by the local H2 washout technique. After scalding, RCF decreased markedly in all series whereas AP was relatively well preserved. In accordance with previous experiments, 11% of the washout curves recorded 0-75 min after scalding showed abrupt changes in local blood flow, rising to 27% during the next 60 min in drug-untreated rats. In contrast, blocking of serotonin S2 receptors with Ketanserin abolished the phenomenon. However, in rats treated with the prostaglandin synthesis blockers, indomethacin (general) or 3-ethyl pyridin (thromboxane A2 blocker), the phenomenon was observed in only 2-3% of the washout curves. Furthermore, after blocking the AngII receptors by saralasin or alpha receptors by phentolamine in separate series, the frequency of abrupt flow shifts was reduced in comparison to the frequency in untreated rats. The results indicate that intermittent, patchy vasoconstriction is mediated by serotonin and thromboxane A2 (TxA2), probably released from platelets. The occurrence of ischemic episodes also depends on the local AngII and alpha-adrenergic tonus present after scalding.
此前在犬类和大鼠身上观察到，创伤性休克期间肾皮质存在间歇性片状缺血。在最近对大鼠进行的实验中，烫伤后观察到局部血流出现高频率的突然变化。为了试图揭示导致此类缺血发作的内源性因素，我们对六组麻醉大鼠进行了烫伤（在80摄氏度水中烫伤体表的50%，持续30秒），并测量了动脉血压（AP）、血细胞比容（Hct）和局部肾皮质血流（RCF）。RCF通过局部氢气洗脱技术记录。烫伤后，所有组的RCF均显著下降，而AP相对保持良好。与先前的实验一致，烫伤后0 - 75分钟记录的洗脱曲线中，11%显示局部血流突然变化，在接下来的60分钟内，未用药大鼠中这一比例升至27%。相比之下，用酮色林阻断5-羟色胺S2受体可消除该现象。然而，在用前列腺素合成阻滞剂吲哚美辛（全身性）或3-乙基吡啶（血栓素A2阻滞剂）治疗的大鼠中，仅2 - 3%的洗脱曲线出现该现象。此外，在单独的系列实验中，用沙拉新阻断血管紧张素II受体或用酚妥拉明阻断α受体后，与未治疗大鼠相比，血流突然变化的频率降低。结果表明，间歇性、片状血管收缩由5-羟色胺和血栓素A2（TxA2）介导，可能由血小板释放。缺血发作的发生还取决于烫伤后局部存在的血管紧张素II和α-肾上腺素能张力。
