Schmidt M, Kretschmann B, Schuster R, Honig A
Institute of Physiology, Ernst-Moritz-Arndt University of Greifswald.
Biomed Biochim Acta. 1990;49(10):1067-80.
The reactions of renal hemodynamics, as well as of excretory and concentrating function (clearance-technique) in response to arterial chemoreceptor stimulation by almitrine bismesylate were studied in 3 groups of chloralosed, relaxed, and constantly ventilated cats. In 2 groups of chemoreceptor-intact animals an osmotic diuresis was induced by intravenous infusion of an isoionic solution containing equivalent amounts of either sorbitol or mannitol. Under similar conditions the 3rd series of experiments was carried out in cats under mannitol diuresis but with deafferented arterial chemoreceptors. The changes of mean arterial and central venous pressures as well as of the parameters of the arterial acid-base balance were similar in all groups of cats studied. The chemoreceptor-intact animals undergoing sorbitol diuresis did not show any natriuresis in response to the drug but reacted with a remarkable increase in their U/Posm and TCH2O/Cosm ratios. In contrast, the chemoreceptor-intact animals infused with mannitol in saline reacted to almitrine with a transient natriuresis but with only a weak increase in their U/Posm and TCH2O/Cosm ratios. The data suggest that arterial chemoreceptor stimulation inhibits proximal tubular sodium reabsorption. In the sorbitol-experiments during chemoreceptor stimulation the enhanced delivery of sodium by the proximal fluid was reabsorbed in the thick ascending limb of Henle's loop thus increasing medullary osmolality and renal concentrating ability. Mannitol apparently limited this additional sodium reabsorption in the thick ascending limb of Henle's loop; therefore in the mannitol-experiments during chemoreceptor stimulation a natriuresis but only relatively weak changes of renal concentrating function occurred. The data also suggest that a pharmacological chemoreceptor stimulation might support the recovery of renal excretory function post-anaesthetically, although the optimal solution infused to induce an osmotic diuresis remains to be determined.
在三组用氯醛糖麻醉、处于松弛状态且持续通气的猫身上,研究了二甲磺酸烯丙苯哌嗪对动脉化学感受器刺激所产生的肾血流动力学反应以及排泄和浓缩功能(清除技术)的反应。在两组化学感受器完整的动物中,通过静脉输注含有等量山梨醇或甘露醇的等渗溶液诱导渗透性利尿。在类似条件下,对处于甘露醇利尿状态但动脉化学感受器去传入神经的猫进行了第三系列实验。在所有研究的猫组中,平均动脉压和中心静脉压的变化以及动脉酸碱平衡参数的变化相似。进行山梨醇利尿的化学感受器完整的动物对该药物未表现出任何利钠作用,但U/Posm和TCH2O/Cosm比值显著增加。相比之下,在盐水中输注甘露醇的化学感受器完整的动物对烯丙苯哌嗪的反应是短暂利钠,但U/Posm和TCH2O/Cosm比值仅微弱增加。数据表明,动脉化学感受器刺激会抑制近端肾小管钠重吸收。在化学感受器刺激期间的山梨醇实验中,近端液体增强的钠输送在亨氏袢升支粗段被重吸收,从而增加了髓质渗透压和肾浓缩能力。甘露醇显然限制了亨氏袢升支粗段这种额外的钠重吸收;因此,在化学感受器刺激期间的甘露醇实验中,出现了利钠作用,但肾浓缩功能仅发生相对较弱的变化。数据还表明,药理学上的化学感受器刺激可能有助于麻醉后肾排泄功能的恢复,尽管用于诱导渗透性利尿的最佳输注溶液仍有待确定。